GOLLYGEE!

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Tag: parasites

12.18.2012

mistletoe

Mistletoe

The New York Times has an interesting piece on mistletoe’s role in nature. It’s a parasite but it appears to be key in maintaining a health and balanced forest ecosystem:

Dr. Watson, known in academic circles as “the mistletoe guy,” had long suspected that his favorite plant was a keystone species, meaning it punches above its weight, ecologically speaking, but even he was unprepared for the results. He had supposed that creatures that fed or nested on mistletoe would be affected by its removal. Instead, he found that the whole woodland community in the mistletoe-free forests declined.

Three years after the mistletoe vanished, so had more than a third of the bird species, including those that fed on insects. Bird diversity is considered an indicator of overall diversity. Where mistletoe remained, bird species increased slightly. It was a similar story for some mammals and reptiles, but, in another surprise, particularly for those that fed on insects on the forest floor.

“It’s a bit of a head-scratcher,” said Dr. Watson.

Analysis showed that species of mistletoe play an important role in moving nutrients around the forest food web. That has to do with their status as parasites.

Nonparasitic plants suck nutrients out of their own leaves before they let them fall, sending dry containers to the ground. But because the vampiric mistletoe draws water and nutrients from the tree stem or branch it attaches to, it is more nonchalant about leaving that nutrition in falling leaves. That means the fallen leaves still contain nutrients that feed creatures on the forest floor.

Not only that, but mistletoes make and drop leaves three or four times as rapidly as the trees they live off of, said Dr. Watson. As evergreens, they also do it throughout the year, even when trees are dormant. It is like a round-the-calendar mistletoe banquet.

12.13.2012

platelets confer resistance to parasites

Platelets prevent parasitic infestation. Image from Sciencemag.org

From Science magazine this week, a report on how platelets express genes to help kill parasites. An excerpt from the perspective:

The six Plasmodium parasite species that cause disease in humans (P. falciparum, P. vivax, P. malariae, P. ovale wallickerie, P. ovale curtisii, and P. knowlesi) appear to have independently colonized hominids and influenced the genetic composition of different human populations (3). For example, the genes responsible for sickle cell anemia, thalassemia, and glucose-6-phosphate dehydrogenase deficiency have a higher frequency in populations where malaria is, or was once, endemic. These genes provide protection against severe malaria syndromes and likely evolved in response to the disease by providing a survival advantage (4). Another of these genes encodes the Duffy-antigen receptor for chemokines (DARC/Fy glycoprotein/CD234) found on red blood cells. This protein also acts as a receptor for P. vivax (5), and human red blood cells lacking this receptor are resistant to invasion by this species and by P. knowlesi (6, 7). The impact of this genetic selection can be seen in the geographical distribution of P. vivax. This parasite is spread throughout tropical regions of the world, but is rare in large areas of central and western Africa where many individuals lack Duffy-antigen receptor expression on red blood cells. Thus, this “Duffy-negative” phenotype appears to have evolved as an innate resistance mechanism to P. vivax infection.

McMorran et al. extend previous work that demonstrated an important role for platelets in resistance to malaria (8) by identifying platelet factor 4 (PF4) as a key molecule in platelet-mediated killing of P. falciparum. PF4 is released from α granules in activated platelets to promote blood coagulation (9). It binds the Duffy-antigen receptor, along with several other chemokines (10). McMorran et al. found that a functional Duffy-antigen receptor is required for the antiparasitic activity of PF4.

Also check out the scientific research paper here [subscription required].

12.06.2012

parasites have tricks to take over their hosts

The New York Times has an interesting article today documenting some of the interesting ways parasites take over their hosts in order to stay alive and proliferate. Take as an example the Costa Rican spider:

In the case of the Costa Rican spider, the new web is splendidly suited to its wasp invader. Unlike the spider’s normal web, mostly a tangle of threads, this one has a platform topped by a thick sheet that protects it from the rain. The wasp larva crawls to the edge of the platform and spins a cocoon that hangs down through an opening that the spider has kindly provided for the parasite.

To manipulate the spiders, the wasp must have genes that produce proteins that alter spider behavior, and in some species, scientists are now pinpointing this type of gene. Such is the case with the baculovirus, a virus sprinkled liberally on leaves in forests and gardens. (The cabbage in a serving of coleslaw carries 100 million baculoviruses.)

Human diners need not worry, because the virus is harmful only to caterpillars of insect species, like gypsy moths. When a caterpillar bites a baculovirus-laden leaf, the parasite invades its cells and begins to replicate, sending the command “climb high.” The hosts end up high in trees, which has earned this infection the name treetop disease. The bodies of the caterpillars then dissolve, releasing a rain of viruses on unsuspecting hosts below.

David P. Hughes of Penn State University and his colleagues have found that a single gene, known as egt, is responsible for driving the caterpillars up trees. The gene encodes an enzyme. When the enzyme is released inside the caterpillar, it destroys a hormone that signals a caterpillar to stop feeding and molt.

And also the thorny head worm:

Their host is a shrimplike crustacean called a gammarid. Gammarids, which live in ponds, typically respond to disturbances by diving down into the mud. An infected gammarid, by contrast, races up to the surface of the pond. It then scoots across the water until it finds a stem, a rock or some other object it can cling to.

The gammarid’s odd swimming behavior allows the parasite to take the next step in its life cycle. Unlike baculoviruses, which go from caterpillar to caterpillar, thorny-headed worms need to live in two species: a gammarid and then a bird. Hiding in the pond mud keeps a gammarid safe from predators. By forcing it to swim to the surface, the thorny-headed worm makes it an easy target.

Simone Helluy of Wellesley College studies this suicidal reversal. Her research indicates that the parasites manipulate the gammarid’s brain through its immune system.

The invader provokes a strong response from the gammarid’s immune cells, which unleash chemicals to kill the parasite. But the parasite fends off these attacks, and the host’s immune system instead produces an inflammation that infiltrates its own brain. There, it disrupts the brain’s chemistry — in particular, causing it to produce copious amounts of the neurotransmitter serotonin.