Paragordius obamai

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

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

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

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)

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 ^o C. 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

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.