HISTOLOGY ATLAS 3D FOR MEDICAL STUDENTS.

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Balantidium coli

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Balantidium coli

The ciliate protozoa form a large group of organisms that is characterised by numerous cilia. A large number of ciliates are free-living and an equally large number consists of parasites of the digestive systems of termites, cockroaches and herbivores.

A typical ciliate has a conical mouth, the cytostome, near the anterior end and an anal opening, the cytopyge, at the posterior end. Ciliates have two types of nuclei: a large kidney-shaped macronucleus and a small spherical micronucleus, both of which are visible in the cyst and in the trophozoite.

Balantidium coli is the only ciliate that is parasitic to humans. Balantidium coli has a global distribution in pigs, dogs and several species of monkeys. In man, it occurs mainly in warm climates. The parasite occurs in the large intestine of man, pigs and monkeys.

Morphology

The parasite exists as a cyst and as a trophozoite, the trophozoite being the active form. It is ovoid and covered by cilia that are perpetually in motion, which are used for movement. The parasite varies in size, ranging from 50 to 100 µm in length by 40 to 70 µm in width. The anterior end is conical and the posterior end is rounded. To one side of the anterior end, there is funnel-like peristome, which leads to the cytostome or mouth.

Balantidium coli trophozoite (left) and cyst (right)

Life cycle

Balantidium coli lives in the large intestine where it feeds on bacteria, cells and food particles present in the intestinal lumen. Asexual reproduction is by binary fission in which the micronucleus first divides followed by the division of the macronucleus, resulting in two daughter organisms. B. coli can also reproduce sexually by a process called conjugation, which involves the exchange of nuclear material.

Life cycle of B. coli. A, ingestion of cyst; B, trophozoite formed in the colon divides by binary fission;

C, trophozoite in the lumen of the large intestine or in faeces freshly voided.

Pathogenesis

The effect of the infection in the pig is minimal, as the parasite does not seem to penetrate the mucosal surface. In humans and monkeys, the parasite can enter the surface of the large intestine causing extensive tissue erosion. Furthermore, the parasite may penetrate through the muscularis mucosae into the submucosa and spread out radially causing rapid destruction of the tissues. Most of the lesions caused by Balantidium coli are found in the caecal and sigmoid rectal regions.

The symptoms vary from severe diarrhoea and dysentery to mild insignificant, almost asymptomatic condition.

Epidemiology

Infection is acquired by the ingestion of cysts of Balantidium in food or water contaminated with faecal matter. Since balantidiasis is common in dogs and primates, it may be expected that these animals are probably the main source of infection to man. However, human infections are usually associated with people who come in contact with pigs, chiefly pig keepers or butchers.

The infection rate is very low in humans and this is because humans are generally refractory to exposure to Balantidium. However, once the infection has established itself in man, there is usually a rapid transmission from one person to another, particularly where there is no proper sanitation.

Diagnosis and treatment

Slide smears of infected faeces should show characteristic cysts or trophozoites of Balantidium coli. The infection responds to treatment with tetracycline, and metronidazole.

Leishmaniasis

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Leishmaniasis

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 andAfrica
New World
L. braziliensiscomplex	Cutaneous and mucocutaneous, zoonotic	Latin America
L. chagasi	Visceral, zoonotic (dogs)	Latin America
L. mexicanacomplex	Cutaneous, and a few mucocutaneous reported inPanama, 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 isLeishmania 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 isLeishmania 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.

Helminth Therapy

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The Immune System Response to Helminths

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Malaria: No Ordinary Mosquito Bite

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trichomonas vaginalis

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Medical Parasitology (Laboratory) - Trichomonas vaginalis trophozoite 2

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Phylum Aschelminthes

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Phylum Aschelminthes

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.

Microscopic Techniques

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Microscopic Techniques

Most parasitic agents occur within the gastrointestinal region, body tissues and blood system. Most helminth parasites (nematodes, trematodes, cestodes) and some protozoa inhabit the intestine as well as the bile and pancreatic ducts that empty into the intestinal lumen. The helminths produce characteristic eggs, which pass out in faeces that are used for identification. Either the protozoa exist as active trophozoites or as inactive cysts and their presence in a stool sample is an indication of an infection.

Some important stains for blood films

Method for cleaning microscope slides

Slides used in laboratories for identification purposes should be clean from dust and grease. Films do not stick well if the slides are dirty and greasy and stained artefacts may give the wrong results. There are several ways of cleaning blood slides but the most practical method is the one that uses Decon

Make up a 2 – 3 % solution of Decon in hot water.

Place slides into the solution individually.

Allow slides to stand in solution for at least ½ hour (1 – 2 hours is better).

Rinse thoroughly in running tap water for an hour.

Rinse briefly in distilled water.

Store slides in ethanol – dry as required or dry and store in clean boxes.

Giemsa’s Stain

This stain can be used in different dilutions. A one in ten dilution is convenient, as it gives rapid staining, although the time varies according to the quality of the stain.

The stain can be used for thin films and thick films.

Method for the thin films

Pour 2 ml of Giemsa into a measuring cylinder and make up to 20 ml with distilled water. Empty the dilute stain into a staining jar.

Fix the blood film by immersing it in methyl alcohol for 2 – 3 minutes.

Wash the slide containing the film in distilled water.

Drain off the water and transfer the slide into a staining jar containing Giemsa.

Stain for 30 – 60 minutes.

Remove the slide and rapidly wash it in distilled water.

Wipe off stain from the back of the slide and leave it in an upright position to dry.

Examine in immersion oil at 100 % magnification.

Method for thick films

Prepare the final stain as for the thin film.

Without any fixation, place the slide in the stain.

Leave for 15 – 30 minutes in the stain (by agitating the staining jar gently from time to time, haemoglobin is removed from the area of the film).

Remove the slide from the stain and wash in distilled water.

Let it dry

Leishman’s Stain

Method for thin films

Place the slide on a staining rack over sink or dish, with the film facing uppermost.

Cover the film with 12 drops of the stain and leave for 1½ minutes (the methyl alcohol in the stain fixes the film).

Add double the quantity of freshly distilled water.

Mix the solution thoroughly with a pipette or by rocking very gently the slide, taking care not to spill the stain.

Allow to stain for 15 to 20 min, the actual time depending on the quality of the stain. The film should be quite a strong pink colour, when sufficiently stained. The colour is then reduced or the film differentiated by washing with distilled water.

Flood the slide with distilled water, then tip and allow the water to run off. Continue to wash with distilled water until the film is a rather pale pink.

Stand the slide in an upright position to drain and dry. Heat must not be used to dry films but the film can be gently dabbed with blotting paper and waved in the air to expedite drying.

Examine in immersion oil at 100% magnification.

Method for thick films

Thick films must be treated very gently at all stages, as they are not firmly attached to the slides.

Place the slide film side downwards in a dish (or stand it upright in ajar) containing tap or distilled water.

Leave until all the haemoglobin has been removed (2 to 3 min) and the film has become completely white.

Stand the slide in an upright position to drain and dry.

Proceed as for staining thin films.

Field’s stain for thick films

Field’s stain is used for rapid diagnostic and identification purposes. For thin films, fix in methyl alcohol for 2 to 3 minutes prior to staining.

Preparation

A. Methylene blue (medicinal) 0.4 g

Azur 0.25 g

Buffered water (B), pH, and 6.8 – 7.0. 250 ml

B. Disodium hydrogen phosphate 10.0g

Potassium dihydrogen phosphate 12.5 g

Distilled water 1000 ml

C. Eosin 0.5 g

Buffered water (B) 250 ml

Method

Dip slide in A 1- 2 sec

Rinse in B 2- 3 sec

Dip in C 1- 3 sec

Rinse gently in tap water 2- 3 sec

Place slide upwards to drain and dry

Examination of Stool for Intestinal Protozoa

Direct Method

Place a fresh sample of stool, about the size of a bean seed, on a slide, add a drop or two of physiological saline, cover with a cover slip, and examine at a magnification 400 - 500X. This technique should reveal the motile forms of intestinal flagellates.

To identify the cysts and the nuclei of Amoeba, one or two drops of a 4% Lugo’s iodine solution are added to the fresh stool sample.

Examination of Stool for Worm Eggs

a) Direct Examination

A sample of faeces, about the size of a bean seed, is placed on a slide, mixed with tap water or physiological saline, covered with a cover slip, and examined at low microscope magnification (100 to 200X).

The smear should not have lumps of faeces to obscure the eggs. A drop of Lugo’s Iodine can be added to improve the visibility of the eggs.

b) Thick Smear Technique (Kato and Miura)

Preparation of the Kato stain

Distilled water 500 ml

Glycerine 500 ml

Malachite green, 3% in water 5 ml

Place about 100 mg of faeces on a slide and cover it with a cellophane strip (size 26 x 28 mm), which had been soaked in the Koto Stain for at least 24 hr. Press over the strip with a spatula to have a thin uniform spread of the faeces sample. Allow the preparation to stay at room temperature for ½ to 1 hr. Examine the stool. The glycerine clears the faeces and helminth eggs can be seen at a magnification of 100x.

c) Concentration Method

Place 1 g of stool in a test tube and thoroughly mix it with a concentrated salt solution. Remove any plant particles floating on the surface and allow the mixture to remain undisturbed for 20 to 30 min.

Helminth eggs float on the surface because they are lighter than the salt solution, Transfer the eggs to a microscope slide using a wire loop. Examine at a magnification of 100-200x.

d) Universal Concentration Method

Place 1 g of faeces in a small beaker, add 7 ml of 50% hydrochloric acid and the same amount of ether. Mix the mixture to form a homogeneous solution. Pass the mixture into a centrifuge tube over two layers of muslin placed in a funnel. Centrifuge the solution for a minute or two.

Four layers are formed: the uppermost layer is a yellowish zone of ether below which is a zone consisting of food particles and below this is a zone of hydrochloric acid. The bottommost zone consists of small particles and worm eggs. Carefully insert a pipette into the bottom layer, suck out liquid, and examine it for eggs. Be careful, ether is very volatile and can explode!

Sedimentation Concentration Stool Examination Technique

Add an estimated 5 g of stool to 100 ml of formol glycerol solution (5 ml formaldehyde, 10 ml glycerol, 985 ml of water) in a flask and mix with a glass rod.

Sieve through a mesh into another flask.

Add more formol glycerol up to 3 cm below the top and allow to sediment for a minimum of 20 min at room temperature.

Pour off the supernatant to leave approximately 25 to 30 ml of fluid containing sedimented deposit

Resuspend in formol glycerol and sediment for 20 minutes.

Gently pour off supernatant to leave 15 to 20 ml of suspended deposit.

Use straw to transfer about 0.1 ml of the deposit to each of 3 microscope slides and cover each slide with a cover slip.

Examine

Coccidiosis

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Coccidiosis

The family Eimeriidae consists of hundreds of sporozoan organisms that are parasitic to a variety of vertebrates. Coccidiosis is a common name for the diseases due to these sporozoan parasites. Coccidiosis has been reported in chickens, geese, ducks, turkeys, cattle, sheep, rabbits, pigs, fish, reptiles, horses, dogs, and cats, including man.

Eimeria is characterised by the presence of four sporocysts in each spore. The sporocysts occur primarily in the intestinal cells of the host.

Life cycle

Infection is due to ingestion of oocysts by birds. The oocysts are extremely resistant to adverse conditions and will remain viable in the soil for a long time, sometimes even up to more than 15 months. They are minute in size, measuring about 10 to 30 microns. Oocysts are so light that they can be dispersed by wind.

Following ingestion by a bird, the oocysts rupture in the digestive tract and liberate sporocysts that contain sporozoites. The sporozoites invade the cells of the host’s intestinal epithelium where they divide by schizogony to form merozoites.

The infected epithelial cells rupture, releasing more merozoites, which in turn invade more epithelial cells. The process continues until the intestinal wall is severely eroded by the infection.

Some of the merozoites become sex cells. Fusion of these sex cells or gametocytes leads to the formation of oocysts that are passed out in the faeces.

Pathogenesis

E. tenella is a parasite of the caecum of mainly young birds that are under four weeks old. Older birds are increasingly resistant to infection. The severity of the infection depends on the initial dose of the oocysts ingested by the bird. The greater the dose the more serious is the infection. A dose of 200000 oocysts is enough to kill 1 to 2 week old chicks. Death is usually due to severe haemorrhage of the caecal epithelium evident by the fifth day of the infection.

Infection in the young nonimmune chicks is rapid and serious. Spots of blood appear in the faeces around day 5 after infection. By day 7, the faeces are watery and contain oocysts. The birds show signs of loss of appetite and energy, looking very drowsy. About 90% of them die during the first 7 days of infection. E. necatrix causes a milder, chronic infection than E. tenella.

Bovine coccidiosis is not a serious disease but it can kill calves if the infection is quite heavy. The effects of infection in cattle are weight loss, slow growth and a reduction in milk production.

Control

Clean, uncrowded, dry living quarters are of great importance in controlling the infection in chickens and livestock.

Isospora

Isospora belli and Isospora natalensis are two eimerian parasites of man. They invade the small intestine and shed sporocysts that are detected in the faeces of an infected person. Symptoms are usually not serious but include abdominal pain, diarrhoea, flatulence, abdominal cramps, nausea, loss of appetite, lassitude, loss of weight and fever.

Theileria

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Theileria are tick-transmitted protozoan parasites of domestic and wild ruminants. Theileria parva and Theileria annulata are members of this genus that cause debilitating and often fatal disease in cattle. In eastern, central and southern Africa, the most important species is Theileria parva, which causes East Coast fever. In addition to cattle, T. parva infects African buffalo and waterbucks, both of which serve only as reservoirs of infection.

T. parva threatens the lives of over 25 million cattle and is a severe economic constraint to cattle farming in

Burundi

Kenya

Malawi

Mozambique

Rwanda

Sudan

Tanzania

Uganda

, the

Democratic Republic of the Congo

Zambia

, and

Zimbabwe

The existence of three subtypes of T. parva – Theileria parva parva, Theileria parva bovis and Theileria parva lawrenceicomplicates the search for better control methods. All three are transmitted by the brown ear tick, Rhipicephalus appendiculatus, but only two – T. p. parva and T. p. lawrencei produce severe disease in cattle.

T. p. parva and T. p. bovis are transmitted between cattle. T. p. lawrencei is transmitted to cattle mainly from buffaloes, which act only as reservoirs and do not show any clinical symptoms of theileriosis.

Life cycle

The life cycle of T. parva is complex. In both the tick and the mammalian host, the parasite undergoes a series of cellular transformations into different forms. Upon ingestion by R. appendiculatus tick, the parasite undergoes differentiation first in the tick gut, leading to the formation of forms called kinetes. The kinetes migrate to the tick’s salivary glands, where they differentiate into infective sporozoites.

As the tick feeds on cattle, the sporozoites are injected into the blood along with tick saliva. In the host, the parasites attach to and enter lymphocytes. Within two to three days of invading the lymphocytes, the sporozoites develop into intracellular forms called schizonts. The infected lymphocytes grow bigger and begin to divide. These enlarged lymphocytes are known as lymphoblasts. The division of the lymphocytes ensures that each daughter cell is infected. In the end, large numbers of lymphocytes are infected so that the infection spreads throughout the lymphatic system, leading to the widespread destruction of the lymphatic cells.

In the later stages of the infection, some of the schizonts differentiate into merozoites that are released into the bloodstream where they invade red blood cells. In the red cells, the parasites change into forms that are called piroplasms, which are infective to ticks. As the ticks feed on infected animals, they ingest red blood cells that are infected with piroplasms, and this completes the life cycle. The incubation period is usually 10 to 25 days

Pathogenesis and symptomatology

Typical clinical symptoms associated with theileriosis include inflammation and swelling of the lymph nodes, followed by generalized lymphadenopathy, fever, anorexia, and rapid deterioration of condition. Other symptoms include lacrimation, nasal discharge and corneal opacity, an increased respiratory rate and diarrhoea. Death is usually due to pulmonary oedema, severe dyspnoea and discharge. Some animals develop a fatal disease called ‘turning sickness’, in which infected cells block capillaries in the CNS and cause neurological signs. Some animals recover from the infection and become asymptomatic carriers; others may have poor productivity while others may become stunted in growth.

Post-mortem examination shows extensive haemorrhages in different tissues and body organs, they lymphoid system is greatly swollen but may be shrunken in chronic cases, the liver and the spleen are enlarged. The lungs are reddened and both the trachea and bronchi are filled with fluid and froth.

The main effect of theileriosis on the host is the extensive destruction of the lymphatic cells by multiplying schizonts.Morbidity and mortality vary with host’s susceptibility and the strain of parasite. The mortality can reach 100% in susceptible cattle from nonendemic areas in three to four weeks of infection. However, mortality is low in indigenous zebu cattle in endemic areas. Although animals that recover from the infection acquire immunity that may last for a long time, some of the animals act as reservoirs of infection, or show low productivity and appear stunted.

Diagnosis

Theileria should be suspected in tick-infested animals that present with fever and enlarged lymph nodes, and where mortality seems to affect mainly calves. Diagnosis is made by identification of the schizonts in thin blood smears, lymph node and liver biopsies. At necropsy, schizonts may be found in impression smears from internal organs.

Polymerase chain reaction (PCR) tests and DNA probes are sometimes used to identify Theileria species. Antibodies to T. parva, can be detected with an enzyme-linked immunosorbent assay (ELISA) and other immunological tests.

Control

In areas where East Coast fever is endemic, dipping or spraying cattle with an acaricide to kill the ticks is a sure way of controlling the disease. The dipping or spraying of the animals must be carried out regularly. Because cattle that are regularly treated with acaricide are not exposed to T. parva, they develop no immunity and thus have no protection against the parasite or other tick-borne diseases if treatment is interrupted. Regular application of the acaricides has its drawbacks- it is environmentally unfriendly and can lead to emergence of insecticide resistant ticks.

Treatment of theileriosis is possible with drugs and vaccines.

Babesia

2013-01-19T20:44:00.004-08:00

Piroplasms are protozoan parasites that include Babesia and Theileria. These intracellular tick-borne transmitted diseases are of great economic importance because they are responsible for serious losses in domestic livestock, particularly cattle.

Babesiosis

Babesia bigemina and Babesia bovis are economically important parasites of sheep, cattle, goats, horses, pigs, dogs and cats and are responsible for a disease called babesiosis (redwater fever or tick fever). Babesiosis is transmitted by a number of one-host ticks, such as Boophilus microplus, Boophilus decoloratus, and Boophilus annulatus.

Human babesiosis has been reported mainly in North America and Europe and has been linked to B. bovis, which causes cattle babesiosis. The other parasite linked to human infection is B. microti, a natural parasite of rodents.

Life cycle

The infection begins with a bite by an infected tick, which introduces sporozoites into the blood from it salivary glands. The sporozoites invade the host’s red blood cells and undergo several schizogonic divisions, increasing their numbers enormously. Eventually some of the infected red blood cells rupture, releasing thousands of merozoites and gametocytes into the circulation.

When a tick imbibes blood from an infected animal, the female gamete and male gamete unite in the tick’s gut to produce embryos. Some of these motile embryos or ookinetes migrate through the ticks’ tissues and invade the ovaries where they are incorporated into the developing eggs. Consequently, the ticks lay eggs that are already infected.

The nymphs that arise from such eggs are therefore congenitally infected. Some of the merozoites migrate from the ovaries to the salivary glands of the young ticks and after dividing, give rise to sporozoites. These young ticks are able to pass on the infection directly to a host on taking their first blood meal.

Infected animals show increased body temperature, malaise and loss of appetite, constipation or diarrhoea, vomiting, bloody urine and anaemia. Erythrocytic parasites are present in the lumens of capillaries of all internal organs including the brain. Mortality is high and death may occur in one week.

In human babesiosis, malaise, anorexia and fatigue are usually evident a week after being bitten by an infected tick. These are followed several days later by high fever, chills, drenching sweats, muscle pain and headache. The symptoms may continue for months or abate, then recur. Some infected people do not show any symptoms at all.

Individuals who are at risk are those with reduced immunity, especially the elderly and those who have undergone splenectomy. There is no specific treatment for babesiosis, although antimalarial drugs are sometimes used.

Six-legged, fur-covered, sea-faring and conferences - all packed full of parasites!

2013-01-19T20:40:00.001-08:00

It looks like we've made it through another year of parasites, filled with posts on new research that was published this year on all manners of parasitic and infectious organisms. Among many other things, this year we covered some parasitological going-ons in the insect world with Zombee parasitoids, a story of parasitoid wasp, aphids and their symbionts, a wasp that can manipulate the colour of berries, and a cricket-infecting horsehair worm which has abandoned sex.

We also wrote about parasites that are infecting our furry friends including reindeer roundworms, a fleaof desert rodents, echidna gut parasites, anteater parasites, and a caring, maternal bat tick.

There were a lot of parasite action under the sea too, with jellyfish parasites that provide a floating buffet for some fish, a thorny-head worm which infects krill as a way of getting itself into whales, a leech that lives on shrimps, a prickly worm that lives in the stomach of dolphins, and a story of death, sex and fish guts.

Those are just a few example of post from this year; browse through the archives for a lot more parasitological tales.

Also for the first time on this blog, Susan and I had decided to report from conferences that we had attended on our respective continents! I wrote up a series of blog posts from the Australian Society for Parasitology annual conference, and Susan also wrote a few posts reporting from the American Society of Parasitology annual meeting.

Paragordius obamai

2012-11-09T20:41:00.000-08:00

Paragordius obamai

Sex is one of the great mysteries of evolutionary biology - why do organisms have it? It has numerous costs associated with it, including the two big ones, which are that only half the population will produce offspring in the next generation (technically really a problem more of anisogamy than sex, per se) and that successful gene combinations can be broken up via recombination. There are other costs as well. For instance, finding and wooing mates can be costly to an organism.

Nematomorphs, sometimes called hairworms, are parasites that live inside arthropods as larvae, but then exist as free-living aquatic adults. They often induce suicide in their insect hosts, by causing them to jump into water, where the worms then escape (see this previous post for another example). The adults typically seek out the opposite sex and can form "Gordian knots" of mating worms. Today's species, however, is found in larger and faster-moving waters - and in these big, complicated habitats, finding a suitable mate can be really tricky. So, today's parasite, has solved this problem through the evolution of parthenogenesis. Meet Paragordius obamai, (named after President Obama, in honor of it being discovered in Kenya, where his father was raised), a species of nematomorph that has completely given up on males. When brought into the lab, P. obamai only released female worms and nowhere inside these stringy parasites could male reproductive organs be found. Because bacterial symbiontscan sometimes produce severe sex-ratio biases or even male-killing in insects and other invertebrates, the authors used pyrosequencing to look for evidence of these micro-manipulators, yet found no sequences similar to the taxa that have been observed to cause these biases in other hosts.

The authors now plan to use this new species, in comparison with a sexual congener, to test hypotheses on the evolution of and genetic mechanisms responsible for this novel parthenogenetic situation.

Lysiphlebus fabarum

2012-11-09T20:38:00.003-08:00

Lysiphlebus fabarum

Recently there was a widely circulated study about fruit flies consuming alcohol to fight off parasitoid infections. But there are other methods that insects employ to fight off attacks by parasitoids, and the defence employed by aphids against one of its parasitoids -Lysiphlebus fabrum - is multi-layered in more ways than one.

From the parasitoid's perspective, bigger aphids provide more resources - but they are also more dangerous to tackle. Larger aphids can deliver a mean kick against parasitoid wasps, and they also have a more well-developed innate immune system, so even if the wasp can get past the kicking limbs, her eggs may not survive even if they do make their way in. Small aphids are much easier to attack and subdue and have weaker immune systems. But, because of their smaller size, they are also more likely to die from the trauma associated with being stabbed with a wasp's ovipositor, and this would end up being a waste of time and resources for L. fabarum. Therefore, much like Goldilocks, L. fabarum usually selects for the intermediate-size aphids - not so big that they put on too much of a fight, but not so small that they might not even survive the initial infection process.

However, there's another thread weaving through this story and that thread is coevolution. The effectiveness of the aphid's immune system depends on its genetic lineage. In typical co-evolutionary arms race fashion, there is considerable genetic variation in the aphid's innate immune system andcertain aphid clones are better at fighting off parasitoids. But just when you are getting comfortable with the idea of aphid resistance being based on a combination of aphid age and genotype against the adversarial wasps, it's time to throw in another factor to complicate the story - the appropriately named bacterial symbiont Hamiltonella defensa.

Some (but not all) aphids carry this protective symbiont, which acts as an internal guard dog (guard germ?) that enhances the aphid's ability to kill off parasitoids. To complicate the picture further, H. defensa itself has acquired this ability by incorporating a toxin-producing gene into its genome thatoriginated from a virus. Not only does this toxin-producing microbe kill off the parasitoid larvae inside the aphid, they also affect the egg-depositing behaviour of the parasitoid. And much like the aphid's innate immunity, age also plays a role in modulating the defense conferred by the symbiont. Younger aphids have smaller populations of H. defensa to start off, but they increase as they got older, and the more symbionts an aphid has, the better it is at fighting off parasitoids.

So how does this affect the evolutionary pathway of L. fabarum? Researchers found that because H. defensa play such a major role in the aphid's defense, not only are the wasps locked in a coevolutionary race with the aphids, they are also engaged in an even more intense arms race with the H. defensasymbionts carried by the said aphids. Even when H. defensa do not outright kill the L. fabarum larvae, they do still incur a cost; in aphids carrying the symbiont, the wasp took longer to develop, and also emerged slightly emaciated compared with those that infected H. defensa-free aphids.

The most remarkable finding that emerged was when researchers looked specifically at the different strains of symbionts and their interactions with different lines of L. fabrum. For example, they found that one particular strain of H. defensa that they called H323 conferred protection against most lines ofL. fabarum - but offered the aphid no protection against one particular line of L. fabrum. Even the star performer out of all the symbionts - strain H76 - that conferred the greatest protection on average against almost all the lines of wasp tested - had a nemesis. A different genetic line of L. fabarum was able to weather the bacterial guardian's toxins and successfully develop to maturity.

What emerges is a complex series of coevolution that is occurring not just between different genetic lines of aphids and wasps, but also between the wasps and the symbionts carried by the aphids. While superficially, it may seem like the story of a coevolutionary arms race between aphids and wasps, given the strong interactions between the wasps and the bacterial symbionts, it is much more a story of coevolution between L. fabrum versus H. defensa, being played out on an "aphid stage."

Image from figure in the paper.

Reference:

Schmid, M., Sieber, R., Zimmermann, Y-S. and Vorburger, C. (2012) Development, specificity and sublethal effects of symbiont-conferred resistance to parasitoids in aphids. Functional Ecology 26: 207-215

Ligula intestinalis

2012-11-09T20:36:00.000-08:00

Ligula intestinalis

The star of today's post is a fish tapeworm call Ligula intestinalis, and today's post is about a recently published paper that resulted from a 20 year-long study that monitored the presence of this parasite in the fish community of a reservoir in north-eastern France. The reservoir was originally created in 1986 for buffering the thermal discharge of a nuclear power plant, and data about parasitism of fish in the reservoir have been recorded since 1991. The main parasite infecting fish living in the reservoir is the tapeworm Ligula intestinalis. This parasite infects many different species of freshwater fish, but it mainly parasitises cyprinids (the carp family) such as carp, roach, and dace. A fish becomes infected through eating infected copepods and once inside the fish, the tapeworm develops into a larval stage call a plerocercoid in the fish's body cavity, which goes on to infect fish-eating birds such as herons and cormorants. As you can tell from the photo, the plerocercoid can reach alarming size and mass.

Over the 20 years since records were kept about parasitism of fish in that reservoir,L. intestinalis had progressively shifted its preferred host from roach (Rutilus rutilus) to silver bream (Blicca bjoerkna). The data from this study provide a picture of how this host transfer occurred over the two decades. Prior to 1998, the tapeworm was commonly found in roach and only occasionally found in other fish such as bream. But the roach population suffered from a series of sharp declines during the two decades - once in 1993, and then a more severe collapse in 1997. It was after this second decline that everything changed - in 1998, L. intestinalis began showing up frequently in bream.

It is more surprising that the switch hadn't occurred sooner - the bream made an ideal host for L. intestinalis in the reservoir. Not only was it abundant when the roach population collapsed, it was also more resilient to environmental stressors - such as thermal effluents from a nuclear power plant. Although the reservoir was restocked with additional roaches for anglers in 2002 and 2004, by that time, the parasite had already made the switch to having bream as its preferred host, and it was only found sporadically in roaches - the original host. So even though it seems as if the sliver bream made the ideal host for L. intestinalis in that reservoir, it took a dramatic event - the collapse of the roach population in 1997 - to bring them together. Ligula intestinalis adapted to changes in its circumstances by making an occasional host (bream) into their main host of choice.

Another interest finding of this study was the way L. intestinalis exploits the bream host. The tapeworm adopts a different strategy depending on the host's sex. When L. intestinalis infects a female fish, it diverts resources from her reproductive tissue, but if it infects a male fish, the tapeworm obtain nourishment from the fat reserves. This corroborates earlier studies that found L. intestinalis infection inhibits the reproductive capacity of its host.

But, the most surprising finding was that despite the grotesquely large size of the tapeworm compared to its host, the overall health of infected fish was not noticeably different from uninfected fish - which is remarkable when you consider how many resources the worm has to drain from the fish in order to grow so large. The fact that L. intestinalis was able to divert energy from the fish without compromising its health suggests that it is capable of manipulating the host's physiology with great finesse - fine tuning the physiology of its host in a way that diverts as much energy as possible for its own growth, but at the same time keeping the host alive long enough for it to be eaten by the parasite's next host.

Image from: Trubiroha et al. (2009) International Journal for Parasitology 39: 1465–1473

Reference:

Vanacker, M., Masson, G. and Beisel, J-N. (2012) Host switch and infestation by Ligula intestinalis L. in a silver bream (Blicca bjoerkna L.) population. Parasitology 139: 406–417.

Introduction to Protozoa

2012-10-03T01:19:00.002-07:00

Introduction to Protozoa

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.

Malaria( Plasmodium vivax,P. falciparum, P. malariae and P. ovale)

2012-10-03T01:18:00.003-07:00

Malaria scourge

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, particularlyP. 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 asBacillus 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

2012-09-13T02:49:00.003-07:00

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

2012-09-11T19:03:00.002-07:00

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.