Influential environmentalists tell us that nature is interconnected. What they mean is that an impact, good or bad, on one population in an ecosystem, will affect the whole array of organisms.

There are, however, other ways in which organisms may be interconnected. One fascinating situation involves certain parasites or disease causing organisms. In several cases, a parasite passes through two entirely different kinds of host in or­der to continue its nasty parasitic existence. Not only are these situations fascinating, but biologists are mystified how these rela­tionships could ever have developed.

It takes two⤒🔗

Malaria is probably the best known case of alternation of hosts. The blood from a person suffering from malaria cannot in­fect another person. A specific type of mos­quito is required to further incubate and spread the disease. There are about 2500 species of mosquito which are grouped into various genera. These include Aedes, Culex, and Anopheles among others. It is the Anopheles mosquitoes which transmit malaria, but only 60 out of 380 species have this capability.

The disease agent is a tiny protozoan or single celled animal, really a kind of amoeba. When an infected female mos­quito bites a person or a warm-blooded an­imal, she injects tiny amoeboid cells into the victim's blood stream. These amoebas invade red blood cells and multiply therein. The infected red blood cells burst all at the same time and more young amoebas in­vade other red blood cells. Every time such a release occurs, the victim suffers from fever and chills.

After several such cycles, the proto­zoan develops a sexual stage suitable for transmitting to mosquitoes. When a suit­able female mosquito drinks a victim's blood, the malarial parasites end up in her stomach. There sexual cells unite. These then penetrate the stomach wall. They multiply, producing huge numbers of slen­der spore cells which then invade the sali­vary glands of the mosquito. When this insect injects saliva into a victim prior to her next blood meal, the slender cells en­ter the human victim's blood stream and become amoeboid.

Thus we have the amoeboid stage and presexual stage in man, the sexual union and massive multiplication of spore cells which, when injected into another per­son's blood, become the amoeboid stage again. Here we see that a single celled ani­mal depends upon warm-blooded organ­isms and cold-blooded mosquitoes in order to complete its parasitic life cycle. In order to eliminate this nasty disease, the best pro­cedure obviously is to control or eliminate the relevant mosquito populations.

The tea-fungi connection←⤒🔗

The exploiting of alternate hosts by a parasitic organism is also found elsewhere in nature. Most fungi do not indulge in such fancy lifestyles, but there is one fun­gus group which does include parasites fa­mous for their dependence on alternate hosts. The rusts include many highly spe­cialized fungus diseases of plants. Some attack only a single host. For example Hemileia vestatrix attacks only coffee plants. The devastation brought about by this fun­gus on English coffee plantations in Cey­lon (Sri Lanka) and elsewhere during the late 19th century caused the British to switch to tea as their preferred beverage.

Some other rusts require two distinct hosts in order to complete their life cycle. As we saw in the case of malaria, the hosts exploited by the rust fungus are very dif­ferent from each other.

One of the most famous rust diseases is Cronartium ribicola or white pine blister rust. Pine (Pinus) trees, of course are conifers, non-flowering evergreens which reproduce by means of seeds borne in cones.

The fungus was apparently originally native to white pines in Asia. At some point centuries ago, plant collectors introduced diseased material to Europe. At the end of the nineteenth century, imports of infected white pine seedlings from Germany re­sulted in the establishment of the disease in eastern North America. A few years later, ironically, North American eastern white pine seedlings were imported from France to Vancouver. Thus the disease became es­tablished along the west coast of North America too. Apparently at that time the Europeans had better plant nurseries than the North Americans, and so American plants were often propagated in Europe and then resold back to the new world. That was in the days before people from the Netherlands established plant nurseries throughout Canada and the United States!

The offspring of a tree and shrub←⤒🔗

The story of white pine blister rust ap­pears uncomplicated, but this is not so. The fungus, which grows on pine, cannot infect another pine tree or seedling. It needs an alternate host, namely flowering shrubs of the genus Ribes (currants and gooseber­ries). It so happens that Ribes species are na­tive to Europe, temperate Asia and North America. Places where suitable white pine grows also tend to have currant bushes and/or gooseberry shrubs growing on the forest floor.

The disease cycle proceeds like this. During the late summer and early fall, es­pecially when the weather is cool and moist, special fungus spores from Ribes leaves may be carried by the wind to white pine needles. These spores (called basidiospores) are delicate and survive only a couple of days. Ideally they encounter white pine within a few hundred meters. The spores germinate and grow through the needle into the bark. The fungus then overwinters in the pine victim. During the following summer, the fungus produces a swollen area in the bark. Late in that sum­mer season, the fungus breaks through the bark. Sticky drops of sweet liquid from the fungus attract flies which inadver­tently transfer special sexual cells. Follow­ing this sexual union, the fungus settles down for another winter. In the second spring, swollen white to yellow blisters appear where the sticky areas were for­merly. These blisters are full of spores called aeciospores. The fungus on the pine keeps growing farther on the stem. It may kill a whole branch or a whole seedling.

More and more aeciospores are produced season after season.

The aeciospores, however, cannot in­fect another pine tree.

White pine aeciospores can only infect a Ribes bush. These spores are tough and can spread hundreds of kilometers, carried by the wind. Once they light on a suitable Ribes bush, they invade the leaf. Within two weeks, orange uredospores (rust) ap­pear on the bottom of the leaf. These spores infect more currants or gooseberry leaves.

In the fall, dark spores called teliospores ap­pear instead of uredospores. When condi­tions are cool and moist, each teliospore produces a short club-like growth bearing four basidiospores. The basidsiospores are delicate and short lived and can only infect pine. All fungus stages on Ribes die when the leaves drop off in the fall. Only in pine trees does the fungus survive the winter.

The obvious way to control this disease is to eliminate one of the hosts. Since white pine trees are very valuable, the prudent course of action is to eliminate Ribes. In cen­tral Canada and the eastern United States, this policy was vigorously pursued for many years. Several states banned the growth of cultivated Ribes species. Civic minded citizens sought out native plants and uprooted them. In recent years, such initiatives have become less rigorous, but they certainly helped. In western North America, however, the native shrubs are so common, and so hard to kill, that the initiative was soon abandoned and the blister rust continues to extend its toll.

Rusty wheat←⤒🔗

There are other rusts with interesting host choices. In many grain-cultivating re­gions, wheat rust is the most famous dis­ease to exhibit an alternation of hosts. The life cycle goes something like this. Thick walled teliospores overwinter on wheat stems. In the spring, each teliospore devel­ops a tiny club like structure on which four delicate basidiospores are produced. The basidiospores, spread by the wind, land on the leaves of a small shrub called barberry (Berberis). There are native shrubs of this genus in most wheat growing re­gions. The fungus firstly develops sweet sticky pustules on the barberry leaves. These pustules attract flies which inadver­tently spread the sexual cells. Once sexual union is accomplished, the fungus vigor­ously develops aeciospores on the lower leaf surface. The aeciospores, unable to re-infect barberry, are carried by the wind to wheat stems. Subsequent growth on wheat stems and leaves results in large rust coloured areas releasing myriad uredospores. These can and do infect other wheat stems. Eventually in the fall, the fungus produces dark teliospores which overwinter on wheat stubble.

It might seem that if barberry bushes were eliminated, the fungus would likewise be gone. This program was indeed success­ful in some European countries. Similar programs were undertaken in North Amer­ica. During the 1930s in the United States, many jobless citizens were employed in barberry eradication programs. There were still barberry shrubs in Canadian gardens during the 1950s, but later they too were rooted out. Within the past 4-5 years how­ever, new resistant cultivars of barberry (from Japanese stock) have appeared on the market. These attractive small shrubs are quickly becoming popular.

In view of the immense importance of wheat to the Canadian economy, this coun­try has devoted a lot of money to research rust fungus. Eliminating the alternate host (barberry) unfortunately did not result in control of the disease in North America. Non-hardy rust colored uredospores are able to survive the winter in the southern United States. This is a repeating stage which is able to reinfect wheat. Thus the need for an alternate host is bypassed. As the warmer weather moves north each spring, the uredospores proceed northward on native grasses.

It was a Canadian, John Craigie (1887-1987) who in 1927 discovered the function and significance of the sexual stage in rusts. This man spent much of his career re­searching the 200 or so physiologic races of wheat rust. Some strains of wheat are re­sistant to certain fungus strains, but not to all of them. It is the task of the plant breeder to predict which strains will be most prevalent in a given year, and to de­velop wheat cultivars resist to those fun­gus strains. Naturally this is a research program that never ends!

Worms aplenty←⤒🔗

No discussion of alternate hosts could be complete without mention of worm par­asites. Among human diseases, schistoso­miasis ranks third after malaria and AIDS. This disease is caused by a tiny flatworm parasite. The problem is common in 74 de­veloping countries, with the vast bulk of victims living in sub-Sahara Africa. The disease renders victims lethargic, with stunted growth and often reduced mental capacity. The male worm is flat and the fe­male worm nestles up against the male. The pair lodge in a person's blood vessels of the intestine or bladder wall. The female releases perhaps thousands of eggs per day. Inadequate sanitation results in many of these eggs ending up in bodies of water in which people wash, swim or work in irri­gation projects.

The eggs from the worms cannot infect more human victims. Instead, the eggs hatch into tiny swimming structures called miracidia. These need to find a suitable snail host within 8-12 hours or they will die. Each worm species is able to infect only one particular genus of snails. Inside a suitable snail host, the miracidia develop into many cyst-like spores. After two months, the spores develop into forked tailed swimming structures called cer­cariae. Invisible to the naked eye and re­leased in their thousands, cercariae need to find a human victim within 48 hours. Suc­cessful cercariae burrow through the skin to a blood vessel and from there they move to the intestine or bladder. Some may get lost and land in the brain, heart or liver, of­ten with fatal consequences for the victim.

Obviously, as well as improved sanita­tion, control of the alternate host is the most promising control measure. Faster flowing water with fewer places for aquatic vegetation, definitely reduces the preva­lence of the snails and thus of this para­sitic disease in humans.

Conclusion←⤒🔗

Fascinating as all these stories are, the really interesting question is how each of these parasites came to exploit two highly different hosts in one life cycle. While few of us would be sorry to see these parasites disappear, we must admit to a grudging respect for such ingenuity. Who of us would have the imagination to even conceive of such systems? "Ingenuity" of course is a characteristic of intelligent agents, not of random processes. Blind processes never exhibit planning or design skills. It is evident that these life histories were designed.