Introduction to Medical Parasitology

Introduction to parasitism

2010-01-25T00:00:00.000-08:00

The world is full of organisms that interact with one another. Some of these interactions are mutually beneficial; others are harmful. Parasites are minute organisms that derive their livelihood from their interaction with other organisms, plant or animal. This interaction, however, is in the main not beneficial.

In the following pages, we shall examine parasites that affect mainly humans and, to some extent, their livestock, paying particular attention to modes of transmission, the effect on the host and the methods of control.

Significance of parasites

Parasites are dreaded organisms, for they are responsible for some of the worst disease epidemics in memory. The bacterium, Yersiania pestis, transmitted by fleas and rats, was responsible for waves of epidemics of what was then known as ‘Black Death’ that killed thousands of people in the Middle East and Europe between the 6^th and 18^th centuries. Although human plague flare-ups do occur today in some parts of the world, including the African continent, its transmission is mainly sylvatic.

At the dawn of the 20^th century, East and Central Africa were attacked by hitherto unknown epidemic of sleeping sickness during which more than a half a million people lost their lives. Human trypanosomiasis and nagana, its cattle variant, have much to do with Africa’s current economic underdevelopment.

And then there is malaria, one of the worst scourges of man that continues to kill 1-2 million people every year, the majority being African children.

Parasites affect us in many other ways. They not only sap our energies making us weak and unable to work, they are the cause of poverty and hunger. They are responsible for school absenteeism and poor academic performance. They eat our food or make us incapable of utilizing the food we eat, causing physical and mental retardation.

Some human parasites, such as plasmodia and hookworms feed on blood and cause anaemia. Parasites may also cause mechanical damage to host tissues through which they pass during their migratory stages, or lead to the formation of calcified tissue and even cancerous tissue. The thread-like filarial worms that invade the lymphatic system are responsible for elephantiasis and hydrocoele, some of the worst deformations of the human figure. Espundia, a leishmanial parasite found in the jungles of Central and South America, can erode the whole nasopharyngeal region of its victims, turning them into social rejects.

Since parasites impact on our lives daily, it is important that we understand what they are and how they operate if we are to find solutions to their harmful effects. In designing control measures one must take into account those parasite factors that are crucial to its survival, more particularly its transmission pattern, biotic potential and the nature of its interaction with the host.

Control

Control should aim at reducing morbidity and mortality in the population. As their immune systems are underdeveloped, children should always be given special consideration. Ultimately, control should aim at interrupting transmission and eliminating parasites from the population.

The vehicles of transmission are generally arthropods and mammalian animal reservoirs, some fishes and man. Control of arthropods involves the larval stages as well as the adults. In mosquito control, for example, the aim should be to deny the mosquitoes suitable breeding sites so that they have nowhere to lay their eggs. To do this potholes are filled up with soil, man-made receptacles of any kind that can collect water, such as broken bottles, tins, and used car tyres must be destroyed. There should be a proper drainage system so that flowing water in the sewers and streams passing through human living quarters is not obstructed.

Mosquito larvae are destroyed by chemical larvicides. A cheaper alternative is use of used motor oils that block larval gills causing them to suffocate for lack of oxygen.

Adult mosquitoes can be killed by spraying the walls of occupied houses with an insecticide that has long residual effect. This is necessary because most of the mosquitoes that transmit malaria rest on the walls after feeding. Using insecticide impregnated nets is an effective way of avoiding mosquito bites at night.

Man participates in the transmission of a number of parasites and a change in human behaviour and attitudes would go a long way in ridding the community of such parasites. For example, Ascaris, Trichuris and Enterobius enter our bodies through ingestion of food or fluids contaminated with human faeces that contain parasite eggs. To avoid contracting these parasites, requires proper disposal of human faeces and maintaining personal hygiene. Other parasites like Trichinella, T. saginata and T. solium, are acquired by eating undercooked animal products and by cooking these properly before they are consumed the infections can be avoided. The elimination of these parasites is not as simple as it sounds because human behaviours and attitudes are usually so ingrained that it may require years of persuasion to change them. Nevertheless, patience, sustained health education campaigns, at times backed by bye-laws, should yield results.

Role of zoonosis

Control measures may be handicapped by the involvement of domestic and wild animals in the transmission of a parasite. A disease that naturally exists in other animals but that can also infect humans is known as a zoonosis. Some of the most important parasitic zoonoses include trypanosomiases, leishmaniases, echinococcosis and trichinosis. The animals that harbour the infective agent in each of these diseases are known as reservoirs or carriers of infection and are constant sources of infection to humans. Transmission of infection from the reservoir to man may involve a vector, such as a tsetse fly, or consumption of meat from an infected reservoir host as in trichinosis and hydatidosis.

The significance of zoonosis is that the reservoir animal does not usually suffer any clinical disease from the parasite it harbours. The reservoir animal can retain the infection for a long time, while transmitting it to other susceptible animals and humans. Furthermore, wild animals can move widely over a short period of time, either to escape predators or in search of water and food. During social upheavals, animals may be hunted and forced to flee their normal habitats. These movements may create new foci of infection away from its traditional focus.

Attempts to control zoonotic diseases have often met with financial and logistical difficulties. The wanton destruction of reservoir animals associated with disease would not only require enormous infusion of funds and time but would likely be abandoned because of strong opposition from ecologists and environmentalists. However, in some countries, notably

Iceland

New Zealand

and Tasmania, the elimination of stray dogs and the strict control on the slaughter of sheep and cattle have been very successful in controlling hydatidosis. In fact,

Iceland

is now virtually free from hydatidosis primarily because the restrictions on keeping dogs have been extremely stringent.

Role of local population in control activities

There is currently a tendency to rely too much on chemotherapy in the control of parasitic diseases, with very little effort or, none at all, being given to basic sanitation and hygiene. Treatment of infected persons, destruction of vectors and environmental sanitation should constitute a control package. While it is important to provide treatment to infected persons, it should not be forgotten that most of the parasitic infections can be avoided by observing basic sanitary and environmental rules.

The involvement of the local people in disease control activities enables them to have a clear view of the dynamics involved and what role, if any, their own actions may be contributing to the persistence and intensification of infection in their respective areas. The people who are affected by disease are usually passive observers rather than active participants in control programs. This has resulted in meaningless control programs that do not last once the sources of funds dry up.

The impregnation of the nets with insecticides for malaria control, or the making of tsetsefly traps for control of trypanosomiasis are activities that should be undertaken by those who live in the endemic areas with minimum cost. The materials needed and the expertise involved are not beyond their reach.

Malaria

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Malaria is one of the most important parasitic diseases of man. It has a wide distribution in Africa, Asia, the Middle East, Central and South America, the Caribbean and the Pacific Islands. The malaria agent, Plasmodium, is a protozoan parasite that is transmitted by female Anopheles mosquitoes. Four species of Plasmodium are parasites of man, namely Plasmodium vivax, P. falciparum, P. malariae and P. ovale. P. vivax accounts for about 40% of the world’s malaria cases and 5 – 10 % of the malaria cases in East Africa.

Plasmodium falciparum is the most virulent of the malaria parasites and is often fatal. It contributes up to 50% of all the malaria cases in the world and more than 90% of malaria cases encountered in East Africa. Both P. malariae and P. ovale have a low prevalence, accounting for less than 10% of the world’s malaria cases.

The number of people at risk of contracting malaria in the world is estimated at two billion. Of these 270 million are infected while the number of those showing clinical symptoms is around 110 million. The annual mortality is around 1-2 million, mainly among children under five years of age. The majority of these children are found in the sub-Saharan Africa.

The socioeconomic aspects of malaria are significant. In the endemic areas, morbidity is high, rendering a large section of the population economically unproductive. Constant malaria attacks sap the energies of the population and adversely affect its economic productivity Mortality among the vulnerable groups can be frighteningly high.

Money, which is usually scarce, is spent on treatment and on provisions needed to nurse the sick at the expense of other pressing needs. If the breadwinner is sick, the family goes hungry. Absenteeism due to sickness becomes a problem and the children so affected perform badly in school.

Life cycle

Female Anopheles mosquitoes transmit malaria. There are many species of Anopheles involved depending on the region. Anopheles gambiae complex and Anopheles funestus are the main transmitters in Africa. A. gambiae is a particularly an effective transmitter of malaria. It has a wide range of breeding sites such as temporary ponds, potholes, plant leaves, discarded motor tyres, and cans. Under warm, wet conditions, the entire life cycle can take less than two weeks.

Malaria life cycle involves female Anopheles mosquito and man

Mosquitoes become infected when they suck blood from people who carry gametocytes. The gametocytes are the sex forms of the malaria parasites. When the mosquito ingests blood that contains gametocytes, the latter mature in the mosquito’s midgut into microgametes and macrogametes. The microgamete behaves as a sperm cell, the macrogamete as an ovum. The microgametes are flagellated and are formed by a process known as exflagellation. Exflagellation involves the male leaving the host erythrocyte and extruding about eight microgametes, each resembling a long flagellum. After a few minutes, each of these flagellated microgametes swims about and seeks a female gamete. The process of exflagellation is usually completed within ten to fifteen minutes and is immediately followed by fertilisation.

The zygote formed is active and is known as ookinete. The ookinete, a somewhat elongated and worm-like organism penetrates the insect’s gut wall and grows by a form of nuclear division known as schizogony. About three to four weeks later, a sporocyst, which is a kind of a sac that contains thousands of sporozoites, is formed. Later the sporocyst ruptures and releases spindle shaped sporozoites. Released sporozoites migrate to the salivary glands where they will be transferred to a host when the mosquito takes another blood meal.

Exoerythrocytic stage

when an infected mosquito bites, it introduces its saliva together with the sporozoites into the victim’s blood. the saliva contains a coagulant that prevents the blood from clotting so that it does not block the fine proboscis tube. after inoculation, the sporozoites circulate in the blood stream for period of 30 minutes before disappearing within the liver parenchymal cells. once inside the liver, the parasites undergo division and change into schizonts. the schizonts absorb nutrients from the liver cells, become greatly enlarged, and 7 to 8 days after infection, thousands of merozoites appear. this hepatic phase is known as the exoerythrocytic stage.

A stained blood smear shows ,among others, ring forms (1) and gametocytes (2)

Erythrocytic stage

The merozoites spill over into the blood circulatory system, invade the red blood cells and transform into trophozoites. The erythrocytic stage starts with the attachment and penetration of the red blood cells by the merozoites.

each trophozoite is a minute blob of chromatin and a little cytoplasm, which assumes a ring form. stained with giemsa the chromatin appears red and the cytoplasm blue. the young ringlets grow and, in the case of p. vivax, increasingly exhibit amoeboid activity. eventually the parasite rounds up and forms a schizont.

The erythrocytic merozoites feed by ingesting haemoglobin, accumulating malaria pigment as they grow. The chromatin divides by schizogony or segmentation until the chromatin mass is too large for the cell, which ruptures releasing thousands of merozoites into the blood stream. Each erythrocytic cycle in P. vivax, P. falciparum, and P. ovale takes 36 – 48 hrs while that of P. malariae is synchronised at 72 hrs. Some of the merozoites that enter the red blood cells develop into gametocytes. Gametocytes develop only in the vertebrate host.

All the merozoites of P. falciparum leave the liver and enter the blood circulation unlike those of the other species, particularly P. vivax and P. ovale that leave some parasites in the liver cells in a dormant state for months, or even years and give rise to relapsing malaria attacks. .

Because of the risk of relapsing malaria, some countries do not allow travellers to malarious areas to donate blood for up to three years after returning home.

Pathogenesis

The pathogenicity of malaria is related to the erythrocytic infection. The plasmodia in red blood cells grow and segment at the expense of the host’s cells. As the number of parasites increases, with each successive schizogony, the number of erythrocytes decreases due to rupture of the parasitised cells and lysis of nonparasitised cells. As the number of invaded red blood cells increases and the asexual cycles of the parasites become more synchronised, characteristic chills and fever associated with malaria attack appear. The speed with which symptoms develop depends on the species of Plasmodium and on the host’s immune reaction.

P. falciparum is the cause of most of the fatalities associated with malaria. It invades erythrocytes of all ages and is thus capable of producing very high parasiteamias. It has a schizogonic cycle that is not more than 48 hours but frequently less synchronised. Moreover, in P. falciparum infections there is a tendency for more than one parasite, frequently several, to develop in a single red blood cell. Thus in two or more asexual cycles, the number of infected red cells frequently reaches a dangerous threshold, often before the usual symptoms such as fever and chills become apparent.

In addition, erythrocytes containing P. falciparum parasites tend to adhere to one another and to the lining of blood vessels, causing blockage of blood capillaries in vital areas such as the brain, lungs and kidneys, while toxic products interfere with oxygen utilisation by the host cells.

Destruction of the red corpuscles by the parasites leads to anaemia. In pernicious or serious malaria, destruction and agglutination of the parasitised red blood cells may reduce the number of the erythrocytes to a fifth of the normal. This progressive decrease in the number and quantity of circulating erythrocytes, with corresponding reduction in oxygen transport, causing oxygen starvation of the tissues, is followed by multiple thromboses in the smaller blood vessels and progressive decrease in circulating blood volume.

The placenta has a heavy concentration of plasmodia in all stages of development in the maternal blood sinuses. The spleen and liver are characteristically enlarged in malaria infections.

Symptoms

The symptoms of malaria start as flu usually 8 to 30 days after being inoculated with parasites by an infected mosquito. They are characterised by cycles of fever, shaking, chills and sweating. The symptoms may subside. The frequency of the symptoms depends on the species of malaria parasite involved. In P. vivax, P. ovale and P. falciparum, they appear every 2 days, whereas in P. malariae, they occur every 3 days.

The periodicity of the symptoms coincides with the destruction of the red blood cells and the release of haemoglobin and other substances, some of which are probably poisonous. The pathogenesis of malaria is therefore related to the destruction of the red blood cells and the effect of the debris of the ruptured cells and metabolic products released into the circulation. P. vivax and P. ovale tend to invade young red blood cells while P. malariae seems to prefer older red blood cells. P. falciparum, on the other hand, infects red blood cells of all ages. As a result, this species produces the most severe malaria and accounts for a large proportion of the fatalities associated with malaria.

The incubation period is usually 8 to 15 days. Symptoms due to P. falciparum are associated with chills, shivering, high fever and profuse sweating. Other symptoms include headache, bone and muscular pains, malaise, anxiety, mental confusion and even delirium. Leucopoenia and severe anaemia are common. Blood examination shows the predominance of ring stages and gametocytes.

As the infection progresses, the symptoms intensify. The hyperpyrexia or high fever may appear, characterised by hot, dry, pale skin covered with sticky sweat. The skin feels cold but the temperature may be as high as 39 ^oC. Other signs include vomiting diarrhoea, low blood pressure and oedema.

Cerebral Malaria

Cerebral malaria is an acute disease of the brain, which is accompanied by fever, convulsions and paralysis or coma. It is due to the sequestration of brain capillaries and venues with parasitised red blood cells and nonparasitised red blood cells.

Cerebral malaria is more frequent in children under nine years of age and visitors as well as immigrants from nonmalarious areas. Therefore, any cases of mental symptoms in endemic areas should arouse suspicion of malaria first until it has been excluded.

It is only associated with infections that are caused by P. falciparum which appear to cause the membranes of infected red blood cells to become sticky, causing them to stick to and obstruct the small blood vessels of the brain. Ring-like lesions in the brain are a common characteristic of cerebral malaria.

Sickle Cell Anaemia

Common inherited blood disorder is sickle cell anaemia that is caused by the presence of abnormal haemoglobin in the red blood cells. The sickle cell trait is due to a defective gene on the haemoglobin molecule that is inherited as a recessive gene. People who inherit both recessive genes from their parents suffer from sickle cell anaemia but those who inherit one normal gene from one parent and one abnormal gene from the other parent are free from sickle cell anaemia. They are, however, carriers of the sickle cell trait. Those people who inherit only a normal gene from each of their parents are completely free from sickle cell anaemia.

The carriers of the sickle cell trait are protected from attacks of P. falciparum and this has been recognised for a long time among the African Americans and immigrants from the Middle East to North America who must have carried the protective gene with them from their malaria endemic native lands.

European immigrants to

America

and American Indians are not protected against falciparum malaria. The reason for this is not clear but the sickle cell may be deficient in nutritional factors needed to nourish the malaria parasite, in addition to being a poor oxygen carrier.

Endemicity

Endemicity of malaria refers to the degree of prevalence, as regards frequency and intensity, of malaria infection in the natural population in an area. However, if malaria is endemic in an area it means it is always present in that area, perhaps in slowly varying degrees of incidence and intensity , but often to a degree that is measurable in terms of morbidity or splenomegaly.

An epidemic of malaria is caused by a rapid increase in morbidity and mortality in the population. Epidemics occur when there have been increases in incidence and prevalence of cases of malaria, which may have been caused by climatic changes, disasters such as floods, or other human factors.

In endemic areas where malaria rates remain high and relatively stable throughout the year, most people have developed immunity and many have become asymptomatic carriers. This explains why in endemic areas the number of infected people is always greater than the number of people showing clinical symptoms. This may indicate that the population has developed immunity that suppresses parasite multiplication in the blood so that the infection is not heavy enough to generate symptoms of malaria.

However, vulnerable groups like the young children still carry high parasiteamias and suffer from severe attacks of malaria frequently. These groups need to be given particular attention, just as the same attention should be extended to pregnant mothers, visitors and migrant workers who come from nonmalarious areas.

Highland areas sometimes experience a typical form of malaria that is unstable and characterized by epidemic conditions. Under normal climatic conditions, the temperatures are usually not ideal for mosquito breeding. However, occasionally the seasons may become quite warm and wet, resulting in a substantial increase in mosquito numbers within a relatively short time. This is followed by an equally abrupt outbreak of malaria of epidemic proportions. Highland malaria is highly dangerous because it affects people who have very little immunity or none at all and can lead to many deaths before it is checked.

Diagnosis

Routine diagnosis of malaria involves taking thick and thin blood smears, and staining them with Giemsa stain. The stained smears show the presence of different forms of malaria parasites, such as merozoites (ring forms), schizonts and gametocytes. The erythrocytic forms of the various species of the malaria parasite have certain characteristics that distinguish them from one another.

P. Falciparum is characterised by ring-shaped stages (signet ring), sickle-shaped gametocytes and Maurer’s dots.

P. vivax has young ring-shaped stages, multinucleate amoeboid dividing stages with finely granular pigment. These are not present in P. falciparum. They also have the morula stage from which merozoites will arise. Infected erythrocytes show red, orange Schuffner’s stripling. P. malariae has ring form young stages that contain coarse granular yellow pigment. The multinucleated schizonts are barrel-shaped. The gametocytes are similar to those of P. vivax.

Treatment

Drugs used to treat malaria include chloroquine, quinine, fansidar (salfodoxine-pyrimethamine), mefloquine, halofantrine and artemisinin. The problem with these drugs is that all of them are threatened by the development of resistance. Although chloroquine has been the drug of choice against P. falciparum for a long time, its use is now very much hampered by resistance.

Artemisinin extracted from the Chinese plant, Artemisia annua, and melfoquine are currently used to treat multidrug resistant malaria. Proguanil, pyrimethamine and chloroguanil are usually used for prophylaxis. Unfortunately, they have a relatively long half-life and parasites easily develop resistance to these drugs. However, they show a synergistic potency when used in combination with other antimalarial drugs. For example, the antimalarial drug fansidar is made by combining two other drugs, pyrimethamine and salfodoxine.

Drug Resistance

One importance aspect of malaria management is the ease with which the malaria parasites have become resistant to the antimalarial drugs. In much of the Southeast Asia, the strains of P. falciparum have become resistant to almost all the antimalarials in use. This makes the management of malaria a tricky one, as a relentless search for new antimalarials must be kept up. The development of resistance in malaria is due to mutation and the use of subdoses to which the parasites become adapted.

Vector Control

(a) Larval control

Vector control aims at limiting the numbers of larvae and adult mosquitoes. Mosquitoes breed wherever there is standing water, such as potholes, ponds, obstructed drainage channels, discarded vehicle tyres, bushes and leaves. Therefore, the strategy should be to deny mosquitoes breeding sites. This can be done by filling up potholes with soil, getting rid of empty cans, drums, motor tyres and any water receptacles that can serve as breeding sites. Pouring oil such as used diesel on stagnant water destroys mosquito larvae. Water and sewerage drainage systems should be maintained regularly to allow unhampered flow and thus prevent mosquito breeding in them.

(b) Adult mosquito control

Although the mosquito bites habits are diverse, the majority of the mosquitoes bite indoors at night and rest on the walls and ceilings of houses after feeding. Therefore, by spraying the inner walls of houses with an insecticide with a lasting residual effect, the frequency of mosquito bites can be reduced substantially which inevitably causes a reduction in malaria transmission.

In addition, body creams containing insecticide as well as bednets impregnated with insecticides such as permethrin have been found quite effective in preventing mosquito bites as well reducing the rate of transmission and malaria attacks. Insecticide fumigants are also frequently used in homes.

The market is full of insecticides that can kill mosquitoes but their extensive use is very much constrained by environmental considerations.

Biological control has been used to control malaria with some degree of success. Fish such as guppies that breed rapidly and eat mosquito larvae are usually introduced in water tanks and other enclosed water bodies. Water-borne bacteria such as Bacillus thuringiensis and Bacillus sphaericus are used as biological control agents because they produce toxins that kill mosquito larvae. Other biological control agents that have been attempted include viruses, protozoa, fungi and nematodes.

Introduction to Protozoa

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Protozoa are unicellular eukaryotes that seem to live as parasites in all species of multicellular organisms, and some even parasitise other unicellular organisms. Some are intracellular parasites, while others live in extracellular locations such as body fluids, blood or lumen of the host animal. They phylum Protozoa is divided into four classes, of which three are important.

1. Class Mastigophora – consists of flagellates that are equipped with whip-like locomotor structures. The arrangement and number of these flagella are used in classification. Some of the flagellates are classified as plants. Indeed subclass Phytomastigina contains plant like flagellates, which have pigmented bodies called chromoplasts, or chromatophores in which photosynthesis occurs. Like other flagellates, the Phytomastigina move by one or more flagella. Some of them form colonies, thus suggesting an evolutionary trend towards multicellularity.

Subclass Zoomastigina contains animal-like flagellates. They lack chromatophores and are divided into several orders:

Order Rhizomastigida consists of flagellates that move by amoeboid movement, using pseudopodia.

Order Protomastigida is made up of simple flagellates. Included in this group is the family Trypanosomidae that includes disease-causing genera Trypanosoma, Schizotrypanum and Leishmania.

Order Polymastigida contains uninucleate and binucleate species as well as some with polynuclei. There may be as many as five to eight flagella; all must have at least three. This Order includes the family Hexamitidae, to which the intestinal flagellate Giardia, belongs

Order Trichomonadida consists of either uninucleate or multinucleate flagellates with internal rod-like axostyle and a flagella complex of 3 to 6 flagella and a prominent parabasal body. The group contains a number of parasites of man and animals, including Trichomonas vaginalis.

Order Hypermastigida consists of uninucleate flagellates with many flagella. These are symbiotic parasites of wood eating termites

Order Opalinida includes parasites of amphibians.

2. Class Sarcodina- includes free-living and parasitic amoebae of the order Amoebida. Family Endomoebidae contains the genus Amoeba that is parasitic in man. This includes Entamoeba histolytica, E. coli and E. gingivalis.

3. Class Ciliata contains ciliated organisms. The cilia are used for locomotion. Ciliates possess two kinds of nuclei - the macronucleus and the micronucleus. The macronucleus interacts with the cytoplasm in the control of metabolism and growth, while the micronucleus functions in reproduction .The only ciliate parasitic to man is Balantidium coli.

4. Class Sporozoa consists of spore-forming protozoa that are enclosed in tough membranes that are quite resistant to adverse conditions, and can be dispersed by wind and water. They also produce sporozoites that can only survive in the host. Included in this group are malaria parasites and coccidia.

African Trypanosomiasis

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The haemoflagellates are parasites of major medical and economic importance. They include Trypanosoma and Leishmania. They dwell in the blood tissues of man and animals either as extracellular or intracellular parasites and are transmitted by insects. Their contribution to human suffering in terms of morbidity and mortality is immense.

Trypanosomes are protozoan haemoflagellates that affect a variety of domestic and wild animals, as well as humans. Some types of trypanosomes cause a debilitating disease called human sleeping sickness. If not treated, human sleeping sickness is invariably fatal.

The geographical distribution of trypanosomiasis is limited by the distribution of the vector Glossina or tsetse fly. African trypanosomiasis is confined to the continent of Africa south of the Sahara, which corresponds to the distribution of the tsetse flies that serve as its vectors.

The major haemoflagellates transmitted by tsetse flies include Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense, the two species that cause human sleeping sickness, and Trypanosoma brucei, a parasite of livestock and wild game known as nagana that is morphologically identical to the human parasites. Other important trypanosome diseases transmitted by tsetse flies, are Trypanosoma congolense and Trypanosoma vivax, which are important animal parasites, responsible for serious losses in cattle, sheep and goats. Trypanosoma evansi is a parasite of camels in Africa and Asia that is transmitted mechanically by biting flies. T. vivax is a parasite of domestic animals in Africa, the West Indies, Central and South America. In Africa, it is transmitted by tsetse flies, whereas outside Africa where there are no tsetse flies, it is mechanically transmitted by horse flies, indicating that it was probably introduced in those areas from Africa.

Structure of a trypanosome

The flagellum is a thin whip-like structure that originates from a basal body that is not visible but is located close to the kinetoplast. It extends toward the anterior end of the trypanosome, hanging freely in most species. It is used for locomotion. The undulating membrane is a fold of the cell wall that extends from the body of the trypanosome to which the flagellum is attached. In addition to these major features, the trypanosomes may contain various cytoplasmic inclusions and vacuoles. These appear as small granules throughout the surface.

African Trypanosomiasis

Trypanosoma brucei is a common haemoflagellate of mammals in Africa. In domestic animals, it is usually quite virulent, causing high mortality. This parasite is probably a parent form from which both Trypanosoma gambiense and Trypanosoma rhodesiense were derived. The two human trypanosomes have separate but not distinct distribution. The distribution of T. gambiense extends from

Senegal

in West Africa all the way down to

Gabon

Central African Republic

Congo

and the Democratic Republic of Congo. There is a small focus in the West Nile region of

Uganda

, which is probably an extension from the Democratic Republic of Congo. T. rhodesiense is endemic in East Africa,

Malawi

Zimbabwe

Zambia

and

Mozambique

Many species of tsetse flies serve as vectors of trypanosomes but only six are important as vectors of sleeping sickness. These are G. palpalis, G. tachinoides, G. pallidipes, G. fuscipes, G. morsitans and G. swynnertoni. Tsetse flies prefer shade, humidity and temperatures that range from 20 ^oC to 30 ^oC. Each species, however, has slightly different requirements. G. palpalis, G. tachinoides and T. fuscipes are most often found in forest areas, which are shady and have a higher humidity. G. morsitans lives in savannah woodlands and G. pallidipes characteristically is associated with denser thickets in East Africa.

A typical Glossina habitat consists of water holes surrounded by bushes. Glossina rests in the bushes and bites both humans and livestock using the water. The flies are most active during the cool hours before noon and after three in the afternoon.

A woman draws water in a tsetse fly infested pond

Tsetse flies live for a few months under wet conditions and for 3 to 4 weeks under dry conditions. Once a fly is infected, it remains infective throughout its life.

Life cycle

Development in the tsetse fly

Trypanosomes are grouped into Salivaria and Stercoraria depending on where they undergo development within the vector’s tissues. In the Salivaria, the trypanosomes develop in the midgut and salivary glands and enter the host via the saliva. Both T. gambiense and T. rhodesiense are transmitted via the saliva.

Trypanosomes develop in the salivary glands of tsetse

In the Stercoraria, they trypanosomes are taken up in the blood stream, grow, and divide in the hindgut of the insect vector. Infection of the vertebrate host is by contamination. When the insect feeds, it defecates and the trypanosomes gain entry through the feeding site or by skin being scratched. The most important stercorarian trypanosome is T. cruzi, the causative agent of chagas disease.

The life cycles of T. rhodesiense and T. gambiense are indistinguishable. The trypomastigotes are ingested by a feeding tsetse fly. Both male and female tsetse flies are capable of transmitting infection. The parasites multiply in the fly’s midgut for 10 to 15 days during which they become greatly elongated. They then change into epimastigotes and migrate forwards to the proventriculus, where they spend several days undergoing further multiplication.

Life cycle of Trypanosoma rhodesiense. Animals, such as the bushbuck may be involved in the transmission.

The epimastigotes leave the proventriculus and proceed to the salivary glands, where they attach to the walls and continue to multiply. About 20 to 40 days post-infection, the so-called metacyclic trypanosomes or trypomastigote forms appear in the lumen of the salivary glands. The development within the fly takes at least 3 weeks.

Development in the vertebrate

The metacyclic trypomastigotes present in the fly’s salivary glands are transferred to the host’s skin when the fly takes a blood meal. They undergo multiplication within the vicinity of the inoculation site before appearing later in the vertebrate blood one to two weeks after infection. Soon after appearing in the blood stream, the trypanosomes begin to multiply by binary fission and invade all the tissues of the body via the blood and lymphatic systems.

Trypomastigotes found in the blood show morphological polymorphism characterised by long ‘slender’ and short ‘stumpy’ forms. The slender forms have a free flagellum while the stumpy forms are without a free flagellum. The proportions of stumpy and slender forms change as the infection progresses. The slender forms are usually present in large numbers in an active acute infection, whereas the stumpy forms seem to predominate in a chronic infection.

Pathogenesis

The infection occurs in two phases: the early phase and the late phase.

The early phase

A painful local swelling that resembles a boil follows the bite by a tsetse fly. The swelling is known as a chancre. Examination of the chancre shows the presence of trypomastigotes that are dividing. About 2 to 3 weeks later the chancre subsides. The lymph nodes closest to the bite site are swollen while others remain normal at this period.

The incubation period is marked by early clinical symptoms that are extremely variable, depending on the virulence of the trypanosome itself, the resistance of the individual and the presence of other infections. The symptoms may last from a few days to a few weeks, even years. The symptoms are characterized by an intermittent fever which may even disappear later but which is accompanied by headaches, loss of appetite, weakness, joint pains, pruritus (itching) and loss of weight.

Other symptoms include anaemia, cardiovascular and endocrine disorders, and enlargement of the spleen, liver and inflammation of the lymph glands. The cervical, subclavicular and inguinal lymph nodes are particularly palpable. The symptoms are easy to confuse with those of early attacks of malaria infection, or a common cold.

One of the effects of the early infection is the presence of oedema, especially of the ankles, which is due to the leakage of the small blood vessels. The involvement of the lungs at this stage is particularly important because it predisposes to secondary infections, and pneumonia, the latter being a frequent cause of death.

The late phase

As the infection progresses, the parasites cross the blood brain barrier and enter the central nervous system, heralding the second phase of the infection. The involvement of the central nervous system is confirmed by an examination of the cerebrospinal fluid (CSF). It is important to note that the second stage cases may occasionally be asymptomatic. This is a latent stage of infection when only CSF analysis will show the involvement of the central nervous system.

In the late advanced stage of infection, when the parasites are in the central nervous system, the disease takes a dramatic turn. The patient is unable to concentrate and may show moods of irritation, aggressiveness and lethargy.

An advanced case of trypanosomiasis

The patient is overcome by extreme tiredness, apathy and sleep-like unconsciousness as the infection progresses. Because he is unable to eat food, he becomes wasted and eventually falls into a deep coma and dies.

Epidemiology

Trypanosomiasis is endemic in Africa between 20^o N and 20^o S of the equator. It is widely spread throughout the equatorial belt of the continent of Africa with distinct foci where the infection persists and flares up from time to time.

Trypanosomes have rendered huge areas of the most fertile parts of the African continent unsuitable for human settlement and animal rearing. More than one fourth of the arable land in Africa is unavailable for agriculture and livestock keeping because of the high mortalities caused by human trypanosomiasis and nagana. With the exception of probably malaria, both human and animal trypanosomiasis has contributed greatly to the socioeconomic stagnation of tropical Africa.

Complex epidemiology of trypanosomiasis, involving humans, domestic and wild animals.

Reservoir hosts are a source infection to humans. Many animals act as reservoir hosts for trypanosomiasis. Trypanosomiasis is, therefore, a zoonosis. Among the reservoirs are cattle, sheep, dogs, goats, bushbuck, giraffe, warthog, hyena, lion, and hartebeest. These animals play a significant role in the maintenance and as a source of infection to man and compound efforts to control the disease.

T. brucei brucei in game is probably the same parasite that infects man as T. gambiense or T. rhodesiense. There are important differences in the behaviour of T. gambiense and T. rhodesiense. T. rhodesiense infections typically appear in thinly populated areas where game animals are common, such as the savannas of east and southern Africa. T. gambiense occurs in the more densely populated areas, especially riverine-forested areas of West and Central Africa. T. gambiense produces a slowly developing chronic disease that may go on for several years before actual sleeping sickness symptoms appear. On the other hand, T. rhodesiense is much more acute, taking five to seven days for the symptoms to appear and if not treated, the patient dies in a few weeks to a year.

Because of its acute nature, T. rhodesiense is easier to diagnose, making it possible to deal with outbreaks early enough before they spread. Because of its chronicity, T. gambiense is usually mistaken for malaria or other human diseases that present with fever, and may not be diagnosed until it has spread widely and a major outbreak has occurred.

Diagnosis

For a quick demonstration of the trypanosomes, an examination of a drop of blood under the microscope will show actively moving organisms. However, trypanosomes can easily be demonstrated in thick or thin blood smears stained with ordinary laboratory stains.

Trypanosomes stained with Giemsa

Chronic low infections are detected by inoculating laboratory animals with blood from suspected human cases. The laboratory animals, usually rats or mice, are monitored for two to three weeks.

Swollen glands are characteristic of an early infection. One of the neck glands is palpated and then squeezed between the fingers and punctured with a hypodermic needle. Juice is aspirated and examined for the presence of parasites.

To demonstrate whether there is neurological involvement, a hypodermic needle is inserted into the spinal cord through the lumbar region. The cerebral spinal fluid (CSF) is withdrawn and examined. Trypanosomes may be present but if not present, an elevated protein content and increased white blood cell count may be indicative of a current or previous infection. Various serological techniques for detection of trypanosomiasis exist but they are not used routinely. For example, in endemic areas serological findings in animals and humans that indicate high Igm titres have been associated with trypanosomiasis.

Vector Control

The use of insecticides is an integral part of tsetse control. Ground spraying is used along infested streams and rivers, including coastal areas. Aerial spraying is used for large-scale operations. Insecticides are, unfortunately, environmentally unfriendly, as they not only kill the tsetse flies but also other non-target insects, including amphibians and even small mammals. They must therefore be used with care.

Bush clearing has been undertaken to clear large areas of tsetse flies. However, the tsetse flies re-establish unless the cleared areas are used for resettlement and crop production. Traps impregnated with deltamethrin, permethrin and other suitable insecticides are very effective in reducing tsetse fly numbers. For example, a 99 .9 % reduction in tsetse fly numbers was achieved in some

Ivory Coast

villages using insecticide impregnated traps and screens. Similar control methods have been carried out in

Uganda

with equally good results.

A mass of tsetse flies captured by traps

Better catches can be achieved by incorporating fly attractants into the traps. Studies in

Zimbabwe

showed that the flies were attracted to natural odours of calves and oxen in large numbers. Further studies identified specific attractants as carbon dioxide, acetone and octenol.

Fly trapping is an inexpensive method of control that can easily be undertaken by the affected community and should always be encouraged.

biological control methods have been attempted. one of these is the sterile male release technique. this is usually used where spraying has already reduced the population of the flies. under this method, tsetse flies are mass reared and then subjected to gamma ray radiation that sterilizes the males but does not affect their ability to mate. on being released, the mating of the sterilized males with normal females in the wild does not lead to the production of viable eggs and since the female tsetse flies mate only once, these mated females become effectively sterile. with further releases of sterile males, the fly population continues to decline, with a corresponding decrease in the transmission of infection.

Treatment

Drugs are effective against trypanosomiasis. Their main drawback is the fact that they show nasty side effects. Suramin is used to treat the early phase of T. rhodesiense while pentamidine is used to treat T. gambiense. These two drugs do not enter the brain. Another drug, melarsoprol or Mel B, can cross the blood barrier and attack the parasites in the central nervous system. It is therefore used to treat the late stages of the infection. A relatively new drug, eflornithine, is effective against late stage T. gambiense but not against T. rhodesiense and has less side effects than Mel B. Experimental studies with mice show that eflornithine with either suramin or melarsoprol was

Leishmaniasis

2010-01-24T23:45:00.001-08:00

These haemoflagellates of the genus Leishmania are parasites of invertebrates and vertebrates that use small biting sand flies (Phlebotomus), such as P. sargenti, P. papatasii, P. argentipes and many others, depending on the geographical area as vectors. The leishmanias are rounded or oval parasites with a morphologically complex life cycle consisting of a promastigote with a free flagellum and amastigote that has no flagellum.

Human leishmaniasis is scattered over wide areas of the globe, from

China

across Asia to

India

Iran

Afghanistan

, the Middle and Near East, the Mediterranean basin, into

Sudan

and

Ethiopia

and East and West Africa. In the New World, it extends from

Mexico

to the northern part of

Argentina

. There is no continuity in the distribution over these wide areas nor is a single disease involved. The distribution is determined by the kinds of mammals that serve as its hosts and by the distribution of the sand fly.

The diseases attributed to Leishmania range from a mildly inconvenient lesion of the skin, known as Oriental sore, to a serious disease involving the liver and spleen, known as kala-azar. In South America, one form of leishmaniasis (mucocutaneous) extensively involves the mucous membranes of the mouth, nose and pharynx, as well as the skin but does not affect the viscera.

Leishmaniasis is a zoonotic disease that is maintained in nature by many animals including dogs, rodents, wolves, foxes, jackals, raccoons, sloths and marsupials. Numerous species of Leishmania have been described in mammals and of these three are generally accepted as human parasites; two of these cause cutaneous leishmaniasis and the third causes visceral leishmaniasis or kala-azar.

Life cycle, symptomatology and epidemiology

The amastigote forms of Leishmania are ingested by sand flies when they feed on the blood and tissue fluid of vertebrates. Compared with trypanosomes, development of Leishmania in the sand fly seems quite simple, involving the transformation of the amastigote forms to promastigotes. These promastigotes multiply in the digestive canal of the insect and transform into infective promastigotes which are injected into a new vertebrate host when the fly feeds again.

Life cycle

In the vertebrate the promastigotes enter host macrophage cells, roundup and lose their flagella, forming the so-called Leishman bodies or amastigote forms that are the characteristic forms found in the vertebrate. The parasites multiply and increase within the host cells until they cause them to rupture. The rapture of the host cells liberates more parasites that are engulfed by other phagocytic cells.

Table. Leishmania species and main characteristics associated with infections

Species	Characteristics	Major foci
Old World
L. aethiopica	Cutaneous, self-healing, also diffuse, zoonotic	Eastern Africa
L. donovani	Visceral, kala-azar, anthroponotic	India, Eastern Africa
L. infantum	Visceral, zoonotic (dogs)	Europe, North Africa
L. major	Cutaneous, self-limiting, rural, zoonotic	Mediterranean basin and Western Asia
L. tropica	Cutaneous, self-healing, with possible recurring satellite lesions, urban, anthroponotic	Mediterranean basin and Western Asia and Africa
New World
L. braziliensis complex	Cutaneous and mucocutaneous, zoonotic	Latin America
L. chagasi	Visceral, zoonotic (dogs)	Latin America
L. mexicana complex	Cutaneous, and a few mucocutaneous reported in Panama, zoonotic	Latin America

Cutaneous leishmaniasis (Oriental Sore)

Cutaneous Leishmaniasis is characterised by sores on the face, arms and legs especially in children. The aetiological agent is Leishmania tropica, a parasite that has a wide distribution in Asia, Middle East and Africa.

The classical lesion of cutaneous leishmaniasis is the Oriental Sore, which is about 5 to 15 cm in diameter and takes several months to develop following infection. Incubation period is usually between 2 to 7 months or longer. The infection is usually accompanied by spontaneous healing of the sore after 9 to 12 months, sometimes leaving unsightly scars on the skin. There is increasing evidence that the infection is followed by permanent immunity.

The sores do not usually contain pus except when they have been invaded by bacteria. Classical sores are found from the Mediterranean region to

India

and southwestern Asia and parts of Africa. Another form of Oriental sore is the relatively wet one that attacks the lymph nodes. This has a shorter incubation period than the dry Oriental sore. It is probably a zoonosis since it occurs in rural areas where its reservoirs are dogs, ground squirrels and gerbils.

Mucocutaneous leishmaniasis (Espundia)

Mucocutaneous leishmaniasis is a chronic disease that occurs in Central and South America. The aetiological agent is Leishmania braziliensis and the most severe form of the disease is called espundia which is endemic in the jungles of South America, particularly

Peru

Bolivia

and

Brazil

. Leishmania braziliensis prefers to attack the mucus membranes of the mouth and the nasopharynx. The infection is usually complicated by bacterial and infections and may result in the complete destruction of the tissues of the mucus membranes including the associated cartilage, leading to grotesque deformation of the nasopharyngeal region and the palate.

Oriental sore (A and B) and espundia (C)

Visceral Leishmaniasis (kala-azar)

Visceral leishmaniasis is caused by L. donovani, a parasite similar to both L. tropica and L. braziliensis. Visceral leishmaniasis exists in

China

India

Afghanistan

Sudan

Ethiopia

and East Africa, South and Central America. It attacks the reticuloendothelial cells of the spleen, liver, bone marrow and visceral lymphatic nodes. This is a rural disease with dogs, foxes, rodents and other mammals acting as its reservoirs.

Biting sandflies introduce promastigotes into the dermal region of the skin. The promastigotes enter the blood and lymph vessels and make their way to the liver, spleen, and bone marrow via lymph and blood. As the parasites divide and increase in numbers, they cause the rupture of the macrophages and release of more parasites that become available to infect more macrophages. The destruction of the macrophages continues until their numbers are considerably reduced.

To counteract the loss of macrophages, the bone marrow is activated to produce more macrophages at the expense of other important cells such as polymorphonuclear cells. The resulting monocytosis and leucopoenia weaken the defence system of the body very badly. The result is that many of the victims of kala-azar succumb to infections that they would normally resist.

Clinical kala-azar develops when the liver, spleen, kidney, and bone marrow are infected. Very often kala-azar is fatal if not treated. In other people, however, the symptoms may assume a chronic course.

The symptoms of kala-azar include headaches, irregular bouts of fever with a temperature (which can range from 36 ^oC to 40 ^oC) and oedema of the face, trunk and feet. Other symptoms include substantial weight loss, splenomegaly, hepatomegaly, and anaemia, bleeding from the gums, lips, nose and intestinal mucosa.

Leishmania donovani exhibits geographical host-relationships. In

China

, kala-azar has dogs as its reservoirs that suffer from extensive lesions. In

India

, kala-azar has no zoonotic features because it is transmitted easily from man to man by sand flies living in moist vegetation in shaded areas near homes.

In the Mediterranean region where dogs are important reservoirs, children are usually more affected than the adults. In the

Sudan

, mucocutaneous leishmaniasis and kala-azar are present and both are caused by L. donovani. In the

Sudan

as in the

Americas

, mucocutaneous leishmaniasis affects the upper respiratory tract and oral regions of the body. However, in the

Sudan

, it is maintained by several rodents such as Arvicanthis niloticus (the Nile grass rat), Acomys albigena (the spiny mouse), the genet and the serval. In the semi - arid northern districts of

Kenya

and the districts of Karamoja in

Uganda

, sandflies live in anthills and feed on rodents and dogs.

Diagnosis

In cutaneous leishmaniasis, the presence of parasites can be demonstrated in blood smears made from skin scrapings, aspiration of juice from the wound or biopsy. Alternatively, the scrapings from the lesion can be cultured or inoculated into hamsters and examined for the presence of amastigotes. In kala-azar, a biopsy from the bone marrow or spleen can be examined for the presence of amastigotes, cultured on a suitable media or inoculated into hamsters before being examined. In either case, the presence of amastigotes confirms the infection.

Treatment

Proper parasitological identification of the parasites is essential for correct treatment. This is because the treatment of leishmaniasis is long and the drugs are toxic. Cutaneous leishmaniasis is usually self-limiting and most of the wounds heal within 6-9 months. The infection can therefore be left to take its course until it heals, unless the wounds are disfiguring because of bacterial involvement. In many parts of southwest Asia, children are exposed to infection or given live virulent injections of the parasite in order to induce immunity that will protect them against further infection and thus avoid disfiguring lesions and scars on the face.

A case of kala-azar, with enlarged liver and spleen

Mucocutaneous leishmaniasis and kala-azar are more serious than cutaneous leishmaniasis because they are not only incapacitating they can also be fatal. The first line of treatment involves the administration of pentavalent antimonials, such as stibogluconate, or meglumine antimoniate. The second line drugs if the antimonials fail are amphoterin B and pentamidine. If untreated, kala-azar has a mortality rate of 100 %.

Vector Control

The diversity of the epidemiology of the different forms of the disease makes it impossible to control leishmaniasis with a single approach or tool. Infection can be prevented by use of repellents or insecticides against sandflies. The elimination of dogs and other reservoir hosts greatly reduces the risk of infection. Vector control using suitable insecticides are effective against peridomestic transmission.

Chagas Disease

2010-01-24T23:44:00.000-08:00

Chagas disease (American trypanosomiasis) is caused by Trypanosoma cruzi. This flagellate naturally occurs in many mammals in Central and South America. It is transmitted by highly coloured bugs of the genera Triatoma, Rhodnius and Panstrongylus, also known as kissing bugs. These arthropods live in burrows or nests of animals and in dark, sheltered areas of human homes. They particularly prefer to inhabit cracks in the walls of mud or adobe houses in Latin America. Chagasiasis is disease of mainly poor people.

Kissing bugs. The right one is engorged with blood

Life cycle

Most of the vectors of T. cruzi are known to defecate while sucking blood. It is believed that the arthropod is attracted to the carbon dioxide in the host’s exhaled breath and that is why it mainly bites on the face, arms and shoulders. As it sucks blood, it defecates and rubs some of the faeces on the wound causing infection. The host may be prompted to rub the wound and contaminate it with the bug’s faeces. Other methods of acquiring infection include blood transfusion, through the mammary glands, organ transplantation and by accidental ingestion of the infected reduviid bugs. Animals become infected by eating the bugs or licking their bites. Cats can become infected through eating infected rodents.

Life cycle of T.cruzi involves reservoir hosts (right), bugs and man (left).

on entering the body tissues, the parasites or trypomastigotes invade cells in the body, particularly muscle and nerve cells, while some are taken up by the macrophages. these intracellular parasites lose their flagella, transform into amastigotes, and start diving for 4 to 5 days to produce large numbers of trypomastigotes. the parasitised host cells rupture, liberating trypomastigotes into the blood stream and body tissues.

once more, some of the trypomastigotes are ingested by macrophages while others invade new cells and another multiplication process begins. however, trypomastigotes that are free in the blood system do not divide.

Infection in the triatomine vector begins when it sucks blood that is infected with trypomastigotes. On reaching the vector’s midgut, the trypomastigotes transform into epimastigotes, which divide to produce more parasites. After division, the parasites proceed to the hindgut where they change into metacyclic trypomastigotes that are infective to a host.

Pathogenesis and symptomatology

The early phase of the infection is characterised by the inflammatory tissue reaction and acute lymphadenitis. The infection is acute during its early stages with characteristic swollen face especially around the eyes. There may be severe headache, inflammation of the tear gland and swelling of the lymph glands of the neck. These symptoms would seem to suggest that the eye might be the usual site of infection, the insect biting the lids of the eyes, causing the host to rub the infected bug faeces onto the eyes. Other symptoms include enlargement of the spleen and liver, fever and anaemia.

The prognosis, especially in children, is usually bad and fatalities are common.

If the patient survives the acute phase, the infection goes into a chronic stage with mild symptoms that last for months or years.

Swelling of the face is an early sign of T .cruzi infection

The mildness of the symptoms, however, masks the extent of the seriousness of organ damage that may be taking place. Organs that are usually affected by T. cruzi include the heart, kidney, central nervous system, thyroid, adrenal glands, oesophagus and colon.

The most affected organ is usually the heart and most of the deaths are due to heart failure. A person may drop dead suddenly only to discover that he has probably been suffering from chronic chagas disease.

Damage to the sympathetic nervous system of the alimentary canal can lead to enlarged oesophagus and inability to swallow. Examination of the patient during the chronic phase of the infection reveals enlarged spleen, and liver, general oedema and anaemia. The patient may be fidgety and nervous.

Epidemiology

T. cruzi is a very versatile parasite. The natural hosts of T. cruzi appear to be armadillos, opossums, bats, racoons and rodents. It can thrive in monkeys, marmosets, guinea pigs, rats, rabbits, cats, dogs and other mammals. Human infection depends on the interaction between this large array of mammalian hosts and triatomine vectors. In areas of high endemicity up to 10 to 15 % of the population may be infected. The infection in children may be as high as 50% in some places.

A large number of vectors of T. cruzi are known. However, comparatively few species of the vectors invade houses and become human pests. In South America, three species are important in transmitting infection: Panstrongylus megistus, Triatoma infestans and Rhodnius prolixus. Panstrongylus megistus is widely distributed and is a principal transmitter of Chagas disease. It is not only thoroughly domesticated in its habits but it is also a regular resident in the huts.

Diagnosis

The parasites can be detected in blood smears taken from an early infection. However, it is difficult to find parasites in the circulation in chronic infections. A technique known as zenodiagnosis is usually used to detect parasites in old chronic cases.

Zenodiagnosis involves allowing unfed parasite-free bugs to imbibe blood from suspected individuals and if the parasites are present, they are detected in the faeces of insects about 4 weeks later.

Treatment

There is no effective treatment for Chagas disease. However, two compounds, nifurtimox and benznidazole, whose efficacy and safely are still in doubt, have recently been introduced. Both drugs require a long administration of two to three months and are therefore not suitable for a widespread use.

Vector Control

The most important vectors of T. cruzi live in or around dwellings. The disease is mostly prevalent where the bugs have adapted to peridomestic environment especially if the homes are constructed of wood and mud with gaping cracks. The bugs hide in the crevices on the walls and in dark places in the houses and come out to bite at night when the people are sleeping.

Spraying with insecticide

Control involves filling up the walls of dwellings with mud or cement, providing better housing and ensuring that the houses are properly aerated. Pyrethroids with long residual effects such as deltamethrin and cypermethrin, sprayed onto the walls of dwellings or mixed in paints, are effective in reducing transmission. In addition, canisters that release fumes of insecticide when lit can be used to control the bugs.

Filariasis

2010-01-24T23:30:00.000-08:00

The filariases are a group of diseases that are caused by slender thread-like parasites that live in the subcutaneous tissues, lymphatic and blood systems of various vertebrates, ranging from amphibians to man. The vulva in female worms is near the mouth. The males are small with spirally coiled tails. Females produce embryos that live in the blood or subcutaneous layers of the skin where they are picked up by the blood sucking arthropods.

Some of the filarial worms that affect man cause very serious effects on the host while the others are of marginal importance. Eight species namely, Wuchereria bancrofti, Brugia malayi, Brugia timori, Loa loa, Onchocerca volvulus, Mansonella ozzardi, Mansonella perstans and Mansonella streptocerca are endemic in many parts of the world.

Wuchereria bancrofti, Brugia malayi, and Brugia timori are the three major filarial worms of man. W. bancrofti has a wide distribution. It is found in Africa, Asia and parts of Latin America. B. malayi is found mainly in southern and eastern Asia and B. timori is confined to the islands of

Indonesia

and Timor.

Wuchereriasis

Wuchereria bancrofti, the parasitic agent that causes bancroftian filariasis, is widely distributed throughout the tropical and the subtropical regions of the world. Its endemic area extends from about latitudes 42 ^o N to 28 ^oS in the Eastern hemisphere and 30 ^oN to 30 ^oS in the Western Hemisphere. Bancroftian filariasis affects millions of people in Africa,

India

, South-East Asia, the Pacific Islands, South and Central America.

It is particularly common in coastal areas and islands where the temperatures are warm and the humidity is high. The adult worms, found in the lymph glands and lymph ducts, often in tangled masses, are thin, thread-like with a smooth cuticle. The anterior end is bulbous. The females are 65 to 100 mm in length by 0.24 mm in diameter, while the males are about 40 mm in length by 0.1 mm in diameter. The males have sharply curved caudal extremities.

The microfilaria of W. bancrofti measures approximately 244 to 296 µm in length by 7.5 to 10 µm in diameter. Its anterior end is bluntly rounded whereas the posterior end is tapered. The body is enclosed in a sheath. The microfilariae that are born in the lymphatic vessels, take 3 – 15 months to mature and live for many years. Larvae produced by the female worms in the lymphatic system are capable of migration to the blood system, usually during the night hours, and be picked by blood-sucking mosquitoes. However, most of the worms remain in the body as immature forms and die in 2 to 6 years.

W. bancrofti has a wide choice of vectors that include some species of Aedes, Anopheles and Culex mosquitoes. In Africa, especially in the rural areas, Anopheles mosquitoes transmit W. bancrofti, while in cities, species of Culex mosquito that easily breed in latrines, sewage and ditches are the major vectors. In the Pacific, the main vector of infection is Aedes. This mosquito can breed in tiny amounts of clean water in the axils of plants, discarded containers and old motor tyres

Life cycle

Mosquitoes pick up microfilariae from infected persons while taking a blood meal. Shortly after being ingested, the microfilariae shed their sheaths, penetrate the walls of the insect’s midgut, and migrate to the thoracic muscles where they lie lengthwise between the muscle fibres for sometime.

While still in the thoracic muscles, the microfilariae change into short, thick larvae before moulting to the second stage, usually after a period of 8 to 10 days since being ingested. This moulting is followed by a spurt of growth that increases the larva’s length to more than 0.1 mm. Around day 12 to 14, the worms moult once more and transform into third stage infective larvae.

They then leave the thoracic muscles and make their way towards the head and mouthpart of the insect. Some of the larvae never reach the proboscis but get lost on the way. Those infective third stage microfilariae that reach the mouthparts continue to grow until they are transferred to a vertebrate host by a feeding mosquito.

Pathogenesis and symptomatology

After being introduced into the host, the microfilariae travel and enter the lymphatic vessels where they grow and moult twice before attaining adulthood. Symptoms range from none to fever, tenderness of infected parts, eosinophilia and inflammation. The most obvious inflammatory reaction is adenolymphangitis or the inflammation of the lymph nodes.

The attacks are usually recurrent, often being precipitated by physical exercise, and may be accompanied by chills, fever, aches, and general malaise.

In endemic areas, some individuals with microfilariae in their blood show no symptoms at all. In others, symptoms develop slowly and may take years to appear. This is suggestive of the development of acquired immunity.

Most of the pathological picture associated with bancroftian filariasis is due to the presence of adult worms. The lymph vessels occupied by the adult worms and the surrounding tissues, including the lymphatic glands, scrotum, spermatic cords and epididymis, are usually quite inflamed and swollen probably due to sensitising substances released by the worms themselves. The inflammation of the lymphatic system, coupled with the presence of adult worms in the lymph channels, usually in tangled masses, causes the obstruction of the lymph fluid in the lymphatic vessels. Lymph accumulates with the effect that the limbs, breasts and male genitals, such as the scrotum, spermatic cords, epididymis and testes become grossly enlarged with fluid.

The condition in which the limbs are grossly swollen is known as elephantiasis. Elephantiasis and a hanging scrotum, called hydrocoele, are usually associated with advanced chronic infections. Bacteria and fungi may infect the wounds exacerbating the wounds.

Epidemiology

Filariasis is not short of vectors. They include mosquitoes of the genera Anopheles, Culex, Mansonia and Aedes. The microfilariae show periodicity in which the numbers are at a peak in the blood circulation at certain hours of the night, which corresponds to the preferred biting hours of the vector. During the day, the microfilariae are virtually absent from the blood stream and may be found concentrated in the pulmonary capillaries.

This periodicity is oriented to the established circadian sleeping and waking cycle of the host instead of day and night as such and is related to the difference in oxygen tension between venous and arterial blood during day and at night. If an experimental host breathes oxygen at night when the microfilariae are normally in the peripheral blood, the parasites accumulate in the lungs.

There is a nonperiodic W. bancrofti is some of the Polynesian islands (Fiji, Tonga, Samoa and Cook Island) that is present in the blood system any time of the day and the mosquitoes there bite at any time of the day. This clearly shows that the purpose of periodicity is to ensure that the parasite reaches new hosts, which guarantees its survival.

Diagnosis

Diagnosis of active bancroftian filariasis is difficult, as blood must be taken at night when the microfilariae circulate in large numbers. Diagnosis is based on the detection of microfilariae in blood smears. With the exception of the South Pacific Islands, the microfilariae are present in appreciable numbers only at night, which coincides with the biting habits of the mosquito vectors. The worms are usually very scanty during the day.

The usual time for taking blood smears is between 10 pm and 2 am, which is quite inconvenient as you can imagine. The microfilariae have been induced to appear in large numbers in the peripheral blood of suspected individuals during the day by administration of diethylcarbamazine.

Treatment

It is now quite clear personal hygiene is extremely important in the management of elephantiasis. This can be accomplished by washing the affected limbs regularly with water and soap, combined with the application of antibiotics and antifungal creams that prevent bacterial and fungal growth that would exacerbate the damage.

In order to reach as many infected people as possible in endemic areas, salt mixed with small amounts of diethylcarbamazine (DEC) has been introduced in

India

China

and

Taiwan

with great success. A small amount of DEC (0.1% - 0.6%), added to table salt and used for 12 months can reduce the prevalence of microfilariae of bancroftian and brugian filariasis by 70 – 100%.

DEC and ivermectin are two effective drugs used in the treatment of filariasis. Both drugs are used separately as single doses against circulating microfilariae. However, a combination of the two drugs, used as a single dose (6 mg/kg DEC and 20 mg/kg ivermectin), is even more efficacious causing a decrease in filarial load of 99% and 96 % one year and two years after treatment, respectively.

Suramin, a drug that is used to treat the early cases of the African trypanosomiasis, can kill adult filarial worms but it has not gained much support because of its side effects.

Vector Control

Filariasis has been eradicated in small islands and much has been accomplished in

China

. The situation remains unchanged in the rest of the endemic areas of the world. Vector control involves limiting mosquito breeding sites and the destruction of larvae by use of larvicides, reduction of mosquito numbers by use of insecticides and use of impregnated bed nets. The culicine mosquitoes, such as Culex quinquefasciatus breed in blocked sewers and fouled stagnant water in urban centres. Therefore, provision of proper sanitation will contribute greatly to the control of urban filariasis.

Brugia malayi

2010-01-24T23:28:00.000-08:00

Brugia malayi is in most instances similar to W. bancrofti. Its geographical distribution includes

India

Sri Lanka

and all the countries of South East Asia, China, and

Japan

. The microfilariae resemble those of W. bancrofti. The males measure 13 to 23 mm in length by 80 µm in diameter, with the posterior end somewhat coiled. The females vary in length from 43 to 55 mm.

The transmitting mosquitoes are species of Mansonia and sometimes, Anopheles as well. Mansonia is an insect of the swamps and Brugia malayi is a parasite of the rural areas unlike W. bancrofti which is a parasite of urban centres.

Like microfilaria of W. bancrofti, that of B. malayi is sheathed but it is distinguished from the former by being somewhat smaller, measuring about 270 µm long, and having a dense column of overlapping nuclei, and a tail with terminal nuclei. In Giemsa stains, the B. malayi sheath stains a bright pink in contrast to that of B. malayi, which remains unstained.

Pathogenesis and symptomatology

The infection is characterised by recurrent fever with inflammation of lymph nodes and the lymphatic vessels. Elephantiasis of the lower limbs is common but the involvement of the genitourinary system is rare.

Epidemiology

Two distinct types of B. malayi differ in larval periodicity and vector requirements. One has nocturnal periodicity whereas the other is described as subperiodic. The nocturnal type is widely distributed and is associated mainly with coastal rice fields, open swamps and ponds, with Anopheles species serving as its natural vectors. The subperiodic form is found in swampy forest areas, with Mansonia species as its natural vectors.

Control

Control strategies are similar to those of W. bancrofti.

Loa loa

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Loa loa is an eye worm that is found in the forests of West and Central Africa. Adult parasites average about 50 mm in length and live in the connective tissues of various parts of the human body.

Life cycle

Larvae produced by the female worms must find their way into the blood stream, where they are picked up by day-biting Chrysops. C. dimidiata and C. silacea are the two natural vectors of Loa loa. Although the vector can feed any time during the day, its usual biting time is about midday.

After being ingested, the microfilariae migrate from the fly’s midgut to the thoracic muscles, where they develop to the infective third stage in about 7 days. The infective microfilariae are introduced into the host’s tissues when the vector takes a blood meal. About 5 to 12 months post-infection, the worms become mature males and females. The adult worms wander in the host’s connective tissues and often enter the orbit and conjunctiva. The worms are known to live for more than 10 years.

Pathogenesis and symptomatology

During their migrations through the superficial body tissues, the worms cause tissue reaction in form of swellings, usually known as ‘Calabar’ swellings. The swellings are painful, the pain lasting on average 2 to 3 days. Sometimes severe symptoms, such as fever, pruritus, pain, renal insufficiency and neurological disturbances may occur. Migration of the worms through the conjunctiva causes considerable pain and oedema of the eye.

Epidemiology

Monkeys possibly serve as host reservoirs for this worm. The parasite can be transmitted practically by all species of Chrysops. The microfilariae are periodic in their cycle. During the day, they remain in the peripheral circulation, where they can be picked up easily by the vector. At night, they are concentrated in lung capillaries.

Diagnosis

People who have visited an endemic area may present with Calabar swellings and eosinophilia. However, specific diagnosis involves demonstrating microfilaria in peripheral blood during the day, or by removal of adult worms from the skin or conjunctiva.

Control

Loaiasis can be controlled by surgical removal of microfilariae migrating through the corneal conjunctiva and treatment of infected persons with diethylcarbamazine and ivermectin. The larval stages of Cyclops are controlled using insecticides.

Schistomiasis

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Schistosomes are among the most important blood parasites of man. Human schistosomiasis (bilharzia or bilharziasis) is due to three species of Schistosoma: Schistosoma haematobium, Schistosoma mansoni and Schistosoma japonicum. S. haematobium is responsible for urinary schistosomiasis in Africa, and the Middle East; S. mansoni is responsible for intestinal schistosomiasis in Africa, Central and South America and the Caribbean and S. japonicum causes intestinal schistosomiasis in the Far East, particularly

China

Japan

and the

Philippines

. Two more species, S. mekongi and S. intercalatum, are intestinal parasites of man but they have a limited distribution.

Although the three major human schistosomes are primarily parasites of man, S. japonicum is present in many other mammals including cattle, goats, pigs, dogs and cats. These animals serve as reservoirs from which infection can be passed to man. The role played by wild animals in human infections of S. haematobium and S. mansoni has not been clarified.

The schistosomes are digenetic trematodes with relatively complex life cycles. The male that measures about 8 to 16 mm long has a groove, the gynecophoric canal, in which the longer and more slender female is held. The male and the female are in permanent copula and usually live for many years.

Life cycle

The adult worms live in the small mesenteric veins of the small intestine or pelvic veins where the females deposit their eggs. Each female S. japonicum lays about 1300 eggs daily. This is about four times the number of eggs shed by the female S. mansoni or S haematobium, which are around 350 eggs per day.

Each species of Schistosoma has characteristic eggs. The eggs of S. haematobium have a large terminal spine; those of S. mansoni have a lateral spine while those of S. japonicum have a rudimentary lateral spine that is often difficult to locate.

As the eggs are laid, they work their way out of the small blood venules aided by their own hydrolytic secretions. The eggs of S. japonicum and S. mansoni reach the lumen of the small intestine by traversing the intestinal musculature before being expelled in faeces. Those of S. haematobium move from the surrounding pelvic blood vessels into the bladder and pass out in urine.

Some of the eggs are carried to the liver and lungs where they cause serious inflammatory tissue reactions, which usually culminate in the formation of fibrous tissue around them.

The shelled eggs are fully developed embryos and hatch into free - swimming ciliated miracidia upon contact with water of low salt content. The miracidia survive for up to 24 hours. For continuation of life, the miracidium must penetrate a snail host during this period. On finding a suitable snail, the ciliated epithelium is shed, the larva becomes a tubular sporocyst that grows to about 1 mm in length and for the next two to three weeks produces daughter sporocysts. Daughter sporocysts emerge from the mother sporocyst, undergo growth and migrate from the snail’s viscera to the digestive gland.

The larvae are very specific in their choice of snails. S. japonicum miracidia can only penetrate the tissues and establish in freshwater snails of the genus Oncomelania, while S. mansoni will only invade snails of the genus Biomphalaria, and S. haematobium those of the genus Bulinus.

In the molluscan digestive gland, sporocysts divide repeatedly into daughter sporocysts, first and second-generation rediae. About six weeks since the miracidium entered the snail, fork – tailed cercariae emerge from the snail. The cercaria is a free-swimming organism that must enter the skin of a mammalian host within two to three days or it dies.

During the penetration of the skin of a mammalian host, the cercariae shed their tails and within a few hours, the young flukes, called schistosomulae, migrate through veins and lymph vessels to the lungs. From there they migrate to the liver, where they develop into young male and female worms within portal blood vessels.

After 4-6 weeks, mating takes place and worm pairs move to their final destinations, which, in urinary schistosomiasis, are the blood vessels of the bladder, and intestinal mesenteries in the case of S. japonicum and S. mansoni. Thereafter, the female worms begin shedding eggs. Some of the eggs make their way through the walls of the blood vessels and enter the bladder or the intestinal lumen. Those of S. haematobium pass out in urine, while those produced by the two intestinal schistosomes are voided in faeces.

Pathogenesis

The main pathological features associated with schistosomiasis are mechanical damage caused by the movement of the eggs through the venules to the intestine or urinary bladder, the formation of fibrotic tissue around the eggs and inflammation. Large numbers of eggs cause extensive rupture of the membranes of the bladder and intestine, resulting in haemorrhage and blood in urine and faeces. About 50 % of the eggs produced by the female worms are trapped in the tissues. Depending on the species of Schistosoma, the clinical manifestations involve inflammatory reactions due to eggs lodged in the liver, intestinal and urinary systems.

Urinary schistosomiasis is characterised by painful urination, and progressive damage to the bladder and ureters. This in turn leads to narrowing of the urinary tract and obstruction of urine flow. In serious cases, there may be total kidney failure. Bladder cancer is common in advanced cases.

The pathology of S. mansoni and S. japonicum is largely similar. However, tissue damage in the Oriental parasite is more severe mainly because of the large numbers of eggs it releases. The fact that S. japonicum is also a parasite of many kinds of mammals seems to suggest that it could have started as an animal parasite that later adapted to man. That being the case, it explains why it is normally considered more virulent than the other two species of human schistosomes.

The damage to the liver and intestinal walls is common and is caused by the fibrotic lesions that develop around eggs trapped in these organs. Long-term chronic infections eventually lead to hypertension of the abdominal blood vessels and progressive enlargement of the liver and spleen.

Long-standing portal hypertension causes secondary enlargement of other vessels such as the superficial veins of the abdominal wall, particularly varicose oesophageal veins from which bleeding can be fatal.

Symptoms

During the early stages of infection, patients with S. japonicum or S. mansoni experience tiredness, recurrent afternoon fever, night sweats, diarrhoea, loss of appetite and loss of weight. The symptoms due to S. haematobium at this stage are not very different from those of the other two species. The patient complains of fever, moderate hepatic and epigastric pain. More often, the obvious symptoms of infection are the presence of blood in the urine and a sharp pain during micturation.

Epidemiology

The usual means of human exposure to infection consists of wading, swimming, and bathing or washing clothes in shallow freshwater along the banks of rivers, lakes and ponds infested with infected snails. Urine and excreta deposited by infected persons that find their way to the water are the major source of infection for the snails. Reservoir animals in S. japonicum contribute to the pollution of water with their infected faeces and increase the chances of human infection.

Schistosomiasis may well be described as an occupational hazard in as far as it affects mostly paddy rice farmers and fishermen. Other groups of people that are usually more exposed to infection than the rest of the population because of their nature of work are women and children. In rural areas, women spend a lot of time in contact with water as they wash family clothing and fetch water for domestic use. Likewise, young children spend a lot of their time swimming and playing in water, thereby exposing themselves to infection.

As the human population increases, there is a corresponding increase in the demand for food. To meet this demand, farmers turn to damming rivers to create large water reservoirs for irrigation. More fishponds are dug and swamps are exploited for rice and other agricultural production. These activities create favourable conditions for the snails to multiply and increase the transmission and prevalence of schistosomiasis.

The construction of the Aswan dam in

Egypt

for irrigation and hydroelectric power generation led to a dramatic increase in the incidence of schistosomiasis. For example, the incidence in children 5 years of age was found to have increased from 0.5 to 60% following introduction of irrigation. Four years following the completion of the Akasombo dam in

Ghana

, the infection rate in children 5-19 years old rose from 15 to 90%. Similar high figures have been reported from other large dams: Kariba in

Zambia

, Kaidji in

Nigeria

and Selingue in

Mali

A few wild animals have been found naturally infected with S. haematobium but their role in human infection is unclear. However, rodents, baboons and velvet monkeys are known to harbour of S. mansoni in East Africa. Whether these animals are natural reservoirs of human infection remains to be resolved.

Diagnosis

Examination of the faeces reveals characteristic eggs of S. mansoni or S. japonicum. For S. haematobium, the eggs are detected in urine.

Control Methods

A successful control method will have to take into account provision of piped water, wearing of protective gear by fishermen and farmers, use of toilets and avoidance of swimming in infected waters.

Snail intermediate hosts are controlled using molluscicides, applied along river and lakeshores and along irrigation canals. Although molluscicides are effective in limiting infection, most of them are unfortunately quite toxic and end up killing many other nontarget organisms including the fish.

Drugs used for treatment of schistosomiasis include metrifonate, oxamniquine and praziquantel. Metrifonate is cheap but requires three doses and is only effective against S. haematobium. Oxamniquine is effective as a single dose against S. mansoni. Praziquantel is a safe, effective drug against all species of Schistosoma and is given as a single dose. Treatment with praziquantel is followed by a dramatic decrease in parasite numbers and egg production. A reduction in parasite numbers means there are fewer eggs, which means fewer snail intermediate hosts will be infected. Eventually, there is a decrease in the transmission of infection. Praziquantel is also effective against trematodes and cestodes.

Guinea Worm

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Dracunculus medinensis (guinea worm) is chiefly a parasite of man that causes very painful, debilitating skin ulcers. The disease, dracontiaisis or dracunculiasis, associated with stagnant water in semiarid areas, has been known since ancient times. The parasite affects many people in East Africa, Central Africa, West Africa,

India

Pakistan

Saudi Arabia

Yemen

Iraq

Iran

Afghanistan

, and parts of South East Asia. The prevalence can be quite high in semi arid and desert areas where water is scarce so that the few available water sources serve many people.

Adult males measure 30 to 40 mm in length by 0.4 mm in diameter, while the females are much bigger measuring 70 to 120 mm in length by 0.9 to 1.7 mm in diameter. The head end is bluntly rounded in the female and commonly ruptured when it has begun expelling larvae. The tail is hooked and sharp.

Life cycle

Patent infection of D. medinensis is characterized by skin ulcers, from which the female worms discharge a milky fluid consisting of thousands of tiny larvae into the water. This occurs whenever the ulcer is exposed to water. The larvae swim actively until they are ingested by a freshwater copepod of the genus Cyclops. The larvae measure 500 to 700 µm long and have a long tail that makes up almost one third of the whole body.

On being ingested, the tiny larvae bore through the copepod’s gut wall and enter the body cavity where they undergo two moults. About three weeks later, the larvae become infective to man. Human infection is due to drinking water contaminated with infected copepods. The crustacean intermediate hosts are killed within the host’s gut, releasing infective larvae. The larvae of both sexes undergo development in deep somatic and visceral connective tissues, taking about 9 to 12 months to reach maturity. After mating, the males die and the females migrate to the subcutaneous tissues near the skin surface. They move particularly to the softer subcutaneous layers of the skin, especially ankles, wrists or any other soft parts of the exposed skin.

When ready to bring forth her young, the female worm moves towards the upper layers of the skin, particularly those parts of the body that are exposed to water, such as the arms, legs and shoulders. Then the worm pierces the skin with the front end of her body and secretes a toxic substance that irritates the tissues.

The skin immediately above the position of the female worm develops a blister that becomes an ulcer with a central hole. On exposure to water, the ulcer opens, the anterior end of the worm ruptures and a fluid containing large numbers of larvae is discharged from the uterus into the water. The female worm continues to discharge larvae each time the host’s body is exposed to water until the uterus is empty and the flabby worm is removed from the skin.

Pathogenesis

There are virtually no symptoms during the early stages of the infection. Symptoms normally appear later when the worms are migrating to the skin, and the ulcers are forming. The symptoms are usually allergic reactions, characterized by vomiting, a rash, nausea, diarrhoea, itching, asthma, dizziness and faintness. The ulcer appears as a reddish papule measuring 15 to 20 mm in diameter. The blister can be found anywhere on the body including the arms, hands, shoulders, neck, buttocks, legs, feet and space between the toes or fingers

Some people are disabled by the symptoms so much that they are unable to work for weeks. When the blister eventually breaks, the symptoms subside. Bacteria may attack the ulcer and aggravate the wound. In northeastern

Uganda

where dracunculiasis is endemic, it is estimated that 60 % of the infected individuals are usually unable to work for at least one month. One person in ten is so affected that he or she is unable to work for at least six months. School performance among infected children is affected by frequent absenteeism and, sometimes, social rejection.

Epidemiology

Factors that promote dracunculiasis are warm temperatures and shortage of water for the population, especially during the dry season, forcing many people to crowd at the few available water reservoirs. The water reservoirs become the centres of activity for bathing, swimming, and performing other family chores. The water becomes contaminated with larvae discharged from individuals with patent infections whenever the ulcer is exposed to water.

Control

A number of measures can be taken to protect the community. These include provision of safe drinking water by protection of the existing water springs or ponds and construction of boreholes. The population should be sensitised adequately about the steps they can take to protect themselves, such as drinking only water that has been boiled or filtered. People, particularly those with wounds, should be prevented from bathing or swimming in water or springs from which the community draws its drinking water.

The use of chemicals to kill copepods in drinking water sources forms part of the control strategy. It is imperative that the chemical used is not toxic to humans and animals that use the water source. Several insecticides can kill the copepods but the most suitable one so far is temophos (Abate) because it is active at low concentrations and has been used as mosquito larvicide for many years. It is safe for humans and animals.

There is no effective drug for treatment of people with guinea worm infection. Anthelminthics, such as albendazole, thiabendazole, metronidazole or mebendazole when given as the gravid females emerge from the skin seem to hasten the worms’ expulsion and reduce the pain. A more practical way to hasten the extrusion of the parasite from the skin is to keep the affected wound covered with a wet bandage.

Onchocerciasis

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Onchocerciasis is a filarial disease that is caused by Onchocerca volvulus and transmitted by black flies of the genus Simulium. The disease is endemic in extensive areas of Africa, isolated foci in Central and South America, including Guatemala, Mexico Venezuela, Brazil and Columbia and the Middle East, particularly Yemen and Saudi Arabia. In Africa, the main vectors include Simulium damnosum and S. naevi. The major vectors in South and Central America include S. ochraceum, S. metallicum, S. callidum and S. exiguum.

Adult worms are very long, slender, and highly coiled, resembling pieces of thread. Males measure 19 to 42 mm in length. The females are larger and measure 33 to 50 cm long.

Life cycle

The embryos leave the uterus of their mother by way of the vulva. They wander in the skin, occupying both the dermal layers and deeper layers of the epidermis. From these tissues, the microfilariae may be ingested by blackflies when they suck blood and juice from infected persons. Ingested microfilariae are carried to the midgut where they penetrate the midgut epithelium within a matter of minutes to avoid being trapped in the insect’s coagulating meal. From the midgut, the microfilariae migrate to the thoracic muscles via the homocoel where they will spend 6 to 7 days growing and undergoing morphological changes that include shedding the cuticle twice. The larvae that emerge are infective to the next person. These infective third stage larvae migrate to the insect’s mouthparts where they remain until they are inoculated into a new host when the fly feeds again.

When an infected black fly bites man, the larvae are released into the wound caused by the bite. They then migrate and grow under the skin where they become trapped by dense fibrous tissue known as a nodule formed by the host. The encapsulated microfilariae continue to grow, differentiate into sexes and mate. About two to three months after being ingested, the microfilariae escape from the nodular cysts within which their parents are trapped and move into the surrounding tissues. Female worms live in the nodules for up to 14 years, during which time they produce millions of microfilariae.

Pathogenesis

Onchocerciasis is characterised by the formation of nodules that enclose the adult worms. The nodules are probably caused by the host’s reaction to sensitising substances that are secreted by the worms. The location of the nodules in the African and American onchocerciasis differs somewhat, probably reflecting the dressing styles of the people in the two areas and the amount of body surface exposed to Simulium.

In Africa, the nodules occur mainly in the lower parts of the body, particularly the abdomen, buttocks and the legs. In contrast, in the

Americas

, particularly

Mexico

and

Guatemala

, more than half of the nodules occur on the head, 15% on the chest wall and only 25% on the pelvis.

The dispersal of microfilariae into the dermal layers of the skin throughout the body causes various types of acute and chronic skin lesions. The most common is intense pruritic dermatitis. There may be diffuse changes of chronic nature including atrophy, hypertrophy and pigmentation. Papular eruptions associated with itching and scratching can appear within a few days and can disappear spontaneously within a few weeks or months. In Africa, these typically affect the trunk and the legs.

In some cases, the affected area of the skin is markedly pruritic, dark and thickened and shows a papular or pustular eruption. Enlarged lymph nodes are commonly associated with onchocerciasis. Some individuals with chronic onchocerciasis may have hanging groin, a saclike projection of loose atrophied skin that contains a mass of large fibrotic lymph glands.

The involvement of the eye is a common feature of onchocerciasis; hence, the disease is popularly known as river blindness. The infiltration of the eye, especially the cornea, retina and the conjunctiva by the microfilariae causes inflammation, haemorrhage, congestion and degeneration. The actual cause of blindness is not very clear but it is possible that substances released by the dead worms are responsible for the degeneration of the eye. The severity of the ocular complications is influenced by several factors including the duration and the intensity of the infection, and the strain of the parasite involved. In some parts of Africa, the parasite strain is very virulent and the rate of blindness can be as high as 10 % in the population.

The socio-economic aspects of onchocerciasis can be serious. In central Africa, some fertile, riverine villages have had to be abandoned by the population because of onchocerciasis. This social dislocation causes economic loss and impoverishes the people. The effects of the disease on the skin texture and pigmentation can be a source of social stigma and mental anguish. Furthermore, the chronic itching of the skin that is commonly associated with the infection makes the patient feel very uncomfortable.

Epidemiology

Black flies have rather unusual breeding habits. They lay their eggs on wet leaves, stones or debris at the edge of flowing streams. The larvae that hatch are attached to the substrates by silk threads and are protected by open-ended cocoons. They feed on microscopic organisms that they catch using buccal fans (brush-like appendages) that sift food from the water and propel it into the mouth.

Dermatitis in a patient with onchocerciasis

Adult flies are not only veracious suckers they cause painful bites that result in persistent itching of the skin, sleepless nights, tiredness and mental anguish. These diurnal feeders, preferring bright light, can fly considerable distances (of up to 20 km) and start an outbreak of infection where it has not existed previously. Black flies in tropical regions need no more than four weeks for a complete generation. These facts have a considerable bearing to transmission of infection and attempts to control onchocerciasis.

Diagnosis

Specific diagnosis relies on the identification of typical microfilariae in the skin. This involves examining a skin snip. A snip is taken from a nodule and placed on a slide containing saline for at least 30 minutes. The worms crawl out of the skin snip into the saline. Alternatively, the snip can be teased onto a slide. To identify the microfilariae, the slides are stained to reveal the presence or absence of the sheath. Unlike the microfilariae of W. bancrofti or B. malayi, the microfilariae of O. volvulus are not sheathed. They are found in the upper layers of the dermis of the skin. They are frequently found in urine and occasionally in stained cytological smears and rarely in blood.

Control

Nodulectomy has been used in some endemic areas, particularly

Mexico

and

Guatemala

. Although it lessens the risk of eye disease, it does not reduce the prevalence of the infection in the population. Diethylcarbamazine (DEC) and suramin have been the only two effective drugs against onchocerciasis.

However, the sudden death of large numbers of microfilariae caused by DEC produces serious hypersensitivity reactions known as “Mazzotti” reactions in the host. Further studies have led to the development of a single dose of DEC that has been found to reduce the microfilarial burden by as much as 90 – 95 %, during a protective period lasting two years. Suramin, one of the drugs that are used to treat African trypanosomiasis is effective against adult Onchocerca volvulus but it is quite toxic, at times to the point of being fatal.

The latest addition to the arsenal against onchocerciasis is ivermectin. Since 1987, ivermectin, originally developed as a veterinary drug, has proved to be an excellent, safe microfilaricide that seems not to have any side effects. The drug is given as a single dose of 150 mg/ kg. The dose can be increased up to 800 mg/ kg without serious side effects.

Vector control

DDT and Abate are among the larvicides that have been used effectively against both Simulium damnosum and Simulium naevi in a number of endemic areas. In West Africa, aerial application of insecticide has been successfully used to control onchocerciasis over a large area, comprising 11 countries. The current methods are only useful for control purposes but not for the eradication of onchocerciasis. However, it is obvious that reliance on the use of insecticides is quite costly. Moreover, if used alone, they would have to be continued for 10 to 15 years (the time it takes the adult worms to die in their human hosts) to interrupt transmission.

Phylum Aschelminthes

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Six different classes, dominated by the Class Nematoda, represent Aschelminthes as a phylum. The nematodes (Nema, thread) or roundworms are ubiquitous small worms that dwarf in numbers all other groups of multicellular animals except insects and mites.

Aschelminthes are pseudocoelomate, unsegmented worms that are covered with a cuticle. An unusual aschelminth trait is parthenogenesis (development of an unfertilised egg). In the classes Nematoda, Rotifera and Gastrotricha, males may be lacking and successive generations of females are produced parthenogenetically

Still another remarkable characteristic of the phylum is the consistency of cell numbers (eutely), in which a precise and relatively small number of cells, remaining unvaried throughout the animal’s life, comprise both specific organs and the entire animal. The number, constant not only for the species but also for the taxonomic group, can be used as part of its morphological definition (for example, the central nervous system in Ascaris and many other nematodes consists of 162 cells)

Class Nematoda

The class Nematoda is very important to us among the group as it consists of parasites of medical and veterinary importance. The class is characterized by the presence of a complete digestive system, consisting of a mouth, intestine, anus and absence of cilia.

Nematodes are found practically in every ecological setting. They live in animals and plants as parasites and in mud, marine, fresh and brackish waters, soil and mud as free-living organisms. They vary in size from a few microns to slightly over a meter in length.

Morphology

Nematodes are cylindrical in shape, tapering at both ends of the body. The digestive system is a long tube that runs from the buccal cavity to the anus. In hookworms, the mouth is armed with teeth or cutting plates. Some nematodes are provided with lips, papillae or a leaf crown around the external opening of the mouth. The pharynx (oesophagus) is a strong muscular tube with walls that can contract and expand, creating a pump-like suction mechanism. The neuromuscular system consists of a circumesophageal ring or nerve ring around the oesophagus and dorsal and ventral nerve cords, which give rise to motor and sensory nerves. The excretory organs lie within the lateral lines and open via a pore ventral to the oesophagus.

Internal structure of a nematode

The gonads lie in the pseudocoele, a space between the intestine and the body wall that is filled with a fluid. The rugged cuticle is not only an extraordinary effective protection against harmful external substances but also serves as an exoskeleton to which muscles are attached.

Female nematodes have a pair of ovaries consisting of cells (oogonia) that produce the eggs. The uteri are usually packed with eggs. The eggshell material is produced by the uterine cells. The uteri unite to form the vagina, which may contain a seminal vesicle for storing male sperm. The vagina opens to the outside by a pore or vulva at the middle of the body, though it may also be near either end of the body.

The male genital system consists of one testis and a seminal vesicle, which continues posteriorly as a muscular ejaculatory duct that opens into the rectum or cloaca. The cloaca serves as a conduit for sperm and digestive wastes. Copulatory spicules protrude through the cloaca opening. The spicules, usually two in number, unite and form a tube through which spermatozoa are injected into the vulva and vagina of the female.

Generalized structure of male (A) and female (B) nematode

Nematodes are classified into two subclasses: Phasmidia (have caudal sensory organs) and Aphasmidia (lack caudal sensory organs). The phasmids include most soil nematodes, most parasites of insects and vertebrates. The aphasmids are mainly aquatic forms and a few parasitic ones.

Life cycle

Life cycles differ greatly among the many nematodes that are parasites of man. Mature female worms produce eggs, which pass out of the body with faeces. Most of the eggs are produced when they are not embryonated and become embryonated in the soil. The embryonated eggs are ingested and under the action of the gastric juices of the host, the larvae are liberated from the eggs. In some parasites, such as Ascaris, the larvae penetrate the wall of the small intestine and migrate to the lungs via the blood. From the lungs, they reach the pharynx and finally settle in the small intestine, where they will attain maturity, mate and produce eggs.

In other nematodes, such as hookworms, the larvae hatch from eggs in the soil and after going through several moults become infective. These third stage infective forms enter the body through the skin. Trichinella has a unique life cycle in nematodes in that the entire life cycle is spent in the host. Transmission from one host to another is through predation, cannibalism or carrion feeding.

Hookworm infections

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Hookworms are present in most of the countries of the world. Two species of hookworms are parasites of man. These are Ancylostoma duodenale and Necator americanus. They differ slightly in structure but have identical life cycles. They also somehow differ in distribution although very often this overlaps. A. duodenale is found mainly in the northern regions - Europe, North Africa, Asia,

China

and

Japan

. N. americanus is dominant in the southern United States, Mexico, Central America, the West Indies, South America, East Africa, Central and southern Africa. Nevertheless, the two seem to coexist in much of the continent of Africa. In East Africa, N. americanus is more predominant than A. duodenale.

Hookworms are among the most important parasites of man accounting for thousands of deaths each year. In 1949, the global prevalence of hookworm infection was estimated at 457 million but in 1962, the figure was revised to 600 million. The current estimate puts the number of people infected with hookworms at between 800 million – 1500 million with about 60000 deaths per year.

A. duodenale females measure 12 mm and the males 9 mm long. N. Americanus, on the other hand, is smaller and more slender than A. duodenale with the females being about 10 to 11 mm long. Its vulva, which is anterior to the middle of the body, lacks a spine.

The male has a longer and narrower bursa than that of A. duodenale. The buccal capsule of N. americanus is provided with cutting plates unlike that of A. duodenale, which consists of paired tooth-like processes. In both species, the adult worms live in the small intestine attached to the intestinal mucosa by their armed teeth. They feed on blood and other nutrients present in the small intestine. The female N. americanus produces between 5000 to 10000 eggs daily while A. duodenale produces about 30000 eggs per day.

Life cycle

The two species of hookworms produce thin-shelled, transparent and ovoid eggs that are indistinguishable. In fresh stool, the eggs are usually in a four–celled stage of development. Under warm, wet temperatures, embryonation proceeds faster and hatching takes place in 24 to 48 hrs. Optimal conditions include good aeration, moisture, shade and a temperature of around 36 ^oC. The emerging tiny rhabditiform larvae feed on bacteria and organic debris, while undergoing growth and after shedding the cuticle, continue to feed and grow bigger. After a period of 5 to 8 days, they cease feeding, shed their cuticles and become third stage infective filariform larvae. The filariform larvae are slender with a closed mouth, an elongated oesophagus and a sharply pointed tail.

Under favourable conditions, the larvae move from the lower parts of the faeces to the surface and to the surrounding vegetation. However, if the sun is too hot, they retreat to the lower parts of the faeces to avoid desiccation. The larvae can remain in the soil for several days, even weeks, depending on the environmental conditions.

Human infection occurs when the infective larva is in contact with any part of the skin. Often it is the hands and feet that are in contact with soil contaminated with human faeces.

The larvae enter the body by penetrating the skin where they remain dormant for 1 to 2 days. The larvae reach the lungs via the blood and enter the air sacs. From the lungs, the larvae migrate to the throat where they are swallowed.

On reaching the small intestine, the larvae, now much larger and in their fourth stage of development, invade the spaces between the villi and moult one more time into sexually mature males and females. Mating ensues and about 6 weeks post-infection, the females start passing out eggs in the faeces. Adult hookworms can live in the human intestine for up to 6 to 5 years, depending on the strain of the parasite and the nutritional status of the host.

Parthenogenesis

The penetration of the skin by the larvae is followed by itching and pain at the entry site. The migrating larvae damage the tissues through which they pass, especially the alveolar sacs of the lungs. On reaching the intestine, the worms attach themselves to the mucosal surface of the small intestine by their buccal cavities, puncturing the local blood and lymph vessels in the process. Hookworms feed on blood; the amount of blood lost by the host is dependent on the number of worms present. It has been estimated that each adult worm drinks approximately 1 ml of blood daily.

The important damage produced by hookworms is haemorrhage from the intestinal wall. This is usually proportional to the number of worms present. Counts of less than 50 eggs per gm of faeces are not associated with serious haemorrhage and rarely evoke any clinical symptoms. However, people with more than 200 eggs per gm of faeces, lose a lot of blood and develop anaemia. Hookworm anaemia is typically of microcytic and hypochromic nature.

N.americanus compared with A.duodenale

Useful substances like food nutrients, mineral salts and immunoglobulins are lost through leakage. The picture may further be complicated by a secondary bacterial infection. In addition to loss of blood and other nutrients, a heavy infection impairs the intestinal mucosa causing malabsorption and aggravating the nutritional status in persons who do not have enough to eat and are already malnourished.

The diet is important in influencing the severity of infection. In light and moderately heavy infections, the blood loss can be compensated for by an adequate, well-balanced diet that is rich in minerals, including iron, animal proteins and vitamin A. In severe hookworm disease, however, even with a highly balanced diet, the body is unable to produce new supplies of normal red blood cells as rapidly as they are lost. Moreover, the perennial protein deficiency in the diet of inhabitants of the developing world, does contribute greatly to the anaemia of hookworm patients, whose ordinary diet is predominantly carbohydrate.

In endemic areas infection is acquired in childhood and by the time the individual reaches maturity he will have been exposed to the hookworm infection repeatedly a number of times. For that reason, a large section of the population will have developed some protective immunity. Immune individuals carry fewer worms and do not experience serious symptoms.

Symptoms

Nausea, headache and an irritating cough are the usual symptoms of an acute early infection. The symptoms are mainly caused by larvae migrating through the tissues and lung air sacs. Between 4 and 6 weeks post-infection, the patient experiences severe colicky pains, flatulence, diarrhoea, and loss of weight, dyspnoea, dizziness, and marked paleness. During this period, a significant leucocytosis may persist at a significant level for months.

In severe cases, the haemoglobin may be reduced to 30% or less, with 200 000 or less corpuscles. The most noticeable symptoms are a severe pallor, tiredness, indifference and withdrawal from participating in social activities, enlarged and palpating heart, irregular weak pulse, oedema making the face puffy and pot-bellied abdomen. Children suffer physical and mental retardation, stupidity and backwardness in school.

Epidemiology

Hookworm infection is one of the commonest parasitic diseases in the tropics. It thrives well under warm, moist temperatures and ample rainfall that are needed for the survival of the eggs and development of the larval stages in the soil. Human infection is caused by two species of hookworm - N. americanus and A. duodenale. Wherever these parasites are endemic, they result from unsanitary disposal of human faeces.

The continued propagation of hookworm disease depends largely on the frequency of contact with contaminated soil. People working in fields that have recently been fertilised with human faeces are at risk of being infected whenever the hands or feet touch the soil, while miners in unsanitary underground tunnels may become infected on practically any area of the skin.

Diagnosis and Treatment

Diagnosis is based on the detection of eggs in faeces. The presence of more than 200 eggs /gm of faeces indicates a severe infection in both Necator americanus and A. duodenale. In general, the latter is more prolific than the latter, usually producing twice as many eggs as the former and causing more damage.

A light infection may be treated directly with drugs without prescribing any supportive diet. There may, however, be need to prescribe a diet rich in protein if the patient’s haemoglobin level is low, and iron to replace that lost through haemorrhage caused by the worms. The most effective drugs for treatment of hookworms are mebendazole and pyrantel pamoate.

Control

Proper disposal of human faeces are mandatory to a successful control of hookworm infection. The use of toilets and pit latrines is essential part of the strategy to control transmission of hookworms in order to prevent soil pollution. Where the pollution of the soils with eggs and larvae is deemed high, it might be necessary to use chemicals to disinfect them.

Infected individuals should be treated to clear the infection and allow the damaged intestinal tissue to heal. If the infection is rampant in the population, mass treatment of the entire community should be undertaken at regular intervals. This helps to reduce each individual’s worm load and concentration of eggs in the soil.

In severe hookworm disease, infected persons should be given dietary supplements rich in animal minerals, proteins and vitamin A to reinforce the iron and other minerals lost. As the infection is acquired through the contact of the infective larvae with the skin, particularly the foot, the wearing of shoes reduces the contact with the larvae. It is quite helpful to encourage people, especially children to wear shoes regularly.

Ascaris

2010-01-24T22:18:00.000-08:00

Ascaris lumbricoides is the largest roundworm of man and mammals. It is a common human parasite in the tropics and subtropics, with a high prevalence in children. It prefers warm, moist conditions and is normally present together with another roundworm, Trichuris trichura.

These are large elongated and cylindrical worms, tapering at the ends. The posterior end of the male is curved ventrally. The male measures 12 - 31 cm long by 3 mm in diameter and the female measures 20 - 35 cm in length by 3 – 6 mm in diameter. A closely related form, Ascaris suum, infects pigs and occasionally humans.

Life cycle

The female worm is highly prolific producing more than 200000 eggs daily. These relatively large and ovoid eggs have thick transparent shells with coarse rough appearance. They are covered by a cuticle that is quite resistant to desiccation and chemicals but shows less resistance to heat, freezing and direct light. If kept in a 10 % formalin solution, the eggs remain viable for weeks.

Favourable conditions for the survival and persistence of viable eggs are moist, well-aerated shady soils, especially loamy soils. In some parts of the world, coffee and banana plants, which are grown around the dwellings, provide ideal conditions for Ascaris and other intestinal parasites.

Unembryonated eggs are passed out in faeces. Embryonation occurs in moist environment and normally takes about two to three weeks. Under favourable conditions of temperature, moisture and air, the eggs develop active embryos, which do not become infective until they have moulted to the second larval stage.

Following the ingestion of the embryonated infective eggs, the larvae are liberated in the duodenum. The larvae penetrate the intestinal wall, enter mesenteric blood veins and lymphatic vessels and reach the lungs, where they spend at least a week. Around the 10th day since hatching, the larvae, which are now quite large, leave the lungs via the tracheal passages to the throat, where they will be swallowed and taken to the small intestine. The third moult takes place in either the lungs or intestine. A final moult that occurs in the small intestine produces mature worms. It has taken at least 8 to 12 weeks since ingestion of the eggs for the worms to become sexually mature and begin mating. Adult worms remain in the small intestine for 9 to 12 months. Quite often, however, they are expelled spontaneously before that.

Pathogenesis and symptomatology

Migrating larvae cause a lot of damage to the liver and the lungs. However, this depends on the numbers of larvae involved. A few larvae will usually provoke no response from the host, especially if it is an initial infection. However, subsequent migrations cause intense tissue reaction in the liver and lungs, even when relatively few larvae are involved.

Headache, muscular pain, pneumonitis consisting of a dyspnoea often of the asthmatic type, a productive cough, wheezing and fever are common symptoms associated with Ascaris infection. During the period of the productive cough, the sputum may contain many eosinophils and larvae. Lesions due to larvae are also found in the spinal cord, brain, and heart muscle.

Infection in children is usually associated with abdominal pain, loss of appetite, listlessness and at times nervous symptoms.

Adult worms in the small intestine frequently provoke no symptoms. However, susceptible individual and people lacking proper nutrition tend to carry heavy parasite burdens and may experience mild abdominal discomfort, lack of appetite, diarrhoea and constipation. A heavy ascarial infection is likely to interfere with the host’s protein nutrition, something of great concern in areas of the world where a protein-rich diet is rare.

Sometimes when disturbed by the drugs or other factors, adult worms tend to migrate forwards or backwards and become entangled with one another and cause obstruction of the intestine, resulting in gangrene and even death. Some of the worms may enter the bile and pancreatic ducts causing jaundice or pancreatic haemorrhage. Worms may enter the appendix and cause appendicitis. But should the worms penetrate the intestine and reach the heart or brain, they can cause death.

An aspect that is more of an embarrassment than injury is when a worm leaves the intestine, wanders up the alimentary canal and creeps out of the nostrils. On rare occasions, larvae have been seen coming out of the lachrymal duct.

Epidemiology

Ascaris is maintained by faecal contamination of the soil. In rural and in congested centres in the developing countries human faeces are usually deposited by small children (and older children during the hours of darkness) in and around the home and since the eggs are quite resistant to desiccation and can remain viable in the soil for months, or even years, the numbers build up in the soil to considerable levels as the time passes. With time, the compound, house floors and even the utensils may be heavily polluted with the eggs of Ascaris and, if the picture is the same in the whole village, the rate of transmission will be high and many people will be infected. With such a high rate of transmission, the intensity of infection in children and other vulnerable groups can be very high indeed.

Human infection is possible in a number of ways. Children can ingestion dirt contaminated with eggs or they may transfer eggs to the mouth via unclean hands. Furthermore, infection may be contracted through eating raw food especially vegetables that have not be cleaned sufficiently, or through drinking water contaminated with faecal matter.

Control Methods

The maintenance of proper sanitary conditions considerably reduces the transmission of infection. This involves the regular use of toilets to prevent soil contamination with human faeces and adhering to personal hygiene by washing hands before eating and eating food that has been properly cooked. Salads that are usually eaten raw should be washed thoroughly.

Mebendazole, pyrantel pamoate and piperazine are effective against ascariasis. All have a wide margin of safety.

Other Ascrids

Ascaris suum is a common pig roundworm that is similar to A. lumbricoides in many ways and is of great economic importance to pig-keepers all over the world. It causes stunting of growth in piglets.

Ascaris suum probably constitutes an occasional source of intestinal ascariasis in man. In some instances, it will develop to adult stage in man. Likewise, A. lumbricoides larvae have been shown to develop in pigs to adult stage.

Other important ascarids include Toxocara canis in dogs, Toxocara cati in cats and Parascaris equorum in horses. The latter is an important parasite of horses throughout the world that inflicts considerable mechanical damage through its migrating larvae on the tissues and lungs of horses, causing pneumonia and even introducing bacteria and viral infections. Like the human Ascaris, adult worms may perforate the intestinal wall, damage the liver and bile ducts and cause general toxaemia from metabolic waste products.

Trichuris trichura

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Trichuris trichura or whipworm derives its name from its whip-like structure, in which the posterior end is thick and the anterior end is thin like a thread. The thick posterior end contains the reproductive organs of the organism. The oesophagus occupies the whole of the anterior end. The male worm measures 30 to 40 mm in length while the female measures between 35 and 60 mm long.

The natural location of Trichuris trichura is the caecum and the lower part of the large intestine.

Trichuris is also found in dogs, pigs and apes. The worm has a cosmopolitan distribution and thrives well under wet, warm conditions. Its distribution is, for the most part, similar to that of Ascaris lumbricoides.

Like all other intestinal nematodes, T. trichura is associated with poverty and ignorance. It is therefore common where the level of poor personal hygiene is low and the general sanitation is poor.

Life cycle

The female worm produces 4000 to 7000 eggs daily. Each spear-like egg is brown with a plug on each end. Under warm wet conditions, the embryonated eggs take about 3 to 6 weeks to become infective. Infection is acquired through drinking water or eating raw vegetables that have been contaminated with the embryonated eggs. Under normal atmospheric conditions, the eggs can remain viable for one to two months, or even longer. Children are particularly vulnerable to infection because of their habits of picking soiled objects and getting their hands dirtied.

After the eggs have been ingested, the larvae hatch in the lower part of the small intestine and the large intestine, penetrate the mucosa of the colon and caecum and undergo development. About 3 months later, mature worms appear and egg production begins.

Pathogenesis

The severity of the infection depends very much on the intensity of the infection and the nutritional status of the individual. Light infections are usually without symptoms. Heavy infections provoke extensive irritation of the mucosa surface of the colon and the caecum, which show evidence of erosion, bleeding and the presence of large numbers of parasites. Observed symptoms are loss of appetite, nausea, diarrhoea, steaks of blood on stools, loss of weight, anaemia, eosinophilia, abdominal discomfort, emaciation and sometimes fever. Heavy infections may also be suggestive of a concomitant hookworm disease or infection with Entamoeba histolytica.

In chronic infections, mucosal irritation of both the colon and the rectum may eventually lead to the prolapse of the rectum.

Children aged 1 to 5 years are frequent victims of trichuriasis and quite often suffer from chronic diarrhoea or dysentery, rectal prolapse and loss of weight. They may also suffer from anaemia of the microcytic type because of lack of adequate nutrition and loss of blood from the affected intestinal mucosa.

Epidemiology

The unembryonated eggs of T. trichura require a shaded soil and warm, moist conditions to develop and after about 4 weeks, a coiled larva can be seen inside the eggshell. The eggs can be ingested with soil or via contaminated hands. The conditions that favour the transmission of A. lumbricoides are the same conditions that favour T. trichura, so that the two are usually found together. It is particularly common in children and, even in localities where the transmission is quite high in the whole population, the incidence and intensity of infection in children remain higher than in the general population.

Diagnosis

Diagnosis is accomplished by the demonstration of characteristic eggs in the faeces. Numerous adult and immature worms are usually attached the mucosal epithelium of a prolapsed rectum.

Control

Effective control measures involve maintenance of high personal standard of hygiene and use of toilets for disposal of human faeces. In addition to the above measures, children in endemic areas should be give regular treatment with mebendazole, which is quite effective and safe.

Enterobius vermicularis

2010-01-24T22:13:00.000-08:00

Pinworm, anal worm, and seat worm are common names given this strictly human cosmopolitan parasite. Although it is found all over the world, it is more common in the temperate regions than in the tropics. Adult Enterobius vermicularis live in the human caecum, appendix and the large intestine. The worms are white in colour with a muscular oesophagus. The females are considerably larger than the males, measuring 8 to 13 mm long and have a tapering posterior end that ends in a long filamentous tail. The males measure 2 to 5 mm and have a curved posterior. The males are not normally found because they die soon after copulating with the female.

Life cycle

Infection is acquired by swallowing embryonated eggs present in contaminated water or food. It may also be acquired by inhaling contaminated dusty air, or by sucking fingers. The eggs hatch in the small intestine and the larvae migrate to the colon and appendix, where they mature into males and females in about four weeks.

Female worms do not usually lay the eggs in the host’s intestine, but crawl to the anus at night when the host is sleeping and deposit the eggs. Each female worm produces 5000 to 10000 eggs daily. Sometimes the pressure exerted by the eggs is too much for it and bursts, scattering the eggs about on the body, bedding, clothes and even the dust in the room.

Pathogenesis

The most obvious symptom associated with E. vermicularis is pruritus ani. This itching of the perianal region is probably caused by substances that are released by the dead worms and their eggs. The intense itching is followed by scratching, both of which make the host quite uncomfortable. The resulting scratching transfers eggs to clothing, hands, and eventually to food. Because of the incessant itching and scratching, the patient is sometimes unable to sleep and shows increasing evidence of restlessness and tiredness. On rare occasions, the worms may wander into female vulva and cause vaginitis.

The immature burrowing worms may cause inflammation of the caecal region, followed by abdominal pain and digestive disturbances.

Epidemiology

Because the eggs of T. vermicularis are quite light, they can be scattered by wind and inhaled. The inhaled eggs reach the intestinal region by way of the digestive tract and cause infection. The usual mode of infection is through ingestion of larvae. The urge to scratch an itching anus leads to the contamination of the hands with worm embryonated eggs, the latter finding their way easily into the mouth during meals, especially in individuals who do not keep their hands clean. By the nature of their habits, more children are usually infected with Enterobius any other groups of people.

Bed sheets, towels, and furniture, soap, bathing basins and even drinking water can easily spread the eggs. The infection spreads quite easily in crowded places such as dormitories, dining halls, classrooms, toilets and many other places where people are crowded.

The eggs are not very resistant to environmental conditions and readily die in dry hot temperatures. They survive well in cool moist temperatures of the temperate regions. Adult worms have a life span of something from 37 to 50 days.

Diagnosis

Pinworm eggs found in the perianal skin are diagnostic. Frequently mothers observe the little white worms creeping out of a child’s anus. The worms may also be seen in water and stool after purging. Faecal examination is not very reliable with only a 25% success. Better results are obtained by applying a Scotch tape over the anus and then examining it for the eggs.

Control

Control should include maintaining personal hygiene and clean living quarters. Children’s clothing and their sleeping quarters should be kept clean. In addition, children’s fingernails should be kept short and clean.

Treatment

Effective drugs include mebendazole, albendazole, and pyrantel pamoate and piperazine hexahydrate. It is usually advisable to treat everybody in the house once an infection has been detected. The treatment can be repeated at least every two weeks until the infection has disappeared.

Strongyloides stercoralis

2010-01-24T22:10:00.000-08:00

Strongyloides stercoralis is one of the smallest nematodes of man. It is very common in the tropics and subtropics. Its distribution is similar to that of hookworms. Adult worms live in the host’s intestinal mucosa in the upper part of the intestine, although they may be found anywhere from the duodenum to the rectum.

Among the domestic animals, dogs are readily susceptible to S. stercoralis and probably contribute to human infections through their faecal contamination of the environment. Cats can become infected but the infection appears to be transitory, the parasites dying after a few months. Other species of Strongyloides occur in monkeys, rodents, sheep and pigs.

Life cycle

Female worms that are extremely slender, measuring about 2 to 2.5 mm long by 40 to 50 µ in diameter, produce eggs parthenogenetically. Each female worm lays slightly less than 50 eggs per day that are deposited in the intestinal mucosa where they undergo development and after hatching the larvae make their way into the intestinal lumen to be expelled with host faeces.

The larvae are rhabditiform, resembling hookworm larvae, only distinguishable by having a very small mouth cavity. Larval development may take either a direct course or an indirect course. Under the direct mode of development, the rhabditiform larvae, after undergoing two moults, transform into infective ensheathed filariform larvae, which then infect the host through skin penetration.

Under the indirect course of development, the rhabditiform larvae deposited with faeces, feed, grow, and after four moults become adult free-living males and females. The females then produce eggs that hatch into rhabditiform larvae, which develop into infective filariform larvae after two moults. These ensheathed filariform larvae appear about 2 days and by day 5 or 6, are numerous in the soil. These larvae infect a new host by skin penetration. There may be more than one free-living generation but this seldom occurs.

Under rare cases, the whole life cycle may take place within the host. Under this so-called hyperinfective mode of development, the rhabditiform larvae produced by parasitic females transform into filariform larvae in the intestinal lumen after undergoing two moults. These then penetrate the host intestinal mucosa, where they develop into adult worms and produce eggs.

The filariform larvae from direct or indirect mode of development that penetrate the skin appear in the lungs three days later and spend sometime there undergoing further growth. They then travel to the small intestine via the tracheopharyngeal route and on arriving in the small intestine, enter the epithelium of the glands. The larvae continue their growth and after moulting twice attain maturity with new larvae appearing in the faeces three weeks post-infection.

Following skin penetration by the larvae, there may be a transient period of cutaneous larval migrans, in which the larvae wander within the subcutaneous tissues before they find their way to the lungs. This causes mechanical damage, intense itching and pain. The passage of the larvae through the lungs causes little reaction in light infections, but in heavy infections, there may be alveolar haemorrhage, oedema, pneumonitis, eosinophilia and coughing.

The presence of adult worms in the small intestine causes little reaction except when large numbers are involved. There is usually moderate leukocyte infiltration and other inflammatory cells. Heavy infections may be accompanied by severe erosion of the intestinal mucosa, which increasingly becomes non-functional, with intense infiltration of inflammatory cells into the submucosa, atrophy of the villi and destruction of large areas of the mucosa. The destructive effect of the infection on the intestinal wall leads to malabsorption and emaciation. Strongyloides stercoralis rarely causes death.

Symptoms

Coughing and pneumonitis follow the migration of the worms through the pulmonary tissue. In rare cases, the filariform infective larvae develop to the adult stage within the lungs causing acute inflammatory reaction. Examination of the sputum reveals the presence of adult worms, filariform, rhabditiform larvae and eggs.

In the intestine, light infections lead to abdominal pain and diarrhoea. The blood picture is characterised by leucocytosis with a moderate to high eosinophilia. Mild to moderate chronic infections elicit symptoms of abdominal pain, nausea, vomiting, and diarrhoea. In severe cases, there may be uncontrollable diarrhoea with blood and undigested food in the stools. The loss of blood and continued fluid drain from the body results in severe emaciation.

Ectopic infections caused by filariform larvae migrating subcutaneously are common with S. stercoralis and are characterised by urticarial creeping eruption of the skin of the buttocks, abdomen and thighs.

Epidemiology

In S. stercoralis infections, rhabditoid larvae rather than eggs are passed in the faeces, and these can mature rapidly in 24 to 36 hours to the infective filariform stage by direct development in faeces, soil or water. Under suitable conditions, indirect development through the free-living adult generation may occur instead and since the progeny of each free-living female is about 30 to 50, this leads to considerable pollution of the soil with larvae.

Strongyloides seems to parallel hookworm in some geographical areas, occurring mainly in warm, humid river basins and coastal areas, and related to poor sanitation. It generally has a lower prevalence than hookworm infection but in some tropical areas such as

Brazil

and

Colombia

, it appears to be more prevalent and serious than hookworms. It is usually common in institutions like mental hospitals, prisons and homes for retarded children.

Dogs are readily susceptible to human strains of S. stercoralis and probably do play a role in the transmission of the parasite to humans.

Diagnosis

Eggs of S. stercoralis are difficult to find in the stool although adult worms can be detected in fresh stool. Detection of active rhabditoid larvae in the fresh stool confirms presence of strongyloidiasis. Filariform larvae may be found in old faeces that have stayed for a day or more.

Control

Proper disposal of human faeces are a sure way of preventing strongyloidiasis. The same steps required to control hookworm and other intestinal parasites apply to S. stercoralis.

Treatment

Both thiabendazole and albendazole are effective drugs for the treatment of strongyloidiasis.

Trichinosis

2010-01-24T22:08:00.000-08:00

Trichinella is a parasite of wild animals, domestic pigs and man. It has a wide distribution that includes all geographical regions of the world. In Europe and North America, human infection is mainly due to eating undercooked pork and pork products, especially sausages. In North Africa, Trichinella is scarce mainly because of dietary habits and Islamic cultural norms that prohibit eating pork. Human infection is low in Africa south of the Sahara with domestic pigs and rodents playing almost no role in the transmission.

Morphology

The trichina is one of the smallest nematodes of man. Adult females are 3 to 4 mm long by 50 to 60 µm in diameter while the males are only about 1.3 to 1.5 mm long by 30 to 40 µm in diameter. They are therefore difficult to see with the unaided eye. The male has no spicule, and bears two conical appendages, which are used in copulation. Adults and larvae have anterior stylets.

Life cycle

Infected pork contains encysted tiny larvae, which are set free by the digestive processes in the gut. Freed larvae enter the mucosal epithelium of the small intestine, particularly the spaces between the villi where they undergo sexual differentiation. Mating takes place soon after and the females that are viviparous start producing larvae within four to five days. The production of larvae reaches its highest point during the second week of infection and continues, albeit at a moderate rate, for 4 to 16 weeks.

These first stage larvae are carried in the lymphatic system and later in the bloodstream through the lungs and left part of the heart to all parts of the body. Only those arriving in the voluntary muscles survive. The most parasitised parts of the body are the diaphragm, larynx, tongue, intercostal muscles, masseter, biceps, pectoral, deltoid, and gastrocnemius muscles. As the larvae undergo growth within the muscle fibres, the host forms a fibrous tissue capsule around them so that they become trapped or encapsulated. After 3 weeks, the encapsulated larvae become infective. The encapsulated larvae appear coiled in concentric rings and can remain viable for many years.

Trichinella has no free-living phase and infection can only be contracted through predation, cannibalism or carrion feeding. The larvae can survive in a rotting carcass for two to three months. Carrion feeders are important in the transmission of trichinosis. The adult worms are very short-lived, the females surviving for about 16 weeks in man and only ten days in the dog.

Pathogenesis

Penetration of the young excysted worms into the intestinal mucosa provokes a cellular response characterised by eosinophilic infiltration, which is particularly noticeable in the heart muscle. Wherever the larvae lodge, as in the capillaries of the brain, eye, lungs, etc, they provoke a cellular inflammatory process around them.

Light infections are seldom symptomatic. However, heavy infections cause severe acute abdominal pain (almost similar to food poisoning) and diarrhoea. Migration of the larvae and their penetration of muscles cause fever, intense muscular pain, and oedema (marked puffiness), difficulty in moving eyes and respiratory distress. Other symptoms include difficulty in mastication, speech and walking. Death is usually due to myocarditis, pneumonia and complete exhaustion.

Epidemiology

It was generally assumed that trichinosis was a disease of flesh eating mammals in the temperate zones where pigs and rats were already known to be the major source of human infection. As no cases of trichinosis had been detected in Africa south of the Sahara, it was assumed that the region was free from trichinosis. However, in 1959, eleven young men, of whom one died later, were admitted to a hospital near Mt

Kenya

complaining of muscular pain and showing oedema of the face or limbs. Although they were originally diagnosed as suffering from typhoid fever, subsequent investigations confirmed the presence of Trichinella. All the affected herdsmen had eaten roasted meat from a bush pig they had killed.

Since then further studies have shown that although human trichinosis is not common in the tropics, sylvatic transmission between carnivores and wild pigs is quite common. Most human infections reported so far have been associated with the eating of meat from the bush pig or warthog.

The reason for the low prevalence of trichinosis among the Africans is probably explained by the fact that most communities in Africa do not eat meat from wild carnivores. Even the warthog and the bush pig are not commonly hunted for their meat. Moreover, the culture of rearing pigs for commercial purposes has only recently come with urbanisation. This therefore explains why the infection in humans is low despite the high prevalence of sylvatic transmission.

The trichina is now thought to consist of at least four geographically distinct species. One of these strains, T. nativa, is an arctic form that is present in polar bears, arctic foxes, wolves, minks, walruses and seals. It affects mainly fishermen and hunters, such as the Eskimos of Greenland. This parasite is highly tolerant to cold temperature (can tolerate a temperature of -12 ^oC to – 17 ^oC for at least six months).

T. spiralis is a temperate parasite of foxes, wild cats, weasels, wild boars, rats and pigs. T. spiralis is mainly maintained in pigs and rats in people’s homes and garbage dumps. Human infection is due to eating pig meat and, less frequently, it may emanate from a butchery contaminated with infected pig meat, which also serves other animal meat. It is now rarely encountered in humans in much of Europe, North America,

Australia

and

New Zealand

because of improvements in sanitation and proper management of pigs.

T. nelsoni is a tropical species that is maintained mainly in warthog, bush pig, hyenas, jackals, leopards and lions. Human infections are very rare in Africa south of the Sahara and the few cases that are reported are probably acquired through eating meat from the bush pig or warthog. Rodents and domestic pigs do not seem to play any demonstrable role in the transmission of T. nelsoni.

Patients infected with T. nelsoni can tolerate unusually large worm burdens that would be fatal with other strains. For example, the average worm burden among the young herdsmen admitted in a hospital near Mt

Kenya

was 2715 larvae/gm of thigh muscle. The worm burdens per gram of muscle in the fatal case were - tongue, 5190, thigh 4560 and diaphragm 4560. In addition, T. nelsoni does not establish as easily in laboratory animals, as does T. spiralis.

T. pseudospiralis is essentially a parasite of birds and mammals although a few human cases infected with this parasite have been reported.

Control

Control involves the treatment of infected individuals and instituting appropriate personal and public health measures to check the transmission. Strict observance of hygienic conditions when handling pork and pork products especially in slaughterhouses and butcheries is necessary to prevent contamination and spreading of the infection.

Serious epidemics have been reported following parties during which the revellers ate uncooked pork seasoned with spices. The trichinae can be killed by freezing pork at -15 ^o C for 20 days (except for artic species) or cooking it at 60 ^o C for at least thirty minutes.

Thiabendazole and mebendazole are effective against intestinal larvae but not against larvae encysted in the muscles. .

Introduction to platyhelminthes

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Flatworms or Platyhelminthes (platy - flat, helminthes - worm) consist of three classes: (1) the free-living nonparasitic, ciliated Turbellaria (2) the Trematoda (flukes) and (3) the Cestoda (tapeworms).

The flatworms have a nerve structure that consists of a central nervous system with ganglia and nerve trunks. The body shape is controlled by longitudinal and circular muscles that underlie the outer epidermal layer of the body. The excretory system consists of flame cells or protonephridia. These special ciliated cells collect body fluids and pump them into a complex series of ducts and channels that drain into an excretory bladder. The fluid is excreted through one or more excretory pores.

Motility is well developed in free-living Turbellaria, as they possess cilia on their ventral body surface and secrete a coat of mucus on which they can easily glide.

Structural adaptations among the flatworms include hooks, spines, and suckers; slaps of tissue, or combinations of these, that provide a mechanism for ‘staying put’ usually in the intestine of vertebrates.

The digestive system is extremely variable. In most of the trematodes, the intestine branches into two blind sacs, or caeca, while in the tapeworms, the digestive system has entirely been lost, so that food absorption takes place across the entire surface of the organism.

The reproductive system is well developed in Turbellaria and is extraordinarily complex in the flukes and tapeworms, which have essentially become reproductive machines. Since the chance of a parasite to transfer its progeny from one host to another is remote and fraught with danger, parasites have a high reproductive potential. Combined with this adaptation certain trematodes have developed complex life cycles that involve intermediate hosts, specialized larvae, and both sexual and asexual reproductive methods.

In tapeworms, sexual reproduction follows mutual exchange of sperm between segments of different worms, or different segments of the same worm. Most tapeworms and flukes are hermaphroditic (monoecious, both sexes occurring in the same individual). Asexual reproduction in tapeworms occurs in the larval forms of certain taenia-like cestodes, such as Echinococcus granulosus. In these, the larvae develop in bladder-like cysts within the tissues of a host. This type of larval reproduction is called polyembryony (many larvae).

The cestode body consists of a chain of segments or proglottids budded out from a growth area near the scolex (head). Each segment contains both sex organs. In some tapeworms, the segments detach themselves from the worm, and crawl out of the host’s intestine as if they were separate worms. Segmentation seems to have the purpose of duplicating reproductive capacity of the tapeworms. Tapeworms produce large numbers of eggs. The beef tapeworm, Taenia saginata, may grow up to 10 m long and produce up to 80, 000 eggs per each mature proglottid.

The order Digenea (two hosts in the life cycle) is by far the most important of the groups of trematodes. The digenetic trematodes are endoparasites of man, domestic animals and innumerable kinds of wild animals.

Life cycles

Digenetic trematodes exhibit interesting complex life cycles that involve more than one host, usually a snail intermediate host (there may be more than one snail host) and a final vertebrate host. The sequence of larval forms in the intermediate host differs so markedly that each is given a special name: miracidium, sporocyst, redia, cercaria and metacercaria.

In all the flukes, the general reproductive pattern is quite similar, but the specific host and manner of development is characteristic of each species. The eggs are laid and expelled in either the faeces or urine depending on the species. The eggs require an aquatic medium to hatch. The ciliated larva, called a miracidium, swims until it meets a suitable snail. After penetrating the snail tissues, the miracidium sheds its ciliated epithelium and eyes and continues to grow. While still in the snail, the miracidium becomes a sac (the sporocyst). Germinal cells lining the walls of the sporocyst develop into second-generation sporocysts or rediae (singular, redia). The rediae develop into tailed cercariae (singular, cercaria) that escape through a birth pore or through the rupture of the sporocyst. The cercariae have many ways by which they access a new host. Some may encyst on vegetation as metacercariae and be ingested by a grazing vertebrate. Others swim about in the water until they find a host and penetrate it; still others may seek another intermediate host, such as a fish, in whose tissues they encyst and gain access to the definitive host when the second intermediate host is eaten. In the final or definitive host, the cercariae grow into sexually mature hermaphroditic (except in one family of blood flukes) worms. It is believed that the sperm and egg unite by cross-fertilisation.

The order Monogenea (single host life cycles) consists mainly of ectoparasites of fishes and amphibians. They share many characteristics with free-living animals (eyes, for instance) but possess well-developed hooks and suckers and have cilia only in the young stages. Unlike the Digenea that lay many eggs and exhibit polyembryony, the Monogenea lay a few eggs and do not

Taenia saginata and Taenia solium

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Introduction

Tapeworms are entirely parasitic and are hermaphroditic. However, they are highly specialised parasites. Many of their organ systems have disappeared and no free-living organism that remotely resembles them exists. Adult cestodes are parasitic in the small intestine of vertebrates where they are attached to the mucosa. Their larvae are parasites of the tissues. A mature cestode consists of a scolex or head, a narrow neck, and a ribbon of segments or proglottids. The scolex may consist of hooks or suckers with which the cestode attaches to the wall of the intestine. The narrow neck, situated immediately below the scolex, is narrow and is a region of growth from which new proglottids arise. Proglottids that are farther away from the neck region are larger and are usually filled with eggs, while the most distal ones are usually gravid, containing mature eggs.

The entire length of the segments, starting from the neck to the last gravid segment, is called the strobila. The smallest strobila is that of Echinococcus granulosus which consists of 3 to 4 proglottids only. The other two major human tapeworms, Taenia saginata and Taenia solium, are made up of hundreds of proglottids. Structurally, a tapeworm is flat dorsoventrally, creamy in colour and with a relatively transparent tegument. It lacks a digestive system and lives on the host’s digested food that it absorbs through its cuticle.

The number of tapeworms present in the human intestine varies according to the size of the tapeworm. For large tapeworms like Taenia saginata and Taenia solium, one or two may be accommodated but, most often, one only.

The beef tapeworm of man

Taenia saginata is a broad tapeworm of cattle and humans. It is common in many parts of the world where cattle are reared, particularly Africa, Middle East, Central and South America, Western and Eastern Europe andAsia.

It has a scolex with four suckers, a narrow neck and proglottids. This worm measures about 4.6 to 6 metres long on average, with 1000 to 2000 segments. The immature proglottids arise from the neck, which is located just behind the scolex. These small immature proglottids contain undeveloped gonads. As the proglottids mature, they increase in length and width until they attain a maximum width of 11 to 12 mm. Each of these fully-grown segments contains a functional set of male and female gonads. The more distal segments of the strobila become more elongated and narrower as they develop a large number of lateral uterine branches. Some of the terminal proglottids, when fully gravid, become separated from the strobila and actively migrate and crawl out of the host’s anus, depositing their eggs on the perianal skin.

T. saginata segments are quite active in freshly expelled faeces and usually move about the surrounding vegetation scattering their eggs. Each gravid segment bears up to 80 000 spherical eggs, each measuring about 30 to 40 µm in diameter with a thick brown shell. The shell-enclosed embryo has three lance-like delicate hooklets.

Life cycle

After the eggs have been ingested by grazing cattle, the six hooked hexacanths hatch in the duodenum. The emerging embryos make their way through the intestinal wall into the surrounding peripheral mesenteric venules or lymphatics. They are then transported to different parts of the body including the heart and skeletal muscles. About two weeks after

Infection, the embryophores develop cysts.

The cyst, known as a cysticercus (Cysticercus bovis), measures 5 by 10 mm and has an invaginated scolex embedded in a fluid-filled bladder. When man eats meat infected with cysticerci, the cysticerci are freed in the digestive canal. They young tapeworms evaginate and attach to the intestinal wall by the suckers. After about 10 to 12 weeks, they attain maturity and start producing eggs.

Pathogenesis and symptomatology

Infection with the beef tapeworm is usually not accompanied by any significant symptoms and, in most cases, there may not be any symptoms at all so that the victims may not know that they are infected until they notice proglottids in the stools or feel them crawling out of the anus. Whenever symptoms occur, they normally include abdominal pain, occasional diarrhoea, loss of appetite and weight loss. Other symptoms include malaise, trouble in breathing, nausea, dizziness and nervousness and insomnia. Convulsions and epileptic fits have also been reported.

In very rare cases, the intestinal mucosa may become inflamed leading to the obstruction of the intestine. In some individuals, the parasite appears to absorb most of the nourishment leaving them with excessive appetite.

Epidemiology

The eggs of T. saginata are relatively resistant to environmental conditions. They will remain viable for about 2 weeks or longer if the temperature does not exceed 24 ^oC, but can stay longer than this under wet warm conditions. Under dry conditions, they dry up quite easily.

T. saginata exists under conditions in which the grazing lands are seeded with eggs present in human faeces, and where meat is eaten undercooked or even raw. Where higher standards of sanitation are practiced, the parasite has virtually disappeared, just as it has happened in Europe and North America.

High infection rates are found in the developing countries where cattle graze in fields that are contaminated with human faeces. In some areas in Africa, over 50% of the carcasses may be infected with Cysticercus bovis. It is estimated that in general about 10% of all the animals have cysts. In

India

where beef is not eaten by many people for religious reasons, the infection is very low, although the surrounding countries, such as

Nepal

, continue to record high rates.

Because of the improvement in sanitation in Europe and North America, cattle are not exposed to human faeces and therefore infection in humans and cattle is now very rare. The few isolated infections that occur are transmitted by birds feeding on the shore, in the sea and sewage farms. Immature onchospheres swallowed by cropless birds such as seagulls pass through the gut unhatched and may be distributed over wide areas where they are picked up by grazing cattle. Cattle may also pick up infection from sluggish streams into which sewage is discharged, or through drinking water or sewage sludge used as fertiliser.

Prenatal infection of calves is another likely source of infection in cattle but this is now considered inconsequential because adult animals are resistant to reinfection.

Diagnosis

Eggs are detected by microscopic examination of the faeces. However, the eggs of T. saginata are indistinguishable from those of another human tapeworm, T. solium. To distinguish between the two, freshly expelled proglottids are compressed between two slides and examined under bright light. This reveals the number of lateral branches of the uterus. T. saginata has about 20 to 23 uterine branches while T. solium has about 8 to 15. Gravid segments of T. saginata are more likely to crawl out of the anus than those of T. solium.

Control of T. saginata

Apart from its effect on human health, T. saginata is of great economic importance to cattle keepers. The losses are incurred through meat condemnation, provision of refrigeration facilities for infected carcasses and losses in the weight of the carcass, estimated at 2%, during refrigeration.

1. Meat inspection at slaughterhouses should always be carried out to detect the presence of cysticerci and their intensity in the muscles. Incisions are usually made in the muscles of the jaws and heart but other parts of the carcass can be examined. Unfortunately, it is not always possible to carry out meat inspection when the slaughter of animals in not done in abattoirs. In many of the developing countries, meat is only inspected in urban centres.

2. Cooking meat at a temperature of 65 ^oC or more kills the cysticerci. Cysticerci are also killed if the meat is kept in cold storage for 10 days at -9 ^oC or at -20 ^oC for 24 hours.

3. There should be regulations that require every household to have toilet facilities for faecal disposal and laws to reinforce compliance.

Niclosamide (Yomesan) and praziquantel are two drugs that are effective in the treatment of T. saginata.

Hymenolepis nana

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Hymenolepis nana, the ‘dwarf tapeworm,’ is the smallest tapeworm found in the intestines of dogs, rats ad humans. . It is more common in children than in adults. Although the parasite has a wide distribution, it is more prevalent in warm areas. It exists in Egypt, Sudan Portugal, Spain, Sicily, India, Japan, South America, Cuba and parts of Eastern Europe

An adult worm consists of about 200 proglottids that are considerably broader than long and measure about 20 to 40 mm long and 0.1 mm wide. The head contains a scolex with a single row of hooklets and four suckers.

Life Cycle

After the six-hooked egg is swallowed, it hatches in the duodenum and the onchosphere penetrates the intestinal villi where in 5 -6 days, it transforms into another larval stage called cysticercoid. The mature cysticercoid returns to the intestinal lumen and the scolex emerges and attaches to the mucosa. Then the cysticercoid goes on to develop into a mature worm. About 3 weeks after infection, the worm sheds eggs, which appear in faeces.. The eggs are set free by partial digestion of mature proglottids.

Under heavy infections, autoinfection may occur when some of the eggs regurgitated into stomach hatch in the upper small intestine.

H. nana can also develop in beetles, fleas or other insects to the cysticercoid stage. If the host accidentally ingests any of these intermediate hosts, the liberated cysticercoid larva attaches to the intestine and develops into an adult worm.

Pathogenesis

The clinical symptoms of infection are mild and sometimes absent. However, if the infection is heavy, the symptoms may include gastrointestinal pain, diarrhoea, vomiting, and loss of appetite and loss of weight. The infection may also cause nervousness and insomnia.

Epidemiology

Transmission of H. nana is usually from anus to mouth and this is why the infection is very common in children. The incidence of infection in humans ranges from less 1% to 25 %. Infection consists of a few worms but occasionally large numbers of worms are present in an individual. Mice and rats can be a source of infection in humans as well as arthropod intermediate hosts.

H. nana is often thought to represent the highest point in cestode evolution, where abandonment of the intermediate host has become possible, enabling both the larval and adult stages to develop in the same individual within a relatively short period of 2 to 3 weeks. .

Diagnosis

Diagnosis is based on finding eggs in stool specimens.

Control

The infection can be prevented by observing personal hygiene and good sanitation, destruction of rats and mice and by treatment of infected persons with a suitable taenicide such as niclosamide.

DIPHYLOBOTHRIUM LATUM

Diphylobothrium latum, also known as ‘broad’ or ‘fish ‘ tapeworm, is one of the biggest tapeworms of man and fish-eating mammals. It exists in the lakes and rivers of temperate regions of the world particularly North America, Europe and Asia. The tapeworm is about 10 m long and 10 to 20 mm wide, with about 4000 proglottids. The elliptical or spatulate scolex measure about 2.5 mm in length by 1 mm in breadth, with deep dorsal and ventral grooves. The broadly ovoid eggs are yellowish to golden brown and operculate, measuring 55 to 70 by 40 to 60 µm. The eggs are unembryonated when expelled in faeces of the host.

Life cycle

Eggs extruded from gravid proglottids pass out with the faeces. After 11 to 15 days, these operculate eggs undergo embryonation to produce ciliated embryos known as coracoids. The ciliated coracidium escapes from the eggshell and swims about until it is ingested by freshwater crustaceans, usually of the genera Cyclops.

After being ingested by a copepod, the embryo invades the hemocoele and develops into another form of larva, the procercoid. The procercoids must be eaten by a fish, which acts as a second intermediate host

Once the copepod is ingested by a fish, the procercoid penetrates the muscles of the second intermediate host and changes into a worm-like plerocercoid that is infective to man and fish-eating mammals. The plerocercoid becomes sexually mature in the human intestine or mammalian intestine where it begins to shed eggs in about 4 weeks. Each worm has been estimated to produce around 36000 eggs daily.

Pathogenesis and symptomatology

Most infections of D. latum produce no symptoms but whenever symptoms occur, they are usually associated with digestive disturbances, diarrhoea, heartburn, loss of appetite, nausea, and vomiting and hunger pains. Other symptoms may be suggestive of peptic ulcer, or appendicitis.

D. latum appears to have quite a high affinity for vitamin B_12, which probably explains the occasional occurrence of severe anaemia in some infected individuals. This vitamin B₁₂deficiency can be cured by giving affected persons a preparation consisting of powered worms and gastric juice.

Epidemiology

In those parts of the world where fish is an important part of the daily diet, notably northern USA, Canada, northern Europe and the Baltic regions, the incidence of D. latum in the population is quite high, ranging between 20-70 % in some areas. Human infection is associated with eating undercooked infected fish, eggs of infected fish or by accidental ingestion plerocercoids. Although cats and dogs are common reservoirs, they do not seem to play a significant role in the transmission of human infection.

Diagnosis and treatment

Diagnosis depends on finding characteristic operculate eggs in the stool (although this is not exclusive to D. latum) or the occasional vomited proglottid.

Control

The control of D. latum involves:

(1) Proper disposal of human faeces to prevent it from contaminating fresh waters in lakes and rivers.

(2) Cooking fish thoroughly or freezing it at a temperature of -18 ^oC for at least 48 hrs.

(3) Elimination of reservoir hosts.

Echinococcosis

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Echinococcus granulosus is a tiny tapeworm with a global distribution, being found in South America (especially Argentina and Uruguay), Europe, North America, New Zealand, Australia and Europe and Middle East. It has a major focus in North Africa around the Mediterranean region, especially Tunisia, Morocco, Libya, and Algeria and, to some extent, Egypt. The other major African focus is in East Africa, an area that includes Kenya, Sudan, Ethiopia, Uganda and Tanzania. The distribution in the rest of the continent of Africa is patchy.

Global distribution of E.granulosus

The adult worm is 3 to 6 mm long and usually consists of 3 to 4 proglottids. The scolex is armed with suckers and a rostellum that is ringed by a row of small hooks. The worms occur in hundreds or thousands in the small intestines of carnivores. The larval form, known as the hydatid cyst, occurs in the tissues of ruminants, such as sheep, cattle, goats and camels. Among its carnivore definitive hosts, the dogs are the main source of infection to man.

E. granulosus is tiny tapeworm

Life cycle

Gravid segments release shelled eggs that are voided with canine faeces. When these are ingested by sheep, cattle, pigs or other ruminants, or by man, the onchospheres emerge from the shells in the small intestine, penetrate the host’s intestinal wall, and reach the circulatory system where they are carried to the liver (50% to 75% lodge here), lungs and other organs of the body. The larvae encyst in these organs while undergoing undergrowth, reaching 1 cm in diameter in about 5 months.

The life of E.granulosus. A, adult parasites in the intestine of a dog lays eggs which are ingested by man or domestic herbivore. B, hydatid cysts develop in the liver of man and herbivores. C, hydatid cyst removed from man or domestic herbivore.

In the viscera, each young worm becomes vacuolated and slowly grows into a cystic structure called the hydatid cyst. The hydatid cyst consists of an outer part or pericyst which is a fibrous cellular envelope formed from the host tissues. Internal to this is another layer, the ectocyst. Inward to the ectocyst is syncytial layer known as the endocyst. The syncytial layer is the embryogenetic or germinal layer out of which brood capsules are budded. The brood capsules in turn give rise to numerous protoscoleces. A mature protoscolex has 4 suckers and a rostellum with hooklets and can be observed in the hydatid fluid.

Growth of the main larval cyst, or hydatid, is slow but the organism may reach a diameter of 20 cm in 10 to 12 years, depending on its location in the host. A mature cyst contains several litres of sterile fluid. The hydatid cyst may live in the intermediate host for up to 50 years.

When a carnivore ingests brood capsules, the protoscoleces are liberated in the stomach. After evagination, the protoscoleces become established in the small intestine, with the rostellum buried in a crypt of Lieberkuhn and for the first four to five days, they undergo little growth. By day 14, the scolex has grown in size, and the first segment has appeared. By the 35th day, the worm is fully developed with fully developed shelled embryos. However, in heavy infections, the worms take a considerably longer time to mature.

Pathogenesis

Hydatid cysts grow slowly at a rate of about 1 cm per year on average. Clinical symptoms usually develop when the cyst is about 10 cm in diameter. The severity of hydatidosis depends on the size, the location and the pressure exerted by the cyst in the host structures. Small cysts do not seem to do any appreciable damage to the host. On the other hand, large cysts exert considerable pressure on the surrounding organs. Rupture of the cyst may cause toxic/allergic reactions such as rash, wheal and redness of the skin. In some individuals, the symptoms may include fever, shortness of breath, cyanosis, vomiting and diarrhoea. Severe anaphylaxis resulting in a sudden death may follow a rupture of a large cyst and release of large quantities of fluid. Moreover, the rupture may spread the protoscoleces to other parts of the body where they will implant themselves and originate secondary hydatidosis.

Brood capsule containing scolices

One of the greatest dangers in hydatidosis is the involvement of the lungs where one side of the pulmonary cavity becomes blocked causing respiratory deficiency. Death usually occurs due to pulmonary oedema. Hydatid cysts in the brain are associated with increasing occurrence of intracranial tumours. Bone hydatidosis erodes the bone gradually until it fractures or crumbles.

Epidemiology

The incidence of echinococcosis in humans and in domestic ruminants is very much tied up with the keeping of dogs. Even in the Islamic countries of North Africa where the keeping of dogs is not encouraged, dogs still play a very important role in the transmission of infection. In East Africa, particularly among the pastoral groups, the prevalence of infection is quite high in the population, which is related to the large numbers of dogs that are usually kept ostensibly for herding, and protection against predators. The owners of these dogs do not look after them well and so the animals are always hungry. They will therefore feed on anything that resembles food, including offal and rotting carcasses and acquire infection.

The dog plays a central role in the transmission of E.granulosus

The Turkana people of

Kenya

are pastoralists, living in the arid northwestern corner of the country. They keep large numbers of dogs, about 70% of them heavily infected with E. granulosus. The incidence of hydatidosis in the population ranges from 20 to 200 cases per 100000 people. Dogs carry heavy parasite loads that are as high as 3000 worms per dog. This is far in excess of the 30 worms per dog that seems to be the case in most endemic areas of the world.

The Turkana keep sheep, camels and goats, all of which are usually infected with hydatid cysts. In addition, many of the wild carnivores, such as the leopards, lions, hyenas, and jackals carry the infection. It is not surprising the incidence of human hydatidosis in that part of

Kenya

has been judged the highest in the world.

Diagnosis

Diagnosis is difficult because cysts grow deep in the internal organs. The liver is the most affected organ, recording 65 – 75 % of all the infections, the lungs, 10 – 20 %, and to a lesser extent the spleen, kidney, bones, orbit and brain. Among the Turkana people, a swollen belly is usually a sure diagnosis of E. granulosus. In mature hydatid infections, the size of the cyst may exceed 20 cm in diameter and contain many litres of fluid. Useful diagnostic tools include x-rays for pulmonary cysts, C T scan or echography and serological tests. Serology has less sensitivity in infections that do not involve the liver or lungs.

Doctor hold cysts removed from a Turkana woman

Control

1. Prevention of E. granulosus involves meat inspection and destruction of cysts by boiling or burying infected meat to prevent it from being eaten by dogs and other carnivores. The eggs of Echinococcus are very resistant to adverse conditions and survive for up to 2 years in water and cool temperatures, and more than a year on the ground under humid conditions. In pure formalin, the eggs remain viable for 2 weeks.

2. Animals should be slaughtered in designated abattoirs where the carcass can be inspected for cysts. Offal from infected animals should be buried or incinerated to prevent dogs from feeding on it.

3. Dogs should be treated regularly with anthelminthics and stray dogs should be eliminated.

4. Human treatment is based on surgical removal of the cyst and\ or treatment. The usual treatment involves albendazole 10 mg/kg body weight. However, success with albendazole is only reported to be about 30%. Administration of praziquantel by itself or in combination with albendazole is 100% effective against the protoscoleces.

The species of Echinococcus

Speciation in this genus is complex and confusing. Initially it was considered that there was only one species of Echinococcus granulosus, although different patterns of development of hydatid cysts were known by parasitologists. These were however thought to be due to development in different intermediate hosts. This view was later refuted and abandoned. Four types of hydatid cysts are now recognised.

Unilocular: characterised by single well-defined bladders, in which the laminated membrane continuously encloses the germinal membrane. Its geographical distribution is global. Example, E. granulosus.

Multivesicular: characterised by many adjoining and connected bladders, each having its own germinal membrane.

Alveolar: characterised by a malignant type of growth with jelly-filled proliferating vesicles embedded in a common dense stroma. The very thin laminated membrane does not restrict the germinal membrane that grows out into the host surrounding tissues. This parasite is restricted to the northern hemisphere.

Multilocular: characterised by many small bladders embedded in a common enclosing membrane. Has the same geographical distribution as E. granulosus.

Fasiolopsiss buski

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Fasciolopsis is a giant fluke of the small intestine of humans and pigs. It is one of the largest human trematodes, measuring between 20 to 80 mm long and 8 to 20 mm wide. Adult worms are capable of producing up to 25000 eggs per day that pass out in faeces.

It is widely distributed in China, Taiwan, and several countries in Southeast Asia, including the subcontinent of India. The infection is common especially in those areas, which rear pigs and consume freshwater plants.

Life cycle

Eggs laid by the flukes pass out in faeces. Like all fluke eggs, they require an aquatic medium to hatch into miracidia. The miracidia swim about until a suitable host is found, usually freshwater snails of the genera Planorbis, Segmentina, or Hippeutis.

The miracidia penetrate the soft tissues of the snails and transform into sporocysts. After a number of multiplications, the sporocysts give rise to first and second-generation rediae. The rediae release thousands of noninfective cercariae, which become infective after they have encysted on vegetation as metacercariae.

Human infection is caused by eating uncooked vegetables that are contaminated with metacercariae or by accidental ingestion of the metacercariae. Ingested metacercariae excyst in the duodenum and attach to the intestinal wall. There they develop into adult flukes in about 3 months. The adult worms have a life span of about 12 months only.

Pathogenesis

Most infections are light and asymptomatic and not life threatening. However, in heavy infections the intestinal muscle is usually inflamed and ulcerated. There may also be evidence of haemorrhage and abscesses in the small intestine. Furthermore, the individual may experience abdominal pain, diarrhoea, oedema of the lower limbs and face.

Control

In the areas of the world where F. buski is endemic, human faeces are usually used as a fertilizer, which seems to perpetuate the infection within the population. The cycle can be broken if the faeces are treated with chemicals that render the eggs unviable before they are used in the fields. Vegetables and salads should be washed thoroughly before being consumed.

With advances in food production methods, the use of night soil for fertilization is now marginal while the use of toilets is becoming more common in tune with the improvements in the socioeconomic conditions of the peoples of Asia. In the end, the transmission of F. buski is bound to decline considerably.

Diagnosis

Diagnosis consists of microscopic identification of eggs or more rarely of the adult flukes in the stool or vomitus. The eggs are indistinguishable from those of Fasciola hepatica. Praziquantel is the drug of choice for treatment.

Paragonimus westermani

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Paragonimiasis is a zoonois which is caused by a trematode called Paragonimus westermani. This parasite lives in the human lung, though some ectopic parasites are found in other locations, suggesting that this parasite is not well adapted to living in man. P. westermani is also found in the lungs of many other mammals. The disease is endemic in Korea, China, Japan, Burma, Vietnam, Cambodia and Laos. It also exists in South and Central America, West and Central Africa. Its reservoir hosts include dogs, cats, lions, leopards, tigers and pigs.

The adult fluke is robust reddish–brown and is covered with minute cuticular spines. It measures 7.5 to 12 mm long by 5 mm wide and 4 mm thick.

Life cycle

Adult trematodes lay golden brown, operculate eggs in the lungs. The eggs are passed out in the air passages of the lungs and are coughed up and spat out or swallowed. Those eggs that are swallowed are voided with the host’s faeces. The eggs take 17 to 21 days at 30 ^oC to hatch into motile ciliated miracidia. At lower temperatures, this period can extend up to 6 weeks. The intermediate hosts of P. westermani are snails of the genera Brotia, Thiara, Melania, and Semisulcospira. Once the miracidia find the right snail, they penetrate it and change into tube-like sporocysts. The sporocysts develop into first generation rediae. These first generation rediae or mother rediae, as they are also called, give rise to daughter rediae or second-generation rediae. Finally, thousands of cercariae emerge from the daughter rediae.

The cercariae that can live for up to 48 hrs do not swim but either crawl or are carried by currents in the water until they find a second intermediate host, usually a crab or a crayfish, which they actively penetrate and then migrate to the muscles or heart and encyst as metacercariae . About six weeks later, the metacercariae become infective.

Human infection is caused by eating raw crayfish or raw crabs. After ingestion, the metacercariae excyst within an hour of ingestion and the young worms penetrate the intestinal wall and make their way via the diaphragm into the pleural cavity. The worms may wander about and invade many other body organs, such as the brain, intestine, reproductive organs, spinal cord, scrotum, etc. Within 2 to 4 weeks post-infection, the worms arrive in the lungs, where they will undergo growth to maturity before shedding eggs. Not all the flukes reach the lungs; some end up in the brain, spleen, liver, and kidneys where they cause inflammation and abscesses.

Pathogenesis

Larvae migrating to the lungs from the intestine cause lesions along their path. Sometimes, they may stray into aberrant locations including the abdomen causing diarrhoea and abdominal pain, or the spinal cord and brain causing cerebral paragonimiasis. Cerebral paragonimiasis is a serious condition that is characterized by epilepsy, meningitis and other neurological complications.

The usual symptoms are chronic cough, severe stabbing pains in the chest and haemorrhage. The sputum is tinged with blood and its examination reveals the presence of operculate eggs. There may also be other symptoms such as fever, chills and sweating and loss of weight. In addition, there may be chest pains and dyspnoea, bronchiectasis and fibrosis of the lung tissue.

Epidemiology

Humans acquire the infection by eating pickled or marinated infected crabs or crayfish. In endemic countries like China, crabs are sprinkled with salt and spices and eaten raw. The salt can kill some of the metacercariae but not all. Another common habit is to soak the crabs in wine overnight and eat them raw. Infection may also be acquired by eating salads contaminated with infected crabmeat. Some people in Japan and Korea use the juice prepared from the crayfish for medicinal purposes, while some communities in West Africa regard eating raw crabs as treatment for infertility.

Paragonimus exists as a zoonois in cats, dogs, pigs and a large number of many other animals. These animals are capable of transmitting infection to humans.

Diagnosis

Diagnosis is done by recovery of eggs of P. westermani in sputum, faeces, and pleural aspirate or from abscesses.

Control

Treatment with bithionol is effective and is the drug of choice. Chloroquine and praziquantel have also been used successfully. Infection may be prevented by avoiding eating raw crabs or crayfish as well as maintenance of sanitary conditions.