Introduction to parasitism

While there are so many organisms that we can see with our naked eyes, there are many other organisms that we can only detect with the aid of an ordinary microscope or an electron microscope. Among these ‘invisible’ organisms are parasites of man and his livestock.

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, there should be proper disposal of human faeces. 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.

Ascarophis

Ascarophis sp.

When I saw the reports of giant amphipods being dragged up from the Kermadec Trench off the coast of New Zealand, my immediate thought was "I wonder what parasites it has?" This promoted me to do a write-up of a paper I've read recently, which is about a parasite that infects amphipods - admittedly those that are more modestly sized. Today, we are featuring a study on Ascarophis, a nematode worm that infects an intertidal amphipod (Gammarus deubeni) in Passamaquoddy Bay, New Brunswick, Canada. Compared with related species this worm has evolved to live the simple life(-cycle), and avoids the complications that come with having a complex life-cycle.

Previously on this blog, we have featured parasites that have evolved to take short-cuts with their complicated life-cycles. When a particular host is absent, such parasites may opt to ditch that host from their life-cycle, and switch up their developmental schedule. This is the case with the fluke Coitocaecum parvum. However, while C. parvum can switch between different life-cycles depending on circumstances, Ascarophis has completely abandoned that altogether, and has evolved to make things simpler by completing its entire life-cycle within its amphipod host. Usually, parasites with complex life-cycles use different hosts for different functions - i.e., one host might merely serve as a transport and/or resources for temporary development, whereas another acts as a mating ground and/or habitat in which it reaches maturity. So how can Ascarophis get so much functionality out of a tiny little crustacean?

Nematodes normally go through 4 larval stages (L1-L4) before becoming a sexual mature "fifth stage" worm (L5). The end of each larval stage is accompanied by a molt (rather like insects). In related nematodes that have retained their complex life-cycle, the L3 worms (which are ready to infect the next host) live encapsulated in the first host, while the L4-L5 live in the digestive tract of the final host. What the researchers found with the Ascarophis they collected from New Brunswick is that L1 and L2 worms were found in the muscle tissue, and upon reaching L3 the worms begin to migrate into the body cavity where they complete their development into adulthood and start producing eggs. Now compare this with Ascarophis from the White and Baltic Seas, which also infect amphipods, but uses a species of sculpin as their final host. Those fish acquire their infection by eating amphipods infected with L3 stage nematode, and the worms develop into adults in the fish's gut.

In effect, the Ascarophis from New Brunswick gets the most out of its little crustacean host by using different parts of the amphipod's body as surrogates for different hosts - instead of being transmitted to a different host, it simply moves to occupy a different part whose function is close enough to its needs for it to complete its development. Unlike the C. parvum, it appears that Ascarophis has abandoned the fish host altogether, and has committed itself to using the amphipod as the sole host for its entire life-cycle. Even though the Ascarophis found in the White and Baltic Seas have retained their complex life-cycle, researchers of this study suggested that they are the same species as the worms they looked at, but the New Brunswick variant has simply adapted to local condition and evolved a different life-cycle. However, it must be noted that the researchers have come to this conclusion based on the worm's morphology and as we have seen before, appearance can be deceptivewith nematodes.

Through all that, this plucky little New Brunswick parasite faces one last problem - getting its eggs out of its crustacean host. For worms that live in inside a fish's gut, passing eggs out into the environment is a pretty straightforward affair - the eggs simply get washed out with the poop. But there is no exit in the body cavity of an amphipod, so how is a worm supposed to cast its eggs out into the environment? Well, this thrifty nematode simply waits for the host to die, and as the body disintegrates, the eggs are released as well. Of course, it helps that these amphipods have a tendency to cannibalise the rotting bodies of their fallen comrades - this presents the perfect opportunity for the parasite to infect a new batch of hosts - yet another reason to not gnaw on any random corpses you may come across.

Halophilanema prolata

Halophilanema prolata

Today's parasite and host are found among the dunes on the coast of Waldport, Oregon. In this story, the host is a little bug - and by bug, I do mean it in the literal scientific sense of the word, as in ahemipteran insect - the shore bug Saldula laticollis. The parasite is a nematode called Halophilanema prolata which, when translated, means "elongated sea salt-loving thread" - which sounds like an item you can find in a specialty gourmet shop or a post on a foodie forum. The mature female worm lives inside the bug's body cavity (top photo), surrounded by her babies (bottom photo). The larval worms reach a very advanced stage of development inside their mother's uterus before they emerge into the bug's body cavity. Each larva then escapes into the sun and surf and undergoes a final molt. It then finds an attractive mate in the sand, and gets on with the business of making the next-generation of bug-infesting worms.

Post-coital, the now fertilised female climbs onto any unfortunate shore bug that happens to be passing through the neighbourhood, and starts digging in. Most of the bugs infected by H. prolata were found among clumps of rushes along a distinct line of yellow-tint sand at the high tide mark. This sand contains a potpourri of algae, microbes, and nematodes - including H. prolata at various stages of development. This is evidently a hot spot for the parasite, because in that area, up to 85% of the bugs are infected.

Now, something must be said about the habitat of today's host and the parasite. The intertidal zone is a harsh habitat, especially for both insects and nematodes. Any organisms living in such areas must be able to endure being periodically immersed in seawater, and then left high and dry by the retreating tide. The combination of saltwater, periodic immersion and exposure poses severe osmoregulationchallenges, which is why despite their great diversity, comparatively few insects have colonised the intertidal habitats. But what about H. prolata?

There are nematode worms which live permanently in marine habitats, and they have bodily fluids that are the same level of saltiness as seawater so they don't suffer from osmotic stress. But H. prolata has evolved from a lineage of terrestrial nematodes which would be subjected to severe osmotic stress (just like how you will dehydrate if you are immersed in seawater for too long - the high solute concentration of seawater draws fluid from your cells). So how do they manage?

Halophilanema prolata has evolved a raincoat of sorts - its cuticle has very low permeability (very difficult for water to move through it) so that it retains its body fluid more readily than animals with more permeable body walls. This also makes these little worms very resistant to other types of chemical stress - they can survive being immersed in 70% ethanol or 5% formalin (which are usually used for pickling biological specimens) - for up to 48 hours - because as well as making it difficult for fluid to diffuse out, a cuticle with low permeability also makes it difficult for other liquid to diffuse in.

So the next time you are at a beach, think about the little insects which are running around with nematodes swimming in their innards, and the microscopic worms getting it on underneath your feet. Why would you want it any other way?

Mysidobdella californiensis

Mysidobdella californiensis

Marine leeches are commonly known to feed on various vertebrate hosts - mainly fish and sea turtles. However, today's parasite stands out from the pack by associating itself with an arthropod.  Instead of fish or turtles, Mysidobdella californiensis sticks its sucker onto mysid shrimps. Mysids are also known as opossum shrimps because the females have a little brood pouch (called a marsupium) in which they carry developing young.

The discovery of Mysidobdella californiensisactually occurred rather serendipitously. Back in the summer and fall of 2010, an unprecedentedly huge swarm of mysid shrimp appeared off the central Californian coast. Some of those shrimps got sucked into the water clarification system at the Bodega Marine Laboratory. With all this shrimp in the system, the lab staff began collecting them opportunistically for fish food. But then, they started noticing these little leeches attached to the shrimps, so they made a concerted effort to collect the shrimps directly from the water clarifier, and examine them under the microscope.

What they found were tiny leeches about 1.5 cm (a bit above half an inch) long. Approximately one in every six shrimp were found to have leeches on them, and each infected shrimp was carrying between one to three leeches. Seeing as this is a new species, at this stage very little is known about its biology except what can be inferred based on what we know of a related species - M. borealis - which has been studied in slightly more details. It is unclear whether M. californiensis (and related species) merely hitch-hike on the shrimp and use it to carry them to potential hosts, or if they in fact feed on the shrimp. In laboratory trials on M. borealis, the leeches refused to feed on any of the fishes that they were presented with, and none of the leeches were found to have fish blood cells in their gut. It is possible that Mysidobdella as a genus specialise in feeding on mysid shrimps. If that is indeed the case, then Mysidobdella would be the only marine leech known to feed on the blood of invertebrates rather than vertebrates. However, mysid blood has yet to be found in the gut of these leeches, so at least at this point, the diet of M. californiensis remains a mystery.

AMEBIASIS

Amoebiasis

Amoebae refer to several organisms that belong to the subphylum Sarcodina. These organisms move by cytoplasmic extensions known as pseudopodia. Many species of Amoeba are free-living organisms and a few are parasites of the digestive tracts of vertebrates and invertebrates 
The amoebae vary considerably in their biology. Entamoeba histolytica infects primates; E. invadens is a parasite of reptiles, while E. coli is a harmless species that is found in the colon of man, monkeys and dogs. E. hartmani is a nonvirulent strain that is easily mistaken for E. histolytica.

Those parasitic to man include Entamoeba histolytica, E. hartmani, E. coli, E. gingivalis, Endolimax nana, and Iodomoeba butschlii. E. histolytica is very pathogenic while the rest of the species are non-pathogenic or harmless.

E. Gingivalis inhabits the crevices between the teeth and feeds on bacteria, particles of food and dead epithelial cells. It is transmitted orally by kissing. Other Amoebae are inhabitants of the caecum and the large intestine.

E. coli is the largest intestinal amoeba of man. It feeds on bacteria that abound in the colon and forms eight nuclei, as opposed to the four nuclei of E. histolytica.

E. histolytica

E. histolytica is an anaerobe that lacks a mitochondrion and obtains its energy by glycolysis. It lives in the lower small intestine and the entire colon. The trophozoite stage is motile and measures 12 to 30 µm in diameter. Sometimes larger trophozoites are found in dysenteric faeces. The parasite’s cytoplasm consists of a clear ectoplasm and granular endoplasm. The vacuoles in the endoplasm are filled with ingested red blood cells that are being digested. E. histolytica naturally feeds on the host’s red blood cells and bacteria fauna present in the colon.

E. histolytica is widely distributed both in the temperate and in the tropical regions of the world. It is, however, more prevalent in the tropics where the prevalence in some communities can be as high as 100%.

Life cycle

Cysts of E. histolytica are passed in faeces. Soon after the faeces are voided, the cyst nucleus divides into two. Then each of the two daughter nuclei divides again into two so that the mature cyst has four nuclei. Cysts are susceptible to environmental conditions and are killed by drying, heat, and sunlight. Cysts formed from trophozoites, measure 5 – 20 µm, and usually have four nuclei

Primary amoebiasis

Infection is contracted through the ingestion of cysts in food or water. On reaching the intestine, the cysts divide into active trophozoites. The trophozoite is the feeding stage and it is amoeboid, using pseudopodia for movement and feeding on bacteria and cell debris.

Aided by hydrolytic enzymes, the trophozoites invade the mucosa of the large intestine and proceed to erode the surface of the muscularis mucosae. The characteristic initial lesion caused by the invasive trophozoites is a superficial minute cavity caused by necrosis of the mucosal surface. This lesion enlarges as the amoebae reach the more resistant muscularis mucosae. The parasites may erode a passage through the muscularis mucosae into the submucosa and spread into the surrounding tissues. This invasive stage affects not only the intestinal wall but also the local blood and lymphatic vessels.

Once inside the intestinal tissue, the trophozoites feed on cell debris and whole red blood cells. As the trophozoites feed, they become larger and divide by mitosis, thereby increasing their numbers enormously. In severe cases, the intestinal epithelium is badly damaged, resulting in open wounds. The ulcerated tissue is subject to infection by other pathogens, such as bacteria. A seriously damaged intestinal mucosa leads to amoebic dysentery with discharge of blood, mucus and amoebae into the intestinal lumen.

Repair of the ulcerated bowel lining eventually occurs, but the flexible, absorptive mucosa is often replaced with fibrous scar tissue. Sometimes, this tissue partially constricts the intestine, blocking peristaltic movements of the bowel and interfering with its normal function.

Secondary amoebiasis

Secondary amoebiasis is due to transportation of amoebae via circulation from a primary abscess in the intestine to other tissues. The liver, lungs, and brain develop amoebic abscesses in the given order of frequency. A liver abscess consists of a hollow eroded region that contains a viscous fluid, and mass of dead amoebae, plus blood and tissue detritus. Around the necrotic centre of the abscess, the liver tissue is full of amoebae, which actively invade healthy tissue as they multiply. No fibrous envelope forms around such an abscess and it spreads steadily with age. Amoebic abscesses are usually sterile or bacteria-free.

Lung abscesses develop directly from liver abscesses through the spread of the latter across the diaphragm. Brain abscesses result from amoebae that have lodged and multiplied in the brain. Brain abscesses are less common than lung or liver abscesses. Other sites of amoebic infection have been reported.

Abscesses contain a large number of leucocytes, which have engulfed amoebae, and systemic or secondary amoebiasis usually produces a raised leukocyte count. In some individuals and with certain races of amoebae this defence is so weak that abscesses form and grow in spite of leukocyte activity.

Certain bacteria seem necessary for amoebic virulence, even if the bacteria themselves are harmless. Thus, mutualistic relationships between amoebae and other inhabitants of the intestine are an important part of amoebic pathogenicity.

Symptoms

The infection has an incubation period of a few days to 3 months or more, depending on the strain of amoeba and the nutritional status of the host. In most cases, it is impossible to determine the time of exposure to infection and the appearance of symptoms. Initial symptoms may involve mild abdominal discomfort and passage of soft stools, which may persist for sometime before the patient is compelled to seek medical attention. In some cases, the onset may be sudden, accompanied by dysentery or severe abdominal pain.

The typical clinical symptoms of acute amoebic dysentery are marked colicky pains and severe bloodstained diarrhoea. The stool then contains blood and mucus and the individual feels the urge to open the bowels several times in a day. The disease, if not treated, is fatal.

A hepatic abscess is associated with fever, an enlarged and tender liver. Pulmonary amoebiasis may present with pneumonia and coughing.

Epidemiology

E. histolytica is found all over the world. It is, however, more prevalent and severe in the tropics than in the subtropics. The infection rates are generally high where sanitary conditions are poor such as in mental hospitals, children’s homes and prisons. Asymptomatic carriers of amoeba are common in endemic areas. It is not clear whether this is an indication of an acquired immunity or merely the presence of nonvirulent strains of the parasite.

Endemic amoebiasis may be interrupted by sudden outbreaks of major proportions, resulting from gross contamination of drinking water with viable cysts of amoeba. Besides water and food contaminated with amoebic cysts, another important mode of transmission is hand-to-hand contact, which is possible with people with unclean hands. The parasite may be carried mechanically by houseflies and cockroaches.

Large numbers of cysts may be discharged in the faeces of an individual. The cysts survive for a few weeks to a few months under moist conditions. Drying kills them. Although monkeys, pigs, dogs and cats are naturally infected with E. histolytica, there is no evidence that shows that they transmit the infection to humans.

Diagnosis

Active trophozoites can be detected by direct examination of the faeces and of biopsy material. Typical amoebic faeces contains exudes, mucus and blood. Formed faeces are of no diagnostic value in amoebiasis. It is possible to distinguish the cysts of E. histolytica from those of E. coli by the number of nuclei.

Control

To prevent contracting amoebiasis, drinking water should always be boiled. Water provided by municipalities is usually chlorinated. Boiling drinking water, even piped water in urban centres is important unless one is quite sure that it is safe to drink it unboiled.

Vegetables should not be eaten raw. Salads should be washed thoroughly before serving. Food handlers can transmit the infection if they do not maintain proper personal hygiene.

Food should be covered to prevent insects landing on it especially houseflies and cockroaches. Disposal of human excreta in toilets and maintenance of personal hygiene limit the spread of infection.

The drug of choice is metronidazole. Alcohol should be avoided while taking this drug. Other drugs include emetine hydrochloride and chloroquine.

Toxoplasmosis

Toxoplasmosis, caused by a coccidian parasite known as Toxoplasma gondii, is an intracellular human and animal disease with a global distribution, especially in warm, moist areas. In human infection, T. gondii exists as active, proliferative trophozoites during the active phase of the infection and as a cyst in chronic infections. The trophozoite is crescent-shaped and measures 4 to 8 µm in length and by 2 to 3 µm in width, with one end more pointed than the other. In an acute infection, the trophozoites are present in the various tissues and tissue fluids but in the chronic stage, the cysts are mainly found in the central nervous system, muscle and tissues.

Toxoplasmosis has been reported from man, cats, pigs, cattle, sheep, dogs, rodents, birds and many other carnivorous animals. It is a common cause of abortion in cattle in England and New Zealand. The main source of human infection is the domestic cat. Other members of the family Felidae develop the infection and are responsible for maintaining it in areas where cats are absent.

Life cycle

T. gondii primarily exists in three forms: oocysts, tachyzoites, and bradyzoites. Oocysts are only produced in the definitive host, members of the family Felidae. When passed in feces and then ingested, the oocysts can infect humans and other intermediate hosts. They develop into tachyzoites, which are the rapidly multiplying trophozoite form of T. gondii. They divide rapidly in cells, causing tissue destruction and spreading the infection. Tachyzoites in pregnant women are capable of infecting the fetus. Eventually tachyzoites localize to muscle tissues and the CNS where they convert to tissue cysts, or bradyzoites. This is thought to be a response to the host immune reaction. Ingestion of cysts in contaminated meat is also a source of infection, as bradyzoites transform back into tachyzoites upon entering a new host.

For a long time, the life cycle of T. gondii remained unsolved. It is now known that the parasite is actually a coccidian of cats and other animals. Oocysts released by infected cats and other animals are very resistant to environment factors and usually remain viable in the soil and in the dust for more than a year. In warm, moist shaded areas, the cysts can survive for a year. Oocysts are ingested by reservoir hosts when they take water or food contaminated with cat faeces. The reservoir hosts may include carnivores and herbivores. Man acquires infection by eating infected raw or undercooked meat from pig or sheep and by accidental ingestion of infected faeces of cats or dogs.

Once ingested, the oocysts form sporozoites that penetrate the intestinal mucosa either by phagocytosis or by active penetration using enzyme-like factor. Within the intestinal mucosa, the sporozoites divide by schizogony to produce merozoites, including gametocytes. Fusion of the gametocytes produces oocysts, which are expelled in the faeces. The incubation period ofT. gondii in the cat is about 21 to 24 days.

Pathogenesis

The large number of humans and animals that have antibodies against T. gondii antigens seems to suggest that the infections are common but with apparently no accompanying symptoms. The newborn babies are the most affected because they are usually infected transplacentally, usually during the second or third trimester of pregnancy, often from asymptomatic mothers.

Toxoplasma gondii occurs chiefly in the cells of the reticulo-endothelial system. The parasites can be found practically in every organ but are particularly numerous in the brain. In children, the infection affects mainly the central nervous system causing meningitis, encephalitis and encephalomyelitis. In adults, the infection is characterized by the enlargement of the lymph nodes. In congenitally acquired infections, the lesions are normally dominant in the brain, spinal cord and the retina or choroid. Hydrocephalus or microcephalus, mental retardation including blindness in the newborn may indicate toxoplasmosis.

Epidemiology

Animals serve as reservoirs for human infection. Being pets, human contact with cats is usually very close and for this reason, cats are the main source of human infection. Farm animals are also important source of infection. Herbivores become infected by eating food and drinking water contaminated with infected faeces of carnivores.

Human infection may be acquired by direct contact with infected animal tissues, by eating contaminated food or meat and through accidental ingestion of oocysts present in water and faeces of domestic and wild animals. Oocysts can survive in moist, shaded soil for over a year. Invertebrates like flies, cockroaches, earthworms, stable fly, Stomoxys and fleas can transmit the parasite mechanically.

Reservoir hosts play a very important role in the maintenance and transmission of T. gondii in the wild. Rabbits, mice, rats and birds serve as reservoirs of T. gondii and frequently transmit infection directly to the predators by predation or by ingestion of oocysts.

Congenital transmission occurs through the placenta but this probably affects only a very small number of people, although it may be responsible for the majority of human fatal cases. In addition, the parasite can be transmitted via blood transfusion and cell transfer. Infection may be transmitted airborne by inhalation of the organisms discharged from the lungs of coughing infected animals or individuals.

Diagnosis

It is always difficult to find the parasites in the body fluids. The infection can be confirmed by demonstrating specific antibodies or the presence of the toxoplasmas in the cerebral spinal fluid when the brain is involved. Mice are very susceptible to infection with T. gondii and are usually used for serological tests.

Control

Although freezing may destroy most of the cysts, proper cooking of the meat is more reliable in ensuring its safety. The main source of human toxoplasmosis, however, is the ingestion of oocysts present in the faeces of domestic cats present in water and food. Therefore, boiling drinking water and maintaining proper hygienic standards help prevent infection. Acquired toxoplasmosis is treatable with sulphonamides

African Trypanosomiasis

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 vectorGlossina 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 bruceirhodesiense 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 andTrypanosoma 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 inAfrica, 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 ofT. 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 theWest 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 andMozambique.

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 inAfrica 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. gambienseor 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. gambienseoccurs in the more densely populated areas, especially riverine-forested areas of West andCentral 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. gambienseis 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 inZimbabwe 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