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.