Coccidiosis

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

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

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!

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

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.