This document deals primarily with the pathogenic helminth worms; while fungi, bacteria, cyanophyte and algal toxins and viruses are mentioned in passing no guidelines are recommended. They are dealt with in other reports. The length of the list of helminth worms gives some indication of the scope of the field. The understanding of helminths is more complete than for many other groups of pathogens. However, there is a growing need for this information to be consolidated and reviewed; some guidelines are needed now. The following table gives a brief capsular overview of the names of the diseases, the organisms responsible, a broad distribution range, some transmission mechanisms, a general prognosis of patients and some pre-disposing epidemiology factors of the disease.
| Parameter | Specific Details |
| Disease Caused | Diphyllobothriasis, fish tapeworm, intestinal infection |
| Organisms Responsible | Diphyllobothrium latum Diphyllobothrium pacificum Diphyllobothrium cordatum Diphyllobothrium ursi Diphyllobothrium dendriticum Diphyllobothrium lanceolatum Diphyllobothrium dalliae Diphyllobothrium yonagoensis |
| Distribution Range | Europe, Asia, North America, Chile, Uganda |
| Transmission Mechanisms | Uncooked or undercooked freshwater fish |
| Prognosis-Healthy People | Asymptomatic, anemia, diarrhea |
| Prognosis-HIV/AIDS | Anemia, diarrhea |
| Epidemiology Factors | Lakes and rivers with fish populations near large human populations which consume raw, undercooked or pickled freshwater fish |
| ..... | |
| Disease Caused | Dipylidiasis, dog tapeworm, intestinal infection |
| Organism Responsible | Dipylidium caninum |
| Distribution Range | Cosmopolitan |
| Transmission Mechanisms | Water, food, fecal/oral, sex, ingesting fleas |
| Prognosis-Healthy People | Asymptomatic |
| Prognosis-HIV/AIDS | Asymptomatic or mild gastro-intestinal |
| Epidemiology Factors | Fleas, dogs, cats, children, poor hygiene |
| ..... | |
| Disease Caused | Echinococcosis, hydatidosis, dog tapeworm |
| Organisms Responsible | Echinococcus granulosus Echinococcus multilocularis Echinococcus vogeli Echinococcus oligarthrus |
| Distribution Range | Cosmopolitan in sheep raising areas |
| Transmission Mechanisms | Food, water, fecal/oral, sex, petting a dog |
| Prognosis-Healthy People | Damage to various internal organs, may be fatal |
| Epidemiology Factors | Sheep and dogs, rodents, stock or game offal or feces |
| ..... | |
| Disease Caused | Gnathostomiasis |
| Organisms Responsible | Gnathospoma binucleatum Gnathospoma didelphis Gnathospoma doloresi Gnathospoma hispidum Gnathospoma miyazakii Gnathospoma nipponicum Gnathospoma procyonis Gnathospoma spinigerum |
| Distribution Range | Southeast Asia, Japan, Mexico, Ecuador, Argentina, Mostly in Thailand |
| Transmission Mechanisms | Food, water; eating raw or poorly cooked meat or drinking water with infected copepods |
| Prognosis-Healthy People | Damage to various internal organs, pain |
| Epidemiology Factors | Cats, dogs, ocelot, raccoon, opossum, otters, other mammals, freshwater fish, reptiles, amphibians, birds (chicken), snakes, copepods |
| ..... | |
| Disease Caused | Hymenolepiasis, rat tapeworm, intestinal infection |
| Organism Responsible | Hymenolepis diminuta |
| Distribution Range | Cosmopolitan |
| Transmission Mechanisms | Water, food, fecal/oral, sex, |
| Prognosis-Healthy People | Usually asymptomatic |
| Epidemiology Factors | Rats, insects, contaminated cereals, flours and grains |
| ..... | |
| Disease Caused | Hymenolepiasis, dwarf tapeworm, intestinal infection |
| Organism Responsible | Hymenolepis nana |
| Distribution Range | Cosmopolitan |
| Transmission Mechanisms | Water, food, fecal/oral, sex, internal auto-infection |
| Prognosis-Healthy People | Usually asymptomatic |
| Epidemiology Factors | Rats, insects, contaminated cereals, flours and grains, poor hygiene |
| ..... | |
| Disease Caused | Sparganosis, dog tapeworm, intestinal infection |
| Organism Responsible | Spirometra erinacei Spirometra mansoni Spirometra mansonoides Spirometra ranarum |
| Distribution Range | Cosmopolitan, Southeast Asia, southern United States |
| Transmission Mechanisms | raw meat, water containing infected Cyclops, some folk medical treatments |
| Prognosis-Healthy People | Swellings, tissue damage, eye and brain damage |
| Epidemiology Factors | Eating raw or undercooked meat, drinking water containing infected Cyclops, raw snake or frog tissue poultices, feral dogs and cats |
| ..... | |
| Disease Caused | Taeniasis, beef tapeworm, intestinal infection |
| Organism Responsible | Taenia saginata |
| Distribution Range | Cosmopolitan where beef is eaten |
| Transmission Mechanisms | Food, water, fecal/oral, sex, poor hygiene |
| Prognosis-Healthy People | Mild intestinal disturbance |
| Epidemiology Factors | Eating raw or undercooked beef |
| ..... | |
| Disease Caused | Taeniasis, cysticercosis, pork tapeworm, intestinal infection |
| Organism Responsible | Taenia solium |
| Distribution Range | Cosmopolitan where pork is eaten |
| Transmission Mechanisms | Food, water, fecal/oral, sex, poor hygiene |
| Prognosis-Healthy People | Mild intestinal disturbance, damage to internal organs |
| Epidemiology Factors | Eating raw or undercooked pork, poor hygiene, close contact with pigs, crowding, subsistence farming |
| ..... | |
| Disease Caused | Ancylostomiasis, hookworm |
| Organisms Responsible | Ancylostoma doudenale Ancylostoma ceylanicum Ancylostoma braziliense Uncinaria stenocephala |
| Distribution Range | Cosmopolitan in warm, moist climates |
| Transmission Mechanisms | Water, food, skin contact, sex, fecal/oral, breastfeeding |
| Prognosis-Healthy People | Anemia, respiratory problems |
| Epidemiology Factors | Poor hygiene, crowding, slums, inadequate sewage or fecal matter treatment, fertilizing with feces or sewage, lack of adequate water filtration, walking barefoot or other skin contact with contaminated soils |
| ..... | |
| Disease Caused | Hookworm |
| Organism Responsible | Necator americanus |
| Distribution Range | Cosmopolitan in warm, moist climates |
| Transmission Mechanisms | Water, food, skin contact, sex, fecal/oral, breastfeeding |
| Prognosis-Healthy People | Anemia, respiratory problems |
| Epidemiology Factors | Poor hygiene, crowding, slums, inadequate sewage or fecal matter treatment, fertilizing with feces or sewage, lack of adequate water filtration, walking barefoot or other skin contact with contaminated soils |
| ..... | |
| Disease Caused | Ascariasis |
| Organism Responsible | Ascaris lumbricoides |
| Distribution Range | Cosmopolitan, more common in tropics and sub-tropics |
| Transmission Mechanisms | Water, food, sex, fecal/oral |
| Prognosis-Healthy People | Asymptomatic or some respiratory problems |
| Epidemiology Factors | Poor hygiene, crowding, slums, inadequate sewage or fecal matter treatment, fertilizing with feces or sewage, lack of adequate water filtration, contaminated soils or dusts |
| ..... | |
| Disease Caused | Capillariasis, intestinal infection |
| Organism Responsible | Capillaria philippinensis |
| Distribution Range | Southeast Asia, Middle East, Columbia |
| Transmission Mechanisms | Food, water, auto-infection, fecal/oral, sex |
| Prognosis-Healthy People | Diarrhea, abdominal pain, rarely fatal |
| Epidemiology Factors | Freshwater fish, eating raw or undercooked fish, |
| ..... | |
| Disease Caused | Capillariasis, hepatic infection |
| Organism Responsible | Capillaria hepatica |
| Distribution Range | Cosmopolitan |
| Transmission Mechanisms | Food, water |
| Prognosis-Healthy People | Hepatitis, may be fatal |
| Epidemiology Factors | Contaminated soil is ingested, poor hygiene |
| ..... | |
| Disease Caused | Capillariasis, pulmonary infection |
| Organism Responsible | Capillaria aerophila |
| Distribution Range | Cosmopolitan |
| Transmission Mechanisms | Food, water |
| Prognosis-Healthy People | Asthma, pneumonia, may be fatal |
| Epidemiology Factors | Contaminated soil is ingested, poor hygiene |
| ..... | |
| Disease Caused | Dracunculiasis, guinea worm |
| Organism Responsible | Dracunculus medinensis |
| Distribution Range | Primarily India and East and West Africa |
| Transmission Mechanisms | Water, food, |
| Prognosis-Healthy People | Skin ulcers, abscesses, arthritis |
| Epidemiology Factors | Cyclops, drinking unfiltered water |
| ..... | |
| Disease Caused | Enterobiasis, pinworm |
| Organism Responsible | Enterobius vermicularis |
| Distribution Range | Cosmopolitan |
| Transmission Mechanisms | Fecal/oral, sex, food, water, bedding, clothing, towels |
| Prognosis-Healthy People | Generally asymptomatic, vulvovaginitis |
| Epidemiology Factors | Crowding, slums, institutions, children, day care centers, poor hygiene |
| ..... | |
| Disease Caused | Toxocariasis, dog and cat roundworms |
| Organisms Responsible | Toxocara canis Toxocara catis |
| Distribution Range | Cosmopolitan where dogs and cats are found |
| Transmission Mechanisms | Water, food, sex, fecal/oral |
| Prognosis-Healthy People | Liver, eye and other tissue reactions |
| Epidemiology Factors | Cats, dogs, poor hygiene, fertilizing with contaminated feces, lack of adequate water filtration, contaminated soils or dusts |
| ..... | |
| Disease Caused | Trichuriasis, whipworm |
| Organism Responsible | Trichuris trichiura |
| Distribution Range | Cosmopolitan, more common in the tropics |
| Transmission Mechanisms | Water, food, dust, soil, fecal/oral, sex |
| Prognosis-Healthy People | Asymptomatic to diarrhea or rectal prolapse |
| Epidemiology Factors | Crowding, slums, institutions, poor hygiene, sewage or feces contaminated soil |
| ..... | |
| Disease Caused | Clonorchiasis, Oriental or Chinese liver fluke |
| Organism Responsible | Clonorchis sinensis |
| Distribution Range | Primarily in Asia, rare elsewhere but in the USA |
| Transmission Mechanisms | Eating uncooked, salted, smoked or pickled fish, food, water |
| Prognosis-Healthy People | Bile duct obstruction, diarrhea, pancreatitis, rarely fatal |
| Epidemiology Factors | Snails, raw freshwater fish |
| ..... | |
| Disease Caused | Fascioliasis |
| Organisms Responsible | Fasciola gigantica Fasciola hepatica |
| Distribution Range | Cosmopolitan in sheep and cattle raising areas |
| Transmission Mechanisms | Eating aquatic plants, water, food |
| Prognosis-Healthy People | Generalized internal organ damage due to migration |
| Epidemiology Factors | Sheep, cattle, watercress or other edible aquatic plants, snails, inadequately washed greens |
| ..... | |
| Disease Caused | Fascioliasis |
| Organism Responsible | Fasciola buski |
| Distribution Range | Primarily in Asia and India in pig raising areas |
| Transmission Mechanisms | Eating aquatic plants, water, food |
| Prognosis-Healthy People | Asymptomatic to diarrhea |
| Epidemiology Factors | Pigs, watercress or other edible aquatic plants, snails, inadequately washed greens |
| ..... | |
| Disease Caused | Heterophyiasis |
| Organism Responsible | Heterophyes heterophyes |
| Distribution Range | Primarily Egypt, Middle East and Far East |
| Transmission Mechanisms | Eating salted or undercooked fish, food water |
| Prognosis-Healthy People | Diarrhea, brain and myocardial damage, rarely fatal |
| Epidemiology Factors | Snails, freshwater fish, eating raw fish |
| ..... | |
| Disease Caused | Metagonimiasis |
| Organism Responsible | Metagonimus yokogawai |
| Distribution Range | Primarily Asia, Spain, Israel |
| Transmission Mechanisms | Eating salted or undercooked fish, food, water |
| Prognosis-Healthy People | Diarrhea, brain and myocardial damage, rarely fatal |
| Epidemiology Factors | Snails, freshwater fish, eating raw fish |
| ..... | |
| Disease Caused | Opisthorchiasis |
| Organisms Responsible | Opisthorchis viverrini Opisthorchis felineus |
| Distribution Range | Primarily Asia and Europe |
| Transmission Mechanisms | Eating salted or undercooked fish, food, water |
| Prognosis-Healthy People | Diarrhea, pancreatitis |
| Epidemiology Factors | Snails, freshwater fish, eating raw fish, cats, dogs |
| ..... | |
| Disease Caused | Paragonimiasis, Oriental lung fluke, flukes |
| Organisms Responsible | Paragonimus westermani other Paragonimus species |
| Distribution Range | Primarily Asia, Europe, America, Africa |
| Transmission Mechanisms | Eating undercooked or pickled crayfish or crabs, food, water |
| Prognosis-Healthy People | Pulmonary and brain damage |
| Epidemiology Factors | Snails, crayfish, crabs, eating raw crustaceans |
| ..... | |
| Disease Caused | Schistosomiasis |
| Organisms Responsible | Schistosoma mansoni Schistosoma haematobium Schistosoma japonicum Schistosoma mekongi Schistosoma intercalatum |
| Distribution Range | South America, Africa, Southeast Asia, Middle East, Caribbean |
| Transmission Mechanisms | Skin contact with water |
| Prognosis-Healthy People | Diarrhea, lesions, cystitis, ureteritis, bladder cancer, pulmonary hypertension, renal and colon damage |
| Epidemiology Factors | Snails, inadequate treatment of feces or urine |
| ..... | |
| Disease Caused | Swimmer's Itch |
| Organisms Responsible | Austrobilharzia variglandi Gigantobilharzia Heterobilharzia americanum Microbilharzia Schistosoma spindale Schistosomatium douthitti Trichobilharzia ocellata Trichobilharzia physella Trichobilharzia stagnicolae |
| Distribution Range | Cosmopolitan |
| Transmission Mechanisms | Skin contact with water |
| Prognosis-Healthy People | Open sores and lesions in the skin |
| Epidemiology Factors | Snails, waterfowl, aquatic animals, aquatic plants, cattle, other mammals |
Importance and Typical Diseases
Many medically important helminths require the invasion, resulting in damage, illness or even death, of a suitable host to complete all or part of their life cycle. Such organisms are therefore termed parasites and medical parasitology is the study of protozoan and helminth infections of man. Exceptions include some free-living organisms that normally live and replicate in the environment, or in other species, but under certain circumstances can infect man causing disease, damage or death, but do not complete their life-cycle when they do so. They are not therefore parasites but are included here as examples of opportunistic pathogens. For example, the swimmer's itch cercaria, flukes, are incidental problems in man. The organisms have a life cycle that alternates between snails and waterfowl, primarily. When the cercaria burrow into the skin of man to avoid dehydration or simply by mistake, they die and provoke an immune and histamine response in the skin which may lead to open sores and secondary bacterial infections.
Parasite infections affect millions of people worldwide afflicting considerable human suffering and economic hardship. Far from declining, many parasite infections are increasing throughout the world. In first world countries helminth infections are relatively uncommon. In many of the descriptions of the life cycles of theses parasites there is a note concerning the geographic range of the parasite. This is the original, and still primary or historical, distribution range of the parasite, its area of evolutionary origin and current area of greatest density of infection. However, such geographical limitations are becoming meaningless in the modern world. Travel is easy and fast. Visitors and immigrants bring in diseases and parasites that are then introduced into our health system, our sewage system and our environment. New cultural behaviours, diets and practices may encourage the survival and spread of these pathogens in their new aquatic habitats. The organisms dealt with in this report, although they comprise a fairly long list, are only a few of the very many parasites that can infect man. Those dealt with here are all transmitted, at least in part, by water.
While many life cycle descriptions do not specifically mention water all the organisms dealt with in this report can be distributed and acquired through water even if water is not the optimal mechanism of spread. If the pathogen is waterborne we are at risk, even though the risk may be small, and should be aware of the potential problems and take the necessary steps to prevent disease outbreaks by treating sewage, irrigation and drinking water as required. Pathogens which are spread only through eating infected meat are not dealt with unless there is also an infective stage found in water. Insect vectors, particularly biting mosquitoes and flies, are the main problem with recreational waters. Many insects, and thus the diseases they transfer, are restricted to the close proximity of aquatic habitats used for recreation such as swimming and boating. Pathogens spread only via insect vectors, and not directly through contact with the water, are not generally covered in this document.
In contrast to the viruses, bacteria and protozoa, the helminths, tapeworms, round worms and flukes, are multicellular with complex reproductive systems and life cycles. There are intermediate hosts for the development of larval stages and a definitive host for the adult form. Adults may be dioecious with separate sexes or hermaphroditic.
Nematodes-filariases
These are insect-borne infections caused by filarial worms. The classic example is elephantiasis caused by Wuchereia bancrofti. Larvae of Wuchereia bancrofti develop in the mosquito and, as in malaria, human infection results from the bite of the insect. When bitten, the larvae, as male and female forms, pass through the lymphatic system and mature to thread-like adults, 4-8 cm long, in the lymphatic glands. After mating the females develop eggs and larvae that are released as microfilariae into the peripheral circulation. The localization of the adult filariae in the lymph glands causes obstructions in the lymphatic drainage. This then results in the grossly disfiguring condition of elephantiasis that typically involves massive swelling of the legs, scrotum and other extremities. There are other insect-borne microfilarial infections of man. Loaiasis is caused by Loa loa. Biting flies spread the disease and the adult worms migrate along connective tissue, usually reaching the conjunctiva of the eye. Onchocerciasis, river blindness, is caused by Onchocerca volvulus, a tissue dwelling nematode, the microfilariae of which are predominantly found in the eye and skin.
Soil Helminths
Soil-transmitted helminthic infections are of two types, the hookworms, which undergo a cycle of development in the soil, the larvae being actively infective, and a group of nematodes that survive in the soil merely as eggs that have to be passively ingested in order for the cycle to continue. The most common hookworms are Ancylostoma duodenale and Necator americanus. Adults attach to the walls of the jejunum and females lay large numbers of eggs that are passed out with the feces. The eggs hatch in the soil and infect man usually by burrowing through the soles of the feet. The larvae then migrate through the body and damage the heart and lungs before passing into the tracheae, pharynx and finally the small intestine. Strongyloides stercoralis females live in the mucosal glands of the small intestine. Eggs hatch in these glands and the larvae are passed with the feces into the soil. As with other hookworms, infection results from the larvae burrowing into the skin. The rest of the life cycle is as for Ancylostoma duodenal and Necator americanus.
Adult worms of Ascaris lumbricoides live in the small intestine where they lay large numbers of eggs that are passed out with the feces. Unlike the hookworms, the eggs are the infectious form in which the larvae develop. When ingested, the eggs hatch in the jejunum, penetrate the mucosa and are carried through the hepatic circulation to the heart and lungs. They again enter the stomach via the tracheae and esophagus before growing to adulthood in the small intestine causing ascariasis. Pneumonitis and intestinal obstruction may accompany heavy infestations.
Toxocariasis results from the accidental infection of man with eggs of the ascarid roundworm of the dog, Toxocara canis, and cat, Toxocara cati. The life cycle is the same as those of Ascaris but the invasive larvae die in various tissues where they are phagocytosed. In the process they induce marked eosinophilia and local tissue reactions commonly involving the liver and eye. Trichuriasis is caused by Trichuris trichiura. The whipworms inhabit the caecum where they attach to the mucosa. Eggs from the mature worms are passed with the feces and develop in the soil. When swallowed, the eggs hatch in the small intestine and the developing larvae move directly to their attachment sites in the large intestine. Heavy infections can cause abdominal pain and chronic bloody diarrhea that may result in rectal prolapse.
Snail Helminthiases
These important groups of snail-transmitted helminthiases are all caused by trematodes, flukes that undergo a complicated cycle involving various species of land or aquatic snails. The most significant of these fluke infections is schistosomiasis and it is estimated that over 200 million people are infected worldwide. The three common species infecting man, Schistosoma mansoni, Schistosoma japonicum and Schistosoma haematobium have similar life cycles. Eggs are passed in the urine by Schistosoma haematobium or feces by Schistosoma mansoni andSchistosoma japonicum, and hatch in natural waters. Miracidia hatch from the eggs, penetrate suitable snails and develop through two generations of sporocysts. The last of these then produces fork-tailed cercariae. These cercariae penetrate the skin when a new host comes into contact with the contaminated water. Once through the skin the cercariae shed their tails and become schistosomulae that migrate through the tissues to the liver. Here male and female flukes copulate and migrate to either the bladder or rectum where eggs are laid. Schistosomiasis can result in chronic liver, spleen and bladder damage. The swimmer's itch organisms, Austrobilharzia variglandi, Gigantobilharzia, Heterobilharzia americanum, Microbilharzia, Schistosoma spindale, Schistosomatium douthitti, Trichobilharzia ocellata, Trichobilharzia physella and Trichobilharzia stagnicolae also belong to this group.
Fasciola hepatica, which causes fascioliasis, is found in most herbivores, but primarily sheep, that graze in wet pastures where the intermediate host, snails of the genus Lymnae, are found. Fasciola hepatica eggs shed from the infected primary host mature into the embryonated form in the environment. These then hatch and release a motile miracidia that seeks out and penetrates the tissue of the intermediate snail host. Cercaria are produced in the snail that, when released into the environment, can encyst to produce metacercariae. In temperate climates man is often infected by eating wild watercress, Nasturtium aquaticu, on which metacercariae have collected. After being ingested, the metacercariae pass through the duodenal wall and penetrate the liver capsule. Following maturation of the young flukes, the adults finally come to lie in the bile ducts or adjacent liver tissue. Here they cause severe damage to the biliary tract and eggs are passed with the bile into the feces to continue the cycle.
Gastrointestinal helminths
Trichinella spiralis is the cause of trichinosis in man. The nematode circulates between rats and pigs with man becoming infected from eating raw or inadequately cooked pork products. Encysted larvae in the meat excyst, hatch, in the intestine and develop into minute adults in the mucosa. These mature and the females deposit larvae that migrate through the tissues to reach skeletal muscles in which they encyst. Human infections may be asymptomatic but can include fever, orbital oedema, myalgia and eosinophilia. In the extreme, infection can be a fatal myocarditis or encephalitis.
Enterobias vermicularis, called a pinworm, is small and thread-like, and mainly infects young children and causing enterobiasis. The females emerge to the peri-anal region usually at night and lay some 10,000-15,000 eggs and then die. In the process they cause severe pruritis or itching. The embryonated eggs are infectious on ingestion and hatch in the duodenum. The larvae pass to the caecum where they mature into adults. Because of the itching, children often re-infect themselves from eggs under their fingernails. Bedding is also a source of infection and can be a means of spreading the organism in families and institutions such as orphanages, day care centers and boarding schools.
Taenia solium is the pork tapeworm. The adult lives in the small intestine of man who is the definitive host. Segments of the worm pass through the anus and release large numbers of eggs that can survive for long periods outside of the body. When ingested by pigs, the eggs hatch and each releases an oncosphere that migrates through the intestinal wall and blood vessels to reach striated muscle where encystment occurs. When man eats inadequately cooked pig meat, excystment occurs in the small intestine and an adult cestode worm develops. If the eggs are released into the upper intestine of man, through regurgitation, they can invade the host setting up a potentially dangerous larval infection known as cysticercosis in muscles and other sites. Taenia saginata is the beef tapeworm. This also infects man through cattle. The life cycle is similar to Taenia solium and in both species the adult tapeworm can grow up to 10 meters in length.
The tapeworm Echinococcus granulosus causes Hydatidosis. The adult worm inhabits the small intestine of dogs from which the eggs of the species are passed. These eggs can be ingested by herbivorous animals and hatch in the duodenum. The embryos enter the circulation where they are carried to various sites to develop into cysts. Dogs become infected when they eat contaminated offal. Humans are infected if they accidentally ingest eggs from infected dogs and the liver is the most common site of infection in which hydatid cysts form.
Table of Diseases and Organisms
Generally only diseases in which the infective stage can be transmitted directly through the water are dealt with in this document; there may be other means of transmission as well. Diseases caused only by insect transmission, even though usually closely associated with water, are rarely discussed.
Helminth Organisms and Diseases
| Organisms | Diseases |
| Cestodes-Tapeworms | |
| Dipylidium caninum | dipylidiasis, dog tapeworm |
| Diphyllobothrium cordatum Diphyllobothrium dalliae Diphyllobothrium dendriticum Diphyllobothrium lanceolatum |
diphyllobothriasis, tapeworm |
| Diphyllobothrium latum | diphyllobothriasis, fish tapeworm |
| Diphyllobothrium pacificum Diphyllobothrium ursi Diphyllobothrium yonagoensis |
diphyllobothriasis, tapeworm |
| Echinococcus granulosus Echinococcus multilocularis Echinococcus vogeli |
echinococcosis, hydatidosis, dog and fox tapeworms |
| Echinococcus oligarthrus | echinococcosis, cat tapeworm |
| Hymenolepis diminuta | hymenolepiasis, rat tapeworm |
| Hymenolepis nana | hymenolepiasis, dwarf tapeworm |
| Spirometra erinacei Spirometra mansoni Spirometra mansonoides Spirometra ranarum |
sparganosis, dog tapeworm |
| Taenia saginata | taeniasis, beef tapeworm |
| Taenia solium | taeniasis, cysticercosis, pork tapeworm |
| Nematodes-Roundworms | |
| Ancylostoma doudenale | ancylostomiasis, hookworm |
| Ascaris lumbricoides | ascariasis, intestinal roundworm |
| Capillaria aerophila | human pulmonary capillariasis |
| Capillaria hepatica | human hepatic capillariasis |
| Capillaria philippinensis | human intestinal capillariasis |
| Dracunculus medinensis | dracunculaisis, guinea worm |
| Enterobias vermicullaris | enterobiasis, pinworm |
| Gnathospoma binucleatum Gnathospoma didelphis Gnathospoma doloresi Gnathospoma hispidum Gnathospoma miyazakii Gnathospoma nipponicum Gnathospoma procyonis Gnathospoma spinigerum |
gnathostomiasis |
| Necator americanus | ancylostomiasis, hookworm |
| Trichuris trichiura | trichuriasis, whipworm |
| Trematodes-flukes | |
| Austrobilharzia variglandis | swimmer's itch |
| Clonorchis sinensis | clonorchiasis, Chinese or oriental liver fluke |
| Fasciola gigantica | fascioliasis, herbivore liver fluke |
| Fasciolopsis buski | fasciolopsiasis, human and pig intestinal fluke |
| Gigantobilharzia | swimmer's itch |
| Heterobilharzia americanum | swimmer's itch |
| Heterophyes heterophyes | heterophyiasis, minute intestinal fluke |
| Metagonimus yokogawai | metagonimiasis, minute intestinal fluke |
| Microbilharzia | swimmer's itch |
| Opisthorchis felineus | opisthorchiasis, cat liver fluke |
| Opisthorchis viverrini | opisthorchiasis, southeast Asian liver fluke |
| Paragonimus westermanni | paragonimiasis, oriental lung fluke |
| Schistosoma haematobium Schistosoma intercalatum Schistosoma japonicum Schistosoma mansoni Schistosoma mekongi |
schistosomiasis, human blood fluke |
| Schistosoma spindale Schistosomatium douthitti |
swimmer's itch |
| Trichobilharzia ocellata Trichobilharzia physella Trichobilharzia stagnicolae |
swimmer's itch |
List of Pathogens and Parasites
Life Cycles and other Pathogen Data
Cestodes
Diphyllobothrium latum (and other Diphyllobothrium species)
The cestode Diphyllobothrium latum, the fish or broad tapeworm, is the largest human tapeworm. Several other Diphyllobothrium species have also been reported to infect humans but less frequently. These include Diphyllobothrium pacificum, Diphyllobothrium cordatum, Diphyllobothrium ursi, Diphyllobothrium dendriticum, Diphyllobothrium lanceolatum, Diphyllobothrium dalliae, and Diphyllobothrium yonagoensis. Diphyllobothriasis occurs in areas where lakes and rivers coexist with human consumption of raw or undercooked freshwater fish. Such areas are found in Europe, North America, Asia, Uganda and Chile. The life cycle is man-feces-copepod-fish-man.
The adult Diphyllobothrium latum tapeworm resides in the small intestine where it attaches to the mucosa. It can reach more than 10 meters in length, with more than 3,000 proglottids. Immature eggs are discharged from the proglottids, up to 1,000,000 eggs per day per worm, and are passed in the feces. Under appropriate conditions, the egg matures in 11 to 15 days and yields an oncosphere that develops into a coracidium. After ingestion by a suitable freshwater crustacean, a copepod that is the first intermediate host, the coracidium develops into a procercoid larva. Following ingestion of the copepod by a suitable freshwater fish, the second intermediate host, the procercoid larva migrates into the fish flesh where it develops into a plerocercoid larva or sparganum. When a larger fish eats the smaller infected fish, the sparganum may migrate into the flesh of the larger fish. Humans, the final, optimal, definitive host, acquire the infection by eating raw or undercooked infected fish. Eggs appear in the feces 5 to 6 weeks after infection. In addition to humans many other mammals can also be infected.
Diphyllobothriasis infections can last for decades. Most infections are asymptomatic but they may include abdominal discomfort, diarrhea, vomiting, and weight loss. Vitamin B12 deficiency with pernicious anemia may occur. Massive infections may result in intestinal obstruction. Migration of proglottids can cause cholecystitis or cholangitis. Microscopic identification of eggs in the stool is the basis of specific diagnosis. Eggs are usually numerous and can be demonstrated without concentration techniques. Examination of proglottids passed in the stool is also of diagnostic value.
Dipylidium caninum
Dipylidium caninum, the double-pored dog tapeworm, mainly infects dogs and cats, but is occasionally found in humans. The dog is the principal definitive host for Dipylidium caninum. Other potential hosts include cats, foxes and people, mostly children. Dipylidium caninum is found worldwide and human infections have been reported in Europe, the Philippines, China, Japan, Argentina and the United States.
The adult tapeworms, up to 60 cm in length and 3 mm in width, reside in the small intestine of the host, where they each attach by their scolex. They produce proglottids, or segments, which have two genital pores. The proglottids mature, become gravid, detach from the tapeworm and migrate to the anus or are passed in the stool. Subsequently they release typical egg packets. Following ingestion of an egg by the intermediate host, the larval stage of the dog or cat flea, Ctenocephalides, an oncosphere is released into the flea's intestine. The oncosphere penetrates the intestinal wall, invades the insect's hemocoel or body cavity, and develops into a cysticercoid larva. Ingesting the adult flea containing the cysticercoid infects the vertebrate host. In the small intestine of the vertebrate host the cysticercoid develops into the adult tapeworm which reaches maturity about 1 month after infection.
Most infections with Dipylidium caninum are asymptomatic. Pets may exhibit behavior to relieve anal pruritis, such as scraping the anal region across grass or carpeting. Mild gastrointesintal disturbances may occur. The most striking feature in animals and children consists of the passage of proglottids. These can be found on the perianal region, in the feces, on diapers and occasionally on floor covering and furniture. The proglottids are motile when freshly passed and may be mistaken for maggots or fly larvae. Demonstrating the typical proglottids or egg packets in the stool or the environment confirms the diagnosis.
Echinococcus granulosus (and other Echinococcus species)
Human echinococcosis or hydatidosis is caused by the larval stages of tapeworms, of the genus Echinococcus. Echinococcus granulosus causes cystic echinococcosis, the form most frequently encountered; Echinococcus multilocularis causes alveolar echinococcosis; Echinococcus vogeli causes polycystic echinococcosis; and Echinococcus oligarthrus is an extremely rare cause of human echinococcosis.
Cystic hydatid disease is primarily a dog tapeworm. Sheep, cattle, deer and other grazing animals are intermediate hosts. Dogs and other carnivores become infected from wild rodents or their feces. Shepherds who use dogs are the most common victims of hydatid disease. Alveolar hydatid disease is primarily the fox tapeworm. Echinococcus granulosus is endemic in sheep raising areas of the Mediterranean, USSR, Australia, South America and Africa. It is found in immigrants to North America in Canada and in the United States, along the Mississippi and in Alaska. Echinococcus multilocularis is endemic in regions where foxes are found, central Europe, Siberia, North America in the north central United States and Canada and in Alaska.
The adult Echinococcus granulosus which is 3 to 6 mm long resides in the small bowel of the definitive hosts, dogs or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host, which under natural conditions are sheep, goat, swine, cattle, horses and camels, the eggs hatch in the small bowel and release oncospheres that penetrate the intestinal wall and migrate through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncospheres develops into cysts that enlarge gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32 to 80 days.
The same basic life cycle occurs with Echinococcus multilocularis which is 1.2 to 3.7 mm. There are a few small differences. The definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes and wolves and the intermediate hosts are small rodents. Larval growth in the liver remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli which is up to 5.6 mm long, the definitive hosts are bush dogs and domestic dogs, the intermediate hosts are rodents, and the larval stage, in the liver, lungs and other organs, develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus which is up to 2.9 mm long has a life cycle that involves wild cats as definitive hosts and rodents as intermediate hosts.
Hydatid disease is caught by humans from dogs that have eaten the raw meat or offal of sheep, cattle, goats, kangaroos or wild pigs carrying hydatid cysts. Dogs and dingoes carry the worm in their gut without becoming ill. Eating with infected hands or other hand-to-mouth contact after patting a dog is enough for eggs of the hydatid worm to be swallowed and cause infection. When swallowed, hydatid eggs are transported by the blood to other parts of the body with resulting release of oncospheres in the intestine and the development of cysts in various organs.
In the early stages of hydatid disease no symptoms may be felt. Symptoms depend on the site of the parasitic cyst which is the cause of the disease. The most common site is in the liver. Symptoms due to a large liver cyst may be a sense of weight, vomiting, feeling overly full after meals, or pain, indigestion and jaundice. Cysts may also occur in the lungs. Early symptoms may be coughing, chest pain or coughing blood. The first symptom may be coughing up salty fluid after rupture of a cyst. This may lead to shock from allergy, itching of the skin or chest infection. Cysts in other body organs may cause seizures, blindness, deafness, kidney pain or heart problems. All these forms are potentially deadly, and the rupture of a cyst at any site can cause death from allergic shock. The only effective treatment is surgery to remove the cysts, sometimes in conjunction with anti-worm drugs. Some cysts in vital organs cannot be readily removed by surgery.
Hymenolepis diminuta
Hymenolepiasis is caused by two cestodes, tapeworm species. Hymenolepis diminuta, the rat tapeworm, is a cestode of rodents which is sometimes diagnosed in humans and has an adult length of 20 to 60 cm. Hymenolepis diminuta has been reported from various areas of the world and requires an arthropod as an intermediate host. Eggs ingested by the arthropod develop into cysticercoid larvae. Ingesting the arthropods infects rodents, and humans can be accidentally infected through the same mechanism, by ingesting insects in precooked cereals. Hymenolepis diminuta infections are most often asymptomatic. The diagnosis depends on the demonstration of eggs in stool specimens. Concentration techniques and repeated examinations will increase the likelihood of detecting light infections.
Hymenolepis nana
Hymenolepiasis is caused by two cestodes, tapeworm species. Hymenolepis nana, the dwarf tapeworm, is the smallest cestode with an adult length of 15-40 mm and the only cestode that causes parasites in humans without requiring an intermediate host. Hymenolepis nana is the most common cause of all cestode infections, and is encountered worldwide. In temperate areas its incidence is higher in children and institutionalized groups.
Adult Hymenolepis nana reside in the ileal portion of the small intestine. They produce proglottids that disintegrate in the small intestine and release eggs that are immediately infective. Eggs passed with the stool cannot survive more than 10 days in the external environment. When an egg is ingested in contaminated food or water or from hands contaminated with feces the oncosphere contained in the egg is released. It invades the intestinal villous and develops into a cysticercoid larva. Upon rupture of the villous, the cysticercoid returns to the intestinal lumen, evaginates its scolex, attaches to the intestinal mucosa and develops into an adult.
An alternate mode of infection consists of internal autoinfection, where the eggs release their oncospheres directly into the intestine without passage through the external environment. The life span of an adult worm is 4-6 weeks, but internal autoinfection allows the infection to persist for years. In addition, when insects ingest eggs, they develop into cysticercoids, which can infect humans or rodents upon ingestion. A morphologically identical variant, Hymenolepis nana var. fraterna, infects rodents and uses insects as intermediate hosts.
Hymenopelis nana infections are most often asymptomatic. Heavy infections with Hymenolepis nana can cause weakness, headaches, anorexia, abdominal pain and diarrhea. The diagnosis depends on the demonstration of eggs in stool specimens. Concentration techniques and repeated examinations will increase the likelihood of detecting light infections.
Spirometra mansonoides
North American human infections are caused by Spirometra mansonoides but there are other species that can also infect man. Spirometra erinacei, Spirometra mansoni and Spirometra ranarum are all found in Asia. Spirometra mansonoides is found in domestic and feral dogs and cats in the southern United States. Spirometra erinacei, Spirometra mansoni and Spirometra ranarum in feral and domestic dogs and cats in Asia.
Cats and dogs are the primary hosts of adult Spirometra and a wide variety of other vertebrates, fish, reptiles, amphibia, birds and mammals are second intermediate and paratenic hosts, they maintain the third stage larvae that infect people. The stage living in copepods can also infect people. People get infected by drinking water containing infected copepods, by eating raw or poorly cooked meat or by using poultices of raw snake or frog tissue. There is no person-to-person transmission. In still fresh or brackish water the larval stages that infect people only occur within copepods in ponds, not free-living, so filtration of the relatively large copepods would serve to break the cycle. Most infected copepods only survive a few weeks in the wild. The third stage larvae likely survive as long as their host.
The life cycle of Spirometra is complex and includes first and second intermediate hosts and paratenic hosts and adult worm hosts. Eggs passed in the feces develop into embryos in the water within several weeks. Ciliated first stage larvae, coracidia, hatch and swim where they are eaten by crustaceans such as Cyclops and other copepods. In several weeks the larvae develop into the third procercoid stage in the body of the copepod. When the copepod is eaten by a tadpole, fish, snake, frog, bird (chicken) or mammal the larvae migrate into the tissues where they develop into the final larval stage, a sparganium, where they may stay a long time. In the US the paratenic hosts are usually frogs and water snakes. Dogs and cats become infected by eating these paratenic or second intermediate hosts, the fish, frogs, snakes, mammals or birds and in them the larvae migrate to the gut where they mature into adults which shed eggs. People may become infectd by drinking water that contains infected copepods or by eating uncooked paratenic hosts. In addition, an Asian folk remedy for wounds is to apply a poultice of raw snake or frog tissue from which the Spirometra larvae may migrate into the human tissues. The immature worms wander through the cutaneous tissues for days to months causing swellings. They may invade the eye and central nervous system, the brain where they can cause serious damage. Surgical removal is the only treatment.
Taenia saginata
Taenia species are worldwide in distribution. Humans are the only definitive hosts for Taenia saginata, the beef tapeworm. The adult tapeworms, usually 5 m long or less, but sometimes up to 25 m, reside in the small intestine, where they attach by their scolex. They produce proglottids, each worm has 1,000 to 2,000 proglottids, which mature, become gravid, detach from the tapeworm and migrate to the anus or are passed in the stool at approximately 6 proglottids per day. The eggs contained in the gravid proglottids, 80,000 to 100,000 eggs per proglottid, are released after the proglottid becomes free and are passed with the feces. The eggs can survive for months to years in the environment. Ingesting vegetation contaminated with eggs or proglottids infects cattle and other herbivores. In the animal's intestine, the eggs release the oncosphere, which evaginates, invades the intestinal wall and migrates to the striated muscles, where it develops into a cysticercus. The cysticercus can survive for several years in the animal. Ingesting raw or undercooked infected meat causes taeniasis in humans. In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for more than 30 years.
Taenia saginata produces only mild abdominal symptoms. The most striking feature consists of the active or passive passage of proglottids. Occasionally, appendicitis or cholangitis can result from migrating proglottids. Microscopic identification of eggs and proglottids in feces is diagnostic for taeniasis, but is not possible during the first 3 months following infection, prior to development of adult tapeworms. Microscopic examination of eggs does not distinguish between the two Taenia species. In addition, taeniid eggs are also morphologically indistinguishable from those of Echinococcus and Multiceps; however, these parasites do not result in eggs in human stools. Repeated examination and concentration techniques will increase the likelihood of detecting light infections. Microscopic identification of gravid proglottids, or, more rarely, examination of the scolex, allows species determination. The life cycle is man-feces-cattle-man.
Taenia solium
Taenia species are worldwide in distribution. Taenia solium, the pork tapeworm, can also cause cysticercosis. Taenia solium can develop not only in humans but also in some other animal species such as monkeys and hamsters. The cysticercus develops not only in striated muscle, but also in the brain (where it may be fatal), liver and other tissues of pigs and other animals, including humans. Taenia solium is more prevalent in poorer communities where humans live in close contact with pigs and eat undercooked pork, but is very rare in Muslim countries. Humans develop taeniasis when they ingest undercooked pork meat containing cysticerci. They develop cysticercosis by ingesting Taenia solium eggs, either by ingestion of fecally contaminated food, or by autoinfection. In the latter case, a human infected with adult Taenia solium ingests eggs produced by that tapeworm, either through fecal contamination or from proglottids carried into the stomach by reverse peristalsis. Infections can be maintained by the fecal/oral route where poor sanitation exists.
The life cycle of Taenia solium is similar to that of Taenia saginata. The adult tapeworms, usually 2 to 7 m long or less, reside in the small intestine, where they attach by their scolex. They produce proglottids, each worm has fewer than 1,000 proglottids, which mature, become gravid, detach from the tapeworm and migrate to the anus or are passed in the stool at approximately 6 proglottids per day. The eggs contained in the gravid proglottids, 50,000 eggs per proglottid, are released after the proglottid becomes free and are passed with the feces. The eggs can survive for months to years in the environment. Ingesting vegetation contaminated with eggs or proglottids infects pigs. In the animal's intestine, the eggs release the oncosphere, which evaginates, invades the intestinal wall and migrates to the striated muscles, where its develops into a cysticercus. The cysticercus can survive for several years in the animal. Ingesting raw or undercooked infected meat causes infection in humans. In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for up to 25 years.
Taenia solium is less symptomatic than Taenia saginata. The main symptom is often the passive passage of proglottids. The most important feature of Taenia solium is the risk of development of cysticercosis. Microscopic identification of eggs and proglottids in feces is diagnostic for taeniasis, but is not possible during the first 3 months following infection, prior to development of adult tapeworms. Microscopic examination of eggs does not distinguish between the two Taenia species. In addition, taeniid eggs are also morphologically indistinguishable from those of Echinococcus and Multiceps; however, these parasites do not result in eggs in human stools. Repeated examination and concentration techniques will increase the likelihood of detecting light infections. Microscopic identification of gravid proglottids, or, more rarely, examination of the scolex, allows species determination. The life cycle is man-feces-swine-man.
Nematodes
Ancylostoma duodenale
The human hookworms include two nematode, roundworm, species, Ancylostoma duodenale and Necator americanus. A smaller group of hookworms infecting animals can invade and cause parasitism in humans, Ancylostoma ceylanicum, Ancylostoma braziliense and Uncinaria stenocephala can penetrate the human skin, causing cutaneous larva migrans, but do not develop any further. In Ancylostoma duodenale the adult females are 10 to 13 mm long and the adult males are 8 to 11 mm. These are the second most common human helminthic infections, after ascariasis. The distribution is worldwide, mostly in areas with a moist, warm, climate. Both Necator americanus and Ancylostoma duodenale are found in Africa, Asia and the Americas. Only Ancylostoma duodenale is found in the Middle East, North Africa and southern Europe.
Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant host blood loss. Eggs are passed in the stool, and under favorable conditions, moisture, warmth and shade, hatch in 1 to 2 days. Larvae are released, grow in the feces and/or the soil, and after 5 to 10 days and two molts have become filariform larvae that are infective. These infective larvae can survive 3 to 4 weeks in favorable environments. On contact with the human host, the larvae penetrate the skin and are carried through the veins and the heart to the lungs. They penetrate into the pulmonary alveolae, ascend the bronchial tree to the pharynx, and are swallowed. Upon reaching the small intestine, they undergo two more molts yielding a fourth stage larvae and then adult worms. Five weeks or more are required from invasion by the larvae to oviposition by the adult female. Most adult worms are eliminated in 1 to 2 years, but some live longer. Some Ancylostoma duodenale larvae, following penetration of the host skin, can become dormant in the intestine or muscle. In addition, infection by Ancylostoma duodenale may also occur by the oral and transmammary route.
Iron deficiency anemia, due to blood loss at the site of intestinal attachment of the adult worms, is the most common symptom of hookworm infection, and can be accompanied by cardiac complications. Gastrointestinal, nutritional and metabolic symptoms can also occur. In addition, local skin itch can occur during penetration by the filariform larvae, and respiratory symptoms can be observed during pulmonary migration of the larvae. It is a chronic debilitating disease leading to malnutrition and mental and physical retardation in children. Microscopic identification of eggs in the stool is the most common method for diagnosing hookworm infection. Examination of the eggs cannot distinguish between Necator americanus and Ancylostoma duodenale. Filariform larvae can, however, be used to differentiate between these two hookworms.
Ascaris lumbricoides
Ascaris lumbricoides is the largest nematode, or roundworm, causing parasitism in the human intestine. Man is the reservoir for this worm. There are similar species in pigs, dogs, cats and horses. The pig species Ascaris suum may alsi infect people in endemic areas. Coprophagous animals like pigs, dogs, cats and chickens disperse and spread the eggs over a wide area. Ascaris eggs are widespread in the environment in surface and ground water, marine, brackish and fresh waters, sewage, sludge, soils, crops and beaches. In temperate climates eggs can remain viable in moist loose soil for seven years, longer buried in wet clay. Viability in arctic tundra may be 100 years.
Chlorine and chloramine are ineffective against Ascaris eggs but coagulation and filtration does remove them from water and UV will destroy them as will temperatures over 37 degrees Celsius. They remain viable in septic systems for about a year; conventional sewage treatment is not effective, the sludge contains large numbers of infective ova.
The adult females reach 20 to 35 cm long and the adult males about 15 to 30 cm. These worms are the most common human helminthic infection with a worldwide distribution. The highest prevalence is in tropical and subtropical regions, especially areas with inadequate sanitation; infections occur in rural areas of the southeastern United States. Fecally contaminated soil, food, water and drinks are vectors.
Adult worms live in the lumen of the small intestine. A female may produce up to 240,000 eggs per day, 25, 000,000 in her lifetime, which are passed with the feces. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions with the optimum being moist, warm, UV shaded soil. After infective eggs are swallowed the larvae hatch, invade the intestinal mucosa and are carried via the portal and then the systemic circulation to the lungs. The larvae mature further in the lungs for 10 to 14 days, penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed. Upon reaching the small intestine they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.
Adult worms usually cause no symptoms but high worm loads can cause abdominal pain and intestinal obstruction. Migrating adult worms can cause symptomatic occlusion of the biliary tract or oral expulsion. During the lung phase of larval migration, pulmonary symptoms can occur. Microscopic identification of eggs in the stool is the most common method for diagnosing intestinal ascariasis. Adult worms are occasionally passed in the stool or through the mouth or nose and are recognizable by their macroscopic characteristics. No specific treatment of pulmonary ascariasis is available though drugs are available for the intestinal infection. Chronic ascariasis is a major contributory factor of poor nutritional status in children who suffer weight and height losses.
Capillaria aerophila
Rare cases of human infections with Capillaria aerophila have been reported worldwide. Capillaria aerophila adult worms reside in the epithelium of the tracheo-bronchial tract of various animals. Eggs are produced, coughed up, swallowed by the animal and excreted in its feces. The eggs embryonate in the soil. Ingestion of infective eggs completes the cycle. Transport or paratenic hosts may also intervene in the cycle. Pulmonary capillariasis due to Capillaria aerophila can present with fever, cough, asthma and pneumonia. It can be fatal. The specific diagnosis of Capillaria aerophila is based on demonstrating eggs in stool or in lung biopsy.
Capillaria hepatica
Rare cases of human infections with Capillaria hepatica have been reported worldwide.Capillaria hepatica adult worms reside in the liver of various animals especially rats. The females produce eggs that are retained in the liver parenchyma. When another animal eats the infected animal the eggs are released by digestion, excreted in the feces of the second animal and embryonate in the soil. Alternately, the eggs can be released following the death and decomposition of the first animal and mature in the soil. Following ingestion by a subsequent host, these infective eggs release larvae in the intestine that migrate through the portal circulation to the liver, where they develop into adults.
Hepatic capillariasis caused by Capillaria hepatica manifests as an acute or sub-acute hepatitis with eosinophilia, with possible dissemination to other organs, and can be fatal. The specific diagnosis of Capillaria hepatica infection is based on demonstrating the adult worms and/or eggs in liver tissue at biopsy or necropsy. The identification of Capillaria hepatica eggs in the stool is a spurious finding, which does not result from infection of the human host but from ingestion by that host of livers from infected animals.
Capillaria philippinensis
The nematode, or roundworm, Capillaria philippinensis causes intestinal capillariasis in man. Capillaria philippinensis is endemic in the Philippines and also occurs in Thailand. Rare cases have been reported from other Asian countries, the Middle East and Colombia. Two other Capillaria species can cause parasitism in animals; with rare reported instances of human infections. They are Capillaria hepatica, which causes hepatic capillariasis in man, and Capillaria aerophila, which causes pulmonary capillariasis in man.
The adults of Capillaria philippinensis males are 2.3 to 3.2 mm and females 2.5 to 4.3 mm. They reside in the human small intestine where they burrow in the mucosa. The females deposit unembryonated eggs. Some of these embryonate in the intestine and release larvae that can cause autoreinfection. Typically, unembryonated eggs are passed in the stool and embryonate in the external environment; after ingestion by freshwater fish, larvae hatch, penetrate the intestine and invade the mesenteric tissue. Ingestion of raw or undercooked fish results in infection of the human host. Humans are the only demonstrated hosts; fish-eating birds probably constitute an animal reservoir.
Intestinal capillariasis caused by Capillaria philippinensis manifests as abdominal pain and diarrhea, which, if untreated, can become severe due to autoinfection. A protein-losing enteropathy can develop which may result in cachexia and death. The specific diagnosis of Capillaria philippinensis is established by finding eggs, larvae and/or adult worms in the stool, or in intestinal biopsies. Unembryonated eggs are the typical stage found in the feces. In severe infections, embryonated eggs, larvae, and even adult worms can be found in the feces.
Dracunculus medinensis
Dracunculus insignis occurs in mink and raccoons in the US but has not been found in people and dracuculiasis infections in dogs are not transmitted to people. Dracunculiasis is caused by the guinea worm, Dracunculus medinensis, which, unlike any other filarial parasite that can be transmitted to humans, uses crustacean copepods, Cyclops, as the intermediate host by which the infective larvae enters the human body. The guinea (dragon, serpent, medina) worm is a parasite of the dog, horse, cow, wolf, leopard, monkey and baboon that also commonly infects man. It is not known in North America. The majority of human infections occur in parts of West Africa, East Africa and India. People get infected by drinking water that contains infected copepods. Filtering water through even as crude a filter as cloth will remove the large copepods and prevent this disease.
The worms live under the skin and the female may be up to a meter long. When the female emerges to lay eggs it causes severe itching. The guinea-worm like all filarial nematodes goes through six developmental stages. After the ingested Cyclops is destroyed by stomach acids the free larvae penetrate the gut lining and migrate to subcutaneous tissues via the lymphatic system. This process takes approximately 43 days and once in subcutaneous tissue the worms mature slowly, reaching full development in one year. They then mate and the small male, 1.2-2.9 cm long, dies and is absorbed into the larger female, 60 cm in length. When the embryos in the female's uterus reach maturity she migrates to areas of the body in contact with water, 90% move to the feet and legs. Once in these areas the worm penetrates the skin, extrudes its uterus through its mouth, discharges larvae into the water and dies.
The larvae, which measure between 500 and 700 micrometers, can live for 6 days in clean water and 2 to 3 weeks in muddy water. The larvae are ingested by Cyclops which actively search them out as food. Once ingested, the larvae mature into their infective stage in approximately 14 days and can then re-infect humans. The female guinea worm lives in the connective tissues of the limbs and trunk where she usually does not cause any noticeable pathological conditions. Although heavy infestations in the joint can cause arthritic conditions and require the removal of the worms most pathology is associated with infection occurring when the female dies after discharging her larvae. The death of the worm causes the formation of a sterile abscess, which when secondarily infected results in cellulitis and local blistering of the skin. However, chills fever and local painful swellings commonly precede the emergence of the worm. Dracunculus medinensis has also been found coiled in the hernial sac and retroplacentally causing bleeding in pregnancy.
Enterobius vermicularis
The nematode, roundworm, Enterobius vermicularis, previously known as Oxyuris vermicularis, is the human pinworm. The adult females are 8 to 13 mm long and the adult male 2 to 5 mm. Humans are virtually the only hosts of Enterobius vermicularis. The species is worldwide, with infections more frequent in school- or preschool-children and in crowded conditions. It is the most common helminthic infection in the United States with estimates of 40 million persons or 20% of the population infected. Personal hygiene and treatment of other household members should be used to stop the spread.
Adult worms live in the lumen of the human colon. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area. The larvae contained inside the eggs develop and the eggs become infective in 4 hours under optimal conditions. Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area. Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Some sexual practices are responsible for person-to-person and self-infection. Food and water are also transmission vectors. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon. The time interval from ingestion of infective eggs to oviposition by the adult females is about one month. The life span of the adults is about two months.
Infections are frequently asymptomatic. The most typical symptom is perianal pruritis, especially at night, which may lead to excoriations and bacterial superinfection. Occasionally there is invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas. Some other possible symptoms include anorexia, irritability, loss of sleep and abdominal pain.
Microscopic identification of eggs collected in the perianal area is the method of choice for diagnosing enterobiasis. This must be done in the morning, before defecation and washing, by pressing transparent adhesive tape on the perianal skin, sticking the tape to a microscope slide and then examining the tape with a microscope. Alternatively, anal swabs can also be used. Eggs can also be found, but less frequently, in the stool and occasionally are encountered in the urine or in vaginal smears. Adult worms are also diagnostic when found in the perianal area or during ano-rectal or vaginal examinations.
Gnathostoma spinigerum
Most human infections are caused by Gnathostoma spinigerum but there are other species that can also infect man. Gnathostoma spinigerum, Gnathostoma doloresi, Gnathostoma hispidum and Gnathostoma nipponicum are all found in the orient; Gnathostoma binucleatum is found in Mexico; Gnathostoma didelphis, Gnathostoma miyazakii and Gnathostoma procyonis are found in North America. Gnathostoma spinigerum is common in wild animals of the Far East and found in the stomach of cats and dogs of Thailand and Japan. Gnathostoma binucleatum is found in the ocelot in Mexico. Gnathostoma didelphis is found in the kidney of the opossum, Diadelphis virginia, in North America. Gnathostoma procyonis is found in the stomach of raccoons, Procyon lotor in North America. Gnathostoma miyazakii is found in the kidney of otters in North America. Gnathostoma doloresi and Gnathostoma hispidum are found in pigs in the orient. Gnathostoma nipponicum is a parasite of the Japanese weasel.
Cats and dogs are the primary hosts of adult Gnathostoma spinigerum and a wide variety of fish, reptiles, amphibia, birds and mammals are second intermediate and paratenic hosts, they maintain the third stage larvae that infect people. The stage living in copepods can also infect people. People get infected by drinking water containing infected copepods or by eating raw or poorly cooked meat, especially fish. There is no person-to-person transmission. In still water the larval stages that infect people only occur within copepods in ponds, not free-living, so filtration of the relatively large copepods would serve to break the cycle. Most infected copepods only survive a few weeks in the wild but have been kept alive for two months in the laboratory. The third stage larvae likely survive as long as their host.
The life cycle of Gnathostoma is complex and includes first and second intermediate hosts and paratenic hosts and adult worm hosts. Eggs passed in the feces develop into embryos in the water within a week. First stage larvae hatch and swim where they are eaten by crustaceans such as Cyclops and other copepods. In two weeks larvae develop to the third stage in the body of the copepod. When the copepod is eaten by a fish, snake, frog, bird (chicken) or mammal the larvae migrate into the tissues where they may stay a long time. Dogs and cats become infected by eating these paratenic or second intermediate hosts, the fish, frogs, snakes, mammals or birds. People may become infectd by drinking water that contains infected copepods or by eating uncooked paratenic hosts; the usual route is raw fish. The immature worms wander through the cutaneous tissues for days to months causing painful swellings. They may invade the eye, pulmonary tract, central nervous system or gut.
Necator americanus
The human hookworms include two nematode, roundworm, species, Ancylostoma duodenale and Necator americanus. A smaller group of hookworms infecting animals can invade and cause parasitism in humans, Ancylostoma ceylanicum, Ancylostoma braziliense and Uncinaria stenocephala can penetrate the human skin, causing cutaneous larva migrans, but do not develop any further. In Necator americanus the adult females are 9 to 11 mm long and the adult males: 7 to 9 mm. These are the second most common human helminthic infections, after ascariasis. The distribution is worldwide, mostly in areas with moist, warm climate. Both Necator americanus andAncylostoma duodenal are found in Africa, Asia and the Americas. Necator americanus predominates in the Americas and Australia.
Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant host blood loss. Eggs are passed in the stool, and under favorable conditions, moisture, warmth and shade, hatch in 1 to 2 days. Larvae are released, grow in the feces and/or the soil, and after 5 to 10 days and two molts have become filariform larvae that are infective. These infective larvae can survive 3 to 4 weeks in favorable environments. On contact with the human host, the larvae penetrate the skin and are carried through the veins and the heart to the lungs. They penetrate into the pulmonary alveolae, ascend the bronchial tree to the pharynx, and are swallowed. Upon reaching the small intestine, they undergo two more molts yielding a fourth stage larvae and then adult worms. Five weeks or more are required from invasion by the larvae to oviposition by the adult female. Most adult worms are eliminated in 1 to 2 years, but some live longer. Necator americanus requires a transpulmonary migration phase.
Iron deficiency anemia, due to blood loss at the site of intestinal attachment of the adult worms, is the most common symptom of hookworm infection, and can be accompanied by cardiac complications. Gastrointestinal, nutritional and metabolic symptoms can also occur. In addition, local skin itch can occur during penetration by the filariform larvae, and respiratory symptoms can be observed during pulmonary migration of the larvae. Microscopic identification of eggs in the stool is the most common method for diagnosing hookworm infection. Examination of the eggs cannot distinguish between Necator americanus and Ancylostoma duodenale. Filariform larvae can, however, be used to differentiate between Necator americanus and Ancylostoma duodenale.
Toxocara canis and Toxocara catis
Toxocariasis results from the accidental infection of man with eggs of the ascarid roundworm of the dog, Toxocara canis, and cat, Toxocara cati. The life cycle is the same as that of Ascaris lumbricoides but the invasive larvae are unable to complete their life cycle in the human body and are killed in various tissues where they are phagocytosed. In the process they induce marked eosinophilia and local tissue reaction commonly involving the liver and eye.
Trichuris trichiura
The nematode, roundworm, Trichuris trichiura, is the human whipworm. This is the third most common round worm of humans. Distribution is worldwide, with infections more frequent in areas with tropical weather and poor sanitation practices, and among children. It is estimated that 800 million people are infected worldwide. Trichuriasis also occurs in the southern United States. Similar species infect other primates, rodents, camels and some domestic animals. Trichuris infections are often highly correlated with Ascaris and Entamoeba infections. Humans are the reservoir but coprophagous animals like pigs, dogs, cats and chickens spread and re-distribute the shed ova. Pigs , lemurs and monkeys may be reservoir hosts.
The adult worms are approximately 4 cm in length and live in the cecum and ascending colon. Female worms in the cecum shed between 3,000 and 20,000 eggs per day. The unembryonated eggs are passed with the stool. In the soil they embryonate and become infective in 15 to 30 days. After ingestion from contaminated soil, water or food, the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60 to 70 days after infection. The life span of the adults is about 1 year.
The infections are most frequently asymptomatic. Heavy infections, especially in small children, can cause gastrointestinal problems such as abdominal pain, diarrhea, rectal prolapse and possibly growth retardation. Microscopic identification of whipworm eggs in feces is evidence of infection. Because eggs may be difficult to find in light infections, a concentration procedure is recommended. Examination of the rectal mucosa by proctoscopy, or directly in case of prolapses, can occasionally demonstrate adult worms.
Trematodes
Clonorchis sinensis
The trematode, Clonorchis sinensis, is the Chinese or oriental liver fluke. Endemic areas are in Asia including Korea, China, Taiwan and Vietnam. Clonorchiasis has been reported in non-endemic areas, including the United States. In such cases, the infection is found in Asian immigrants or following ingestion of imported, undercooked or pickled freshwater fish containing metacercariae.
The adult flukes, 10 to 25 mm by 3 to 5 mm, reside in small and medium sized biliary ducts. Embryonated eggs are discharged in the biliary ducts and in the stool. After ingestion by the suitable snail intermediate host, the eggs release miracidia which go through several developmental stages, sporocysts, rediae and cercariae. The cercariae are released from the snail and encyst as metacercariae in the skin and flesh of freshwater fish. Infection of humans occurs by ingestion of undercooked, salted, pickled or smoked freshwater fish. After ingestion, the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater. Maturation takes approximately 1 month. Adult flukes can survive 20 to 25 years. In addition to humans, carnivorous animals can serve as reservoir hosts.
Most pathologic manifestations result from inflammation and intermittent obstruction of the biliary ducts. In the acute phase, abdominal pain, nausea, diarrhea and eosinophilia can occur. In long-standing infections, cholangitis, cholelithiasis, pancreatitis and cholangiocarcinoma can develop which may be fatal. Microscopic demonstration of eggs in the stool or in duodenal aspirate is the most practical diagnostic method. The adult fluke can also be recovered by surgery.
Fasciola gigantic and Fasciola hepatica
The trematodes, Fasciola hepatica, the sheep liver fluke, and Fasciola gigantica, are parasites of herbivores that can infect humans accidentally. Fascioliasis occurs worldwide. Human infections with Fasciola hepatica are found in areas where sheep and cattle are raised, and where humans consume raw watercress, including Europe, the Middle East and Asia. Infections with Fasciola gigantica have been reported, more rarely, in Asia, Africa and Hawaii.
The adult flukes of Fasciola hepatica are up to 30 mm by 13 mm and those of Fasciola gigantica: up to 75 mm. They reside in the large biliary ducts of the mammalian host. Immature eggs are discharged in the biliary ducts and in the stool. After development in water, each egg releases a miracidium that invades a suitable snail intermediate host. In the snail the parasites undergo several developmental stages, sporocysts, rediae and cercariae. The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity and the liver parenchyma into the biliary ducts, where they develop into adults. Fasciola hepatica infects various animal species, mostly herbivores. Ingesting metacercariae-containing freshwater plants, especially watercress, can infect humans. In humans, maturation from metacercariae into adult flukes takes approximately 3 to 4 months.
During the acute phase, caused by the migration of the immature fluke, manifestations include abdominal pain, hepatomegaly, fever, vomiting, diarrhea, urticaria and eosinophilia, and can last for months. In the chronic phase, caused by the adult fluke, the symptoms are more discrete and reflect intermittent biliary obstruction and inflammation. Occasionally, ectopic locations of infection, such as intestinal wall, lungs, subcutaneous tissue and pharyngeal mucosa, can occur.
Microscopic identification of eggs is useful in the chronic or adult stage. Eggs can be recovered in the stools or in material obtained by duodenal or biliary drainage. They are morphologically indistinguishable from those of Fasciolopsis buski. False fascioliasis or pseudofascioliasis refers to the presence of eggs in the stool resulting not from an actual infection but from recent ingestion of infected livers containing eggs. This situation, with its potential for misdiagnosis, can be avoided by having the patient follow a liver-free diet for several days before the stool examination. Antibody detection tests are useful especially in the early invasive stages when the eggs are not yet apparent in the stools or in ectopic fascioliasis.
Fasciolopsis buski
The trematode Fasciolopsis buski, is the largest intestinal fluke of humans. It is found in Asia and the Indian subcontinent, especially in areas where humans raise pigs and consume freshwater plants.
The adult flukes, 20 to 75 mm by 8 to 20 mm, reside in the duodenum and jejunum of mammalian hosts, humans and pigs, where they are attached to the intestinal wall. Immature eggs are discharged into the intestine and stool. After development in water, each egg releases a miracidium that invades a suitable snail intermediate host. In the snail the parasites undergo several developmental stages, sporocysts, rediae and cercariae. The cercariae are released from the snail and encyst as metacercariae on aquatic plants. Ingesting metacercariae with the aquatic plants infects the mammalian hosts. After ingestion, the metacercariae excyst in the duodenum and attach to the intestinal wall. They develop in approximately 3 months into adults, which have a life span of one year.
Most infections are light and asymptomatic. In heavier infections, symptoms include diarrhea, abdominal pain, fever, ascites, anasarca and intestinal obstruction. Microscopic identification of eggs, or more rarely of the adult flukes, in the stool or vomitus is the basis of specific diagnosis. The eggs are indistinguishable from those of Fasciola hepatica.
Heterophyes heterophyes
The trematode, Heterophyes heterophye, is a minute intestinal fluke. It is found in Egypt, the Middle East and Far East. Adult Heterophyes heterophyes are 1.0 to 1.7 mm by 0.3 to 0.4 mm and reside in the small intestine, where they are attached to the mucosa. They release fully embryonated eggs that are passed in the feces. After ingestion by a suitable snail, the first intermediate host, the eggs hatch and release miracidia which undergo several developmental stages in the snail, sporocysts, rediae and cercariae. The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable freshwater fish, the second intermediate host. Ingesting undercooked or salted fish containing metacercariae infects the definitive host. After ingestion, the metacercariae excyst, attach to the intestinal mucosa, and mature into adults. In addition to humans, Heterophyes can infect various fish-eating animals.
The main symptoms are diarrhea and colicky abdominal pain. Migration of the eggs to the heart, resulting in potentially fatal myocardial and valvular damage, has been reported from the Philippines. Migration to other organs such as the brain has also been reported. The diagnosis is based on the microscopic identification of eggs in the stool. However, the eggs are not distinguishable from those of Metagonimus yokogawai and resemble those of Clonorchis and Opisthorchis.
Metagonimus yokogawai
Metagonimus yokogawai is the smallest, human, intestinal fluke. It is found mostly the Far East, as well as Siberia, Manchuria, the Balkan states, Israel and Spain. Adult Metagonimus yokogawai are 1.0 mm to 2.5 mm by 0.4 mm to 0.75 mm and reside in the small intestine, where they are attached to the mucosa. They release fully embryonated eggs that are passed in the feces. After ingestion by a suitable snail, the first intermediate host, the eggs hatch and release miracidia which undergo several developmental stages in the snail, sporocysts, rediae and cercariae. The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable freshwater fish, the second intermediate host. Ingesting undercooked fish containing metacercariae infects the definitive host. After ingestion, the metacercariae excyst, attach to the intestinal mucosa, and mature into adults. In addition to humans, fish-eating mammals and birds can also be infected.
The main symptoms are diarrhea and colicky abdominal pain. Migration of the eggs to extra-intestinal sites such as the heart and brain can occur, with resulting symptoms. The diagnosis is based on the microscopic identification of eggs in the stool. However, the eggs are undistinguishable from those of Heterophyes heterophyes and resemble those of Clonorchis and Opisthorchis. Specific diagnosis is based on identification of the adult fluke evacuated after antihelmintic therapy or found at autopsy.
Opisthorchis viverrini and Opisthorchis felineus
Opisthorchis viverrini is the Southeast Asian liver fluke and Opisthorchis felineus is the cat liver fluke. Opisthorchis viverrini is found mainly in northeast Thailand, Laos and Kampuchea while Opisthorchis felineus is found mainly in Europe and Asia, including the former Soviet Union area. The adult flukes of Opisthorchis viverrini are 5 mm to 10 mm by 1 mm to 2 mm; those of Opisthorchis felineus are 7 mm to 12 mm by 2 mm to 3 mm. They reside in the biliary and pancreatic ducts of the mammalian host, where they attach to the mucosa. They deposit fully developed eggs that are passed in the feces. After ingestion by a suitable snail, the first intermediate host, the eggs release miracidia, which undergo in the snail several developmental stages, sporocysts, rediae and cercariae. Cercariae are released from the snail and penetrate freshwater fish, the second intermediate host, encysting as metacercariae in the muscles or under the scales. The mammalian definitive host, cats, dogs and various fish-eating mammals including humans, become infected by ingesting undercooked fish containing metacercariae. After ingestion, the metacercariae excyst in the duodenum and ascend through the ampulla of Vater into the biliary ducts, where they attach and develop into adults, which lay eggs after 3 to 4 weeks.
Most infections are asymptomatic. In mild cases, manifestations include dyspepsia, abdominal pain, diarrhea or constipation. With infections of longer duration, the symptoms can be more severe, and hepatomegaly and malnutrition may be present. In rare cases, cholangitis, cholecystitis and cholangiocarcinoma may develop. In addition, infections due to Opisthorchis felineus may present an acute phase resembling Katayama fever, schistosomiasis, with fever, facial edema, lymphadenopathy, arthralgias, rash and eosinophilia. Chronic forms of Opisthorchis felineu infections present the same manifestations as Opisthorchis viverrini, with the additional involvement of the pancreatic ducts. Diagnosis is based on microscopic identification of eggs in stool specimens. However, the eggs of Opisthorchis are practically undistinguishable from those of Clonorchis.
Paragonimus westermani
More than 30 species of trematodes, flukes, of the genus Paragonimus have been reported which infect animals and humans. Among the more than 10 species reported to infect humans, the most common is Paragonimus westermani, the oriental lung fluke. While Paragonimus westermani occurs in the Far East, other species of Paragonimus are encountered in Asia, the Americas and Africa.
Human infection with Paragonimus westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite. The metacercariae excyst in the duodenum penetrate through the intestinal wall into the peritoneal cavity, through the abdominal wall and diaphragm into the lungs. In the lungs, they become encapsulated and develop into adults that are 7.5 to 12 mm by 4 to 6 mm. The time from infection to oviposition is 65 to 90 days. The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with the stool. In the external environment, the egg embryonate, hatch and yield miracidia that enter the first intermediate host, a snail. Cercariae emerge from the snail and invade the second intermediate host, a crustacean, crab or crayfish, where they encyst and become metacercariae. Ingestion of the metacercariae closes the cycle. Infections may persist for 20 years in humans, and occasionally sites other than the lungs are involved. Infection also occurs in many other animal species.
Diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities and eosinophilia may mark the acute phase, invasion and migration. During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum, hemoptysis and chest radiographic abnormalities. Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved. Diagnosis is based on microscopic demonstration of eggs in stool or sputum, but these are not present until 2 to 3 months after infection. Eggs are also occasionally encountered in effusion fluid or biopsy material. Concentration techniques may be necessary in patients with light infections. Biopsy may allow diagnostic confirmation and species identification when an adult or developing fluke is recovered.
Schistosoma mansoni, S. haematobium, . japonicum, S. mekongi and S. intercalatum
Schistosomiasis is caused by digenetic blood trematodes. The three main species infecting humans are Schistosoma haematobium, Schistosoma japonicum, and Schistosoma mansoni. Two other species, more localized geographically, are Schistosoma mekongi and Schistosoma intercalatum. In addition, other species of schistosomes, which are parasites of birds and mammals, also cause cercarial dermatitis in humans. Schistosoma mansoni is found in parts of South America and the Caribbean, Africa and the Middle East. Schistosoma haematobium occurs in Africa and the Middle East; and Schistosoma japonicum in the Far East. Schistosoma mekongi and Schistosoma intercalatum are localized in Southeast Asia and central West Africa, respectively. Human contact with water is necessary for infection by schistosomes. Various animals serve as reservoirs for Schistosoma japonicum and Schistosoma mekongi.
Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species. For instance, Schistosoma mansoni occurs more often in the superior mesenteric veins and Schistosoma japonicum more frequently in the inferior mesenteric veins. However, both species can occupy either location, and they are capable of moving between locations, so it is not possible to state equivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venus plexus of the bladder, but it can also be found in the rectal venules. The females, size 7 to 20 mm, males are slightly smaller, deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine, with Schistosoma mansoni and Schistosoma japonicum, and of the bladder and ureters with Schistosoma haematobium, and are eliminated with feces or urine, respectively.
Under optimal conditions the eggs hatch and release miracidia, which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host, and migrate through several tissues and go through several stages on their way to their residence in the veins. Many infections are asymptomatic. Cercarial dermatitis may occur upon skin invasion by the cercariae of some of the human species of schistosomes, as well as non-human species (see swimmer's itch). Acute schistosomiasis, Katayama's fever, may occur weeks after the initial infection, especially by Schistosoma mansoni and Schistosoma japonicum. Manifestations include fever, cough, abdominal pain, diarrhea, hepatosplenomegaly and eosinophilia. Occasionally central nervous system lesions occur.
Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include colonic polyposis with bloody diarrhea primarily by Schistosoma mansoni. Portal hypertension with hematemesis and splenomegaly occurs with Schistosoma mansoni, Schistosoma japonicum and Schistosoma mansoni. Cystitis and ureteritis occur with Schistosoma haematobium along with hematuria that can progress to bladder cancer. Pulmonary hypertension occurs with Schistosoma mansoni and Schistosoma japonicum. More rarely, Schistosoma haematobium causes glomerulonephritis and central nervous system lesions.
Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. Stool examination should be performed when infection with Schistosoma mansoni or Schistosoma japonicum is suspected and urine examination should be performed if Schistosoma haematobium is suspected. Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear, 1 to 2 mg of fecal material. Since eggs may be passed intermittently or in small amounts, repeated examinations and/or concentration procedures will enhance their detection. In addition, for field surveys and investigation purposes, the egg output can be quantified by using several techniques.
Eggs can be found in the urine in infections with Schistosoma haematobium, the recommended time for collection is between noon and 3 PM, and with Schistosoma japonicum. Centrifugation and examination of the sediment will enhance detection. Quantification is possible by using filtration through a Nucleopore membrane of a standard volume of urine followed by egg counts on the membrane. Tissue biopsy, rectal biopsy for all species and bladder biopsy for Schistosoma haematobium, may demonstrate eggs when stool or urine examinations are negative.
Swimmer's itch
Swimmer's itch is a skin rash caused by certain parasites of birds and mammals. Common genera include Gigantobilhartzia, Ornithobilhartzia, Trichobilhartzia, Schistosomatium, Austrobilhartzia, Heterobilhartzia and Schistosoma. Swimmer's itch or cercarial dermatitis is global in distribution. In the US and Canada, it has most often been reported in areas along the migratory bird flyways where avian hosts are common. Waterfowl, mainly ducks and geese, are the definitive host of the schistosomes that cause swimmer's itch. The cercaria of a large number of non-human schistosome parasites may penetrate human skin, but die almost immediately. This can cause an allergic condition called swimmer's itch or cercarial dermatitis, a reaction caused by release of antigens by the dying parasites embedded in the skin. Organisms that have been implicated in this condition include the following species.
Swimmer's Itch Organisms
| Trematode Species | Host Organisms and Locations |
| Austrobilharzia variglandi | parasitic in water fowl of North America and Hawaii |
| Gigantobilharzia | parasitic in passerine birds |
| Heterobilharzia americanum | parasitic in raccoons and other mammals in Louisiana, USA |
| Microbilharzia | parasitic in gulls, ducks and marine wildfowl on the East Coast, USA and Hawaii |
| Schistosomatium douthitti | parasitic in rodents in North America |
| Schistosoma spindale | a parasite of ruminants, particularly cattle and water buffalo, in South East Asia |
| Trichobilharzia ocellata | parasitic in ducks of Europe, Asia and North America |
| Trichobilharzia physella | parasitic in ducks of North America and Japan |
| Trichobilharzia stagnicolae | parasitic in ducks in the Great Lakes area of North America |
The life cycle of the schistosome begins when the eggs are passed in the feces of the primary hosts, a waterfowl, marsh birds, finch, muskrat, vole or mouse. Once they are deposited in water the fully developed larval stage, miracidium, contained in each egg hatches and begins its search for a snail host. Within the proper snail the miracidia mature into multiple sporocysts. The sporocysts give rise to hundreds of cercariae that leave the host snail to seek a warm-blooded host. If a host is found they attach to the skin and penetrate with the aid of histolytic enzymes. In host animals a systemic infection occurs. Schistosomes develop into adult worms and mate in the waterfowl. Adult trematode flukes then lay eggs in the intestinal wall and the ova penetrate to reach the feces. The schistosome eggs are passed into the water via waterfowl urine and feces. Eggs hatch in the water producing miracidia that invade snails. Here the miracidia develop into infective cercaria that are released into the water where they again penetrate waterfowl and repeat the life cycle.
When the cercaria are shed from the infected snails, they remain very close to the snail unless they are carried great distances by winds or currents. Since the snails become more abundant as summer progresses, there is an increased possibility for swimmer's itch later in the season. The cercaria tends to swim near the surface of the water and are attracted to the warm temperature of the skin. People at greatest risk are those in warm, shallow, calm water near aquatic vegetation which may harbour snails. Children often get swimmer's itch when wading and playing in shallow and weedy water. One man who was pulling weeds from the water with his right arm for several hours got a severe case of swimmer's itch on this one arm. In addition to the typical spots resembling hives or mosquito bites his arm became swollen and inflamed. All people are susceptible. Person-to-person spread does not occur.
Man is an incidental host. The cercaria penetrates the skin and then dies just beneath the epidermis causing an immediate hypersensitivity or allergenic response. This response is variable and is apparently dependent on the degree of hypersensitivity induced by previous exposures. The first exposure to infested water may not result in the itchy rash. Subsequent exposures increase sensitivity to the parasite and the likelihood of rash development. There is a prickling sensation when cercaria penetrates the skin. The tingling lasts up to one hour and is accompanied by swelling and open sores. The primary itching subsides and a quiet period follows during which the sores may subside. After an interval of ten to fifteen hours, open sores accompanied by intensive itching occur. This lasts about one week. Pustules may form if secondary infection occurs. Systemic symptoms are frequent. The lesions are commonly confused with those of contact dermatitis, poison ivy and insect bites from chiggers or mosquitoes. Unless bacteria secondarily infect the rash, the only treatment needed is an antihistamine; since the rash is related to an immune response. Calamine lotion may reduce the urge to scratch in children.
The prevention or control of swimmer's itch can be accomplished by avoidance of all aquatic activities in areas where swimmer's itch is known or elimination of the snail host either through the use of molluscicides or removing aquatic vegetation. A simpler, and more environmentally benign prevention, is simply to dry completely with a towel as soon as you leave the water and before drying out in the sun by evaporation; this requires removing a wet bathing suit and drying all the skin. Allowing water to evaporate from the skin rather than immediately drying the skin with a towel will encourage the cercaria to burrow into the skin to avoid being dehydrated. Drying with a towel after swimming or wading in infested water will remove the cercaria while they are still in the water film on the skin. An immediate hot, soapy, shower will also eliminate the cercaria before they burrow but this is rarely possible. Covering the entire body, including under the bathing suit, with a good waterproof sunscreen may also offer some protection from the cercaria.
Frequency of Helminth Infections by Primary Vector and Country
| Enterobiasis, pinworm-Enterobius vermicularis | |
| Geographic Region | Occurrence Frequency |
| United States | 50,000,000 |
| Canada | 2,000,000 |
| World Total | 52,000,000 |
| Diphyllobothriasis-Diphyllobothrium latum | |
| Geographic Region | Occurrence Frequency |
| Canada | few and isolated |
| Europe | 7,000,000 |
| Eurasia | 2,000,000 |
| Japan | ~1,000,000 |
| World Total | ~10,000,000 |
| Cystercercosis/Taeniasis-Taenia solium | |
| Geographic Region | Occurrence Frequency |
| Central America | 6,500,000 |
| Europe | sporadic |
| World Total | 6,500,000 |
| Ascariasis-Ascaris lumbricoides | |
| Geographic Region | Occurrence Frequency |
| Caribbean | 1,000,000 |
| Africa | over 200,000,000 |
| China | ~100,000,000 |
| Indian sub-continent | 400,000,000 |
| Middle East | 100,000,000 |
| World Total | over 801,000,000 |
| hookworm-Ancylostoma duodenale, Necator americanus | |
| Geographic Region | Occurrence Frequency |
| Africa | over 1,800,000 |
| Indian sub-continent | 300,000,000 |
| Middle East | 60,000,000 |
| World Total | over 361,800,000 |
| Paragonimiasis-Paragonimus westermani | |
| Geographic Region | Occurrence Frequency |
| China | ~1,000,000 |
| Southeast Asia | 2,000,000 |
| Japan | over 1,000,000 |
| World Total | over 4,000,000 |
| Clonorchiasis-Clonorchis sinensis | |
| Geographic Region | Occurrence Frequency |
| Japan | ~20,000,000 |
| World Total | ~20,000,000 |
| Chinese liver fluke-Opisthorchis sinensis | |
| Geographic Region | Occurrence Frequency |
| China | 5,000,000 |
| World Total | 5,000,000 |
| Hydatid disease-Echinococcus granulosus | |
| Geographic Region | Occurrence Frequency |
| Australia | 15 |
| Eurasia | 1,000,000 |
| New Zealand | 5000 |
| Europe | 5000 |
| United States | 7100 |
| World Total | 1,017,115 |
| Dracunculiasis, guinea worm-Dracunculus medinensis | |
| Geographic Region | Occurrence Frequency |
| Indian sub-continent | 60 (1994) |
| Africa | present |
| Middle East | present |
| World Total | 80,000 (being eradicated) |
| Trichuriasis, Whipworm-Trichuris trichuria | |
| Geographic Region | Occurrence Frequency |
| Caribbean | 1,000,000 |
| Africa | present |
| World Total | 1,000,000 |
| Hymenolepiasis-Hymenolepis nana=Vampirolepis nana | |
| Geographic Region | Occurrence Frequency |
| United States | 2,600,000 |
| Eurasia | 1,700,000 |
| World Total | 4,300,000 |
| Schistosomiasis, bilhartzia-Schistosoma japonicum, Schistosoma mansoni Schistosoma haematobium, Schistosoma mekongi Schistosoma intercalatum | |
| Geographic Region | Occurrence [Deaths] |
| Caribbean | 10,000 |
| Africa | 100,000,000 [10,000] |
| China | over 870,000 |
| Middle East | 50,000,000 [5,000] |
| South American | 45,000,000 |
| Japan | over 1,000,000 |
| World Total | over 196,880,000 [15,000] |
Frequency of all Infections by Country
Those that are dealt with in this report are marked with an *. Compare their frequencies of occurrence with that of other parasites, generally having animal, mostly insect, vectors, to get a measure of the relative importance to the health of the human population from water borne helminths.
| United States-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Balamuthia mandrillaris | amoebic encephalitis | rare, few/year, [usually] |
| Cryptosporidium parvum | cryptosporidiosis | 33/year |
| Dirofilaria immitis | pulmonary dirofilariasis | 118 since 1961 |
| Echinococcus | hydatidosis | 7100/year |
| Entamoeba histolytica | amoebiasis | 2893 in 1994 |
| Enterobius vermicularis | enterobiasis | * 50,000,000/year |
| Giardia lamblia | giardiasis | 141/year |
| Plasmodium | malaria | 910/year |
| Plasmodium vivax | malaria | 464/year |
| Plasmodium falciparum | malaria | 282/year |
| Strongyloides stercoralis | strongyloidiasis | up to 1,000,000/year |
| Trichinella spiralis | trichinellosis | * sporadic, ~40/year |
| Vampirolepis nana | vampirolepiasis | 2,600,00/year |
| Canada-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Diphyllobothrium | diphyllobothriasis | * a few isolated cases/year |
| Entamoeba histolytica | amoebiasis | 1778/year |
| Enterobius vermicularis | enterobiasis | * 2,000,000/year |
| Giardia lamblia | giardiasis | 7042/year |
| Plasmodium vivax, Plasmodium falciparum | malaria | 483/year |
| Trichinella spiralis | trichinellosis | sporadic, 5-10/year |
| Central America-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Entamoeba histolytica | amoebiasis | 5,000,000/year |
| Leishmania chagasi, Leishmania mexicana | cutaneous leishmaniasis | 150,000/year |
| Plasmodium | malaria | 500,000/year |
| Strongyloides stercoralis | strongyloidiasis | ~ 3,300,000/year |
| Taenia solium | cystercercosis | * 6,500,000/year |
| Trypanosoma cruzi | chagas, trypanosomiasis | 8,000,00/year |
| Caribbean-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Ascaris lumbricoides | ascariasis | * 1,000,000/year |
| Plasmodium | malaria | 100,000/year |
| Schistosoma mansonii | schistosomiasis | * 10,000/year |
| Trichuris trichiura | trichuriasis | * 1,000,000/year |
| South America-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Leishmania chagasi | leishmaniasis visceral | * 3,000/year |
| Leishmania braziliensis | leishmaniasis cutaneous | * 9,000/year |
| Onchocerca volvulus | river blindness | 500,000/year |
| Plasmodium | malaria | 1,200,000/year |
| Schistosoma mansonii | schistosomiasis | * 45,000,000/year |
| Strongyloides stercoralis | strongyloidiasis | ~ 7,400,000/year |
| Trypanosoma cruzi | chagas, trypanosomiasis | 16-18,000,000/year, [4500] |
| Wuchereia bancrofti | filariasis | 2,000,000/year |
| Australia-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Echinococcus granulosus | hydatidosis | * 15/year |
| Plasmodium | malaria | 93/year (imported) |
| China-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Ascaris lumbricoides | ascariasis | * ~100,000,000/year |
| Opisthorchis chinensis | Chinese liver fluke | * 5,000,000/year |
| Paragonimus | paragonimiasis | * ~1,000,000/year |
| Plasmodium | malaria | 74,000/year |
| Schistosoma japonicum | schistosomiasis | * over 870,000/year |
| Africa-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Ancylostoma duodenale, Necator americanus | hookworm, ancylostomiasis | * over 1,800,000/year |
| Ascaris lumbricoides | ascariasis | * over 200,000,000/year |
| Entamoeba histolytica | amoebiasis | 5,000,000/year, [5000] |
| Leishmania | leishmaniasis | 2-3,000,000/year |
| Onchocerca volvulus, Loa loa, Wuchereia bancrofti | filariasis | 18,000,000/year |
| Plasmodium | malaria | 23,000,000/year, [2,600,00] |
| Schistosoma mansoni Schistosoma haematobium | schistosomiasis | * 100,000,000/year [10,000] |
| Strongyloides stercoralis | strongyloidiasis | ~16,300,000/year |
| Trypanosoma | trypanosomiasis | over 300,000/year |
| Japan-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Anisakis | anisakiasis | ~10,000,000/year |
| Clonorchis sinensis | clonorchiasis | * ~20,000,000/year |
| Diphyllobothrium latum | diphyllobothriasis | * ~1,000,000/year |
| Paragonimus | paragonimiasis | * over 1,000,000/year |
| Schistosoma japonicum | schistosomiasis | * over 1,000,000/year |
| New Zealand-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Echinococcus granulosus | hydatidosis | * 5000/year |
| Southeast Asia-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Brugia malayi | filariasis | 12,500,000/year |
| Opisthorchis sinensis | Chinese liver fluke | * 19,000,000/year |
| Paragonimus westermani | paragonimiasis | * 2,000,000/year |
| Plasmodium | malaria | 500,000/year |
| Strongyloides stercoralis | strongyloidiasis | over 5,300,000/year |
| Eurasia-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Echinococcus granulosis | hydatidosis | * 1,000,000/year |
| Diphyllobothrium latum | diphyllobothriasis | 10,000,000/year |
| Giardia lamblia | giardiasis | * 2,000,000/year |
| Trichinella spiralis | trichinellosis | * 1,500,000/year |
| Vampirolepis nana | vampirolepiasis | 1,700,000/year |
| Middle East-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Ancylostoma duodenale | hookworm, ancylostomiasis | * 60,000,000/year, [2000] |
| Ascaris lumbricoides | ascariasis | *1 00,000,000/year |
| Leishmania tropica, Leishmania major | leishmaniasis cutaneous | 1,300,000/year |
| Plasmodium | malaria | 46,000/year, [2000] |
| Schistosoma mansoni, Schistosoma haematobium | schistosomiasis | * 50,000,000/year, [5000] |
| Europe-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Diphyllobothrium latum | diphyllobothriasis | * 7,000,000/year |
| Echinococcus granulosis | hydatidosis | * 5000/year |
| Strongyloides stercoralis | strongyloidiasis | * 2,000,000/year |
| Taenia solium | taeniasis | * Sporadic outbreaks |
| Trichinella spiralis | trichinellosis | * Sporadic outbreaks |
| India, Pakistan, Sri Lanka-Parasitic Disease Frequencies | ||
| Parasite | Disease | Frequency [Deaths] |
| Ancylostoma duodenale | hookworm, ancylostomiasis | * 300,000,000/year |
| Ascaris lumbricoides | ascariasis | * 400,000,000/year |
| Dracunculus medinensis | dracunculiasis | * 39,792 in 1994; 60 in 1995 |
| Leishmania | leishmaniasis, kala-azar | 500,000/year |
| Plasmodium | malaria | 2,100,000/year, [400,000] |
| Strongyloides stercoralis | strongyloidiasis | * ~7,000,000/yr |
| World Summary-Parasitic Disease Frequencies | |
| Parasite/Disease | Frequency |
| Intestinal roundworms, ascariasis | * 1,400,000,000 |
| Schistosomiasis | * 200,000,000 |
| Lymphatic filariasis | * 120,000,000 |
| Amoebiasis | 40,000,000 |
| Food borne trematode infections | * 40,000,000 |
| Chagas trypanosomiasis | 16,000,000 |
| Leishmaniasis | 12,000,000 |
| African trypanosomiasis | 300,000 |
| Dracunculiasis | * 100,000 |
Nature of Infections
There are many different kinds of diseases caused by these helminth pathogens, many different organs and parts of the body are affected, many different routes of access to the body are used and the outcomes or severity of the diseases caused range from non-symptomatic to fatal. Virtually all organs are affected but the chief or most severe diseases affect the brain, heart, liver, lungs, bile ducts, lymph system and lower gut. Some round worms take the 'grand tour' and wander around much of the body, causing damage as they go, until they settle in their preferred location. Access may be via food or water that is ingested, air or aerosols that are inhaled, direct penetration though the skin, access through the eye, nose and ear or transmitted through sexual activity.
Disease severity ranges from rapidly fatal encephalitis to low grade chronic infections of the gut that may be non-symptomatic for many years. Most commonly there are respiratory problems or diarrhea which are non-life threatening. Tapeworms absorb nutrients from the gut and lead to chronic malnutrition and malaise in heavy infestations. Some worms block passages responsible for bile, lymph or blood flow and the resulting obstruction leads to swelling and tissue damage as well as loss of function. Many pathogens can set up autoinfection cycles within a host whereby they are able to keep re-infecting the host from within without having to shed eggs to the environment and re-infect again. The tables below indicate the main areas of the body which are affected helminth parasites. These are the areas affected during the migration stage and the final destination for growth and reproduction.
The Helminth Organisms and the Part of the Body Affected
| Location in the Body | Helminth Organisms |
| Central nervous system, Brain | Taenia solium, Heterophyes heterophyes, Metagonimus yokogawai, Paragonimus westermani, Schistosoma haematobium,Gnathostoma spinigerum, Gnathostoma binucleatum, Gnathostoma didelphis, Gnathostoma doloresi, Gnathostoma hispidum, Gnathostoma miyazakii, Gnathostoma nipponicum, Gnathostoma procyonis, Spirometra erinacei, Spirometra mansoni, Spirometra mansonoides, Spirometra ranarum |
| Circulatory system, Heart | Ancylostoma duodenale, Ascaris lumbricoides, Heterophyes heterophyes, Metagonimus yokogawai, Schistosoma mansoni, Schistosoma haematobium, Schistosoma japonicum, Schistosoma mekongi, Schistosoma intercalatum, Echinococcus granulosus, Echinococcus multilocularis, Echinococcus vogeli, Echinococcus oligarthrus |
| Eye | Toxocara cati, Toxocara canis, Gnathostoma spinigerum, Gnathostoma binucleatum, Gnathostoma didelphis, Gnathostoma doloresi, Gnathostoma hispidum, Gnathostoma miyazakii, Gnathostoma nipponicum, Gnathostoma procyonis, Spirometra erinacei, Spirometra mansoni, Spirometra mansonoides, Spirometra ranarum |
| Genito-urinary system | Schistosoma haematobium |
| Gut, Colon, Duodenum, Ileum, Small intestine, Lumen, Intestinal tract | Diphyllobothrium latum, Dipylidium caninum, Hymenolepis diminuta, Hymenolepis nana, Taenia saginata, Taenia solium, Ancylostoma duodenale, Ascaris lumbricoides, Capillaria philippinensis, Enterobias vermicularis, Necator americanus, Trichuris trichiura, Clonorchis sinensis, Fasciola gigantica, Fasciola hepatica, Fasciolopsis buski, Heterophyes heterophyes, Metagonimus yokogawai, Opisthorchis viverrini, Opisthorchis felineus, Schistosoma mansoni, Schistosoma haematobium, Schistosoma japonicum, Schistosoma mekongi, Schistosoma intercalatum, Echinococcus granulosus, Echinococcus multilocularis, Echinococcus vogeli, Echinococcus oligarthrus, Gnathostoma spinigerum, Gnathostoma binucleatum, Gnathostoma didelphis, Gnathostoma doloresi, Gnathostoma hispidum, Gnathostoma miyazakii, Gnathostoma nipponicum, Gnathostoma procyonis, Spirometra erinacei, Spirometra mansoni, Spirometra mansonoides, Spirometra ranarum |
| Liver | Taenia solium, Capillaria hepatica, Toxocara cati, Toxocara canis, Clonorchis sinensis, Fasciola gigantica, Fasciola hepatica, Opisthorchis viverrini, Opisthorchis felineus, Echinococcus granulosus, Echinococcus multilocularis, Echinococcus vogeli, Echinococcus oligarthrus |
| Muscle | Taenia saginata, Taenia solium, Ancylostoma duodenale |
| Pancreas | Opisthorchis viverrini, Opisthorchis felineus |
| Respiratory tract, Lungs | Ancylostoma duodenale, Ascaris lumbricoides, Capillaria aerophila, Necator americanus, Paragonimus westermani, Echinococcus vogeli, Gnathostoma spinigerum, Gnathostoma binucleatum, Gnathostoma didelphis, Gnathostoma doloresi, Gnathostoma hispidum, Gnathostoma miyazakii, Gnathostoma nipponicum, Gnathostoma procyonis |
| Skin | Ancylostoma ceylanicum, Ancylostoma duodenale, Ancylostoma braziliense, Uncinaria stenocephala, Necator americanus, Schistosoma mansoni, Schistosoma haematobium, Schistosoma japonicum, Schistosoma mekongi, Schistosoma intercalatum, Austrobilharzia variglandi, Gigantobilharzia, Heterobilharzia americanum, Microbilharzia, Schistosoma spindale, Schistosomatium douthitti, Trichobilharzia ocellata, Trichobilharzia physella, Trichobilharzia stagnicolae, Dracunculus medinensis, Gnathostoma spinigerum, Gnathostoma binucleatum, Gnathostoma didelphis, Gnathostoma doloresi, Gnathostoma hispidum, Gnathostoma miyazakii, Gnathostoma nipponicum, Gnathostoma procyonis |
| Widespread | Taenia solium, Paragonimus westermani, Echinococcus granulosus, Echinococcus vogeli, Spirometra erinacei, Spirometra mansoni, Spirometra mansonoides, Spirometra ranarum |
Sources of Infection
General
While water borne transmission is important for many of these pathogens it is not the only, or in some case the most important, means of spread. The anal/oral shortcut is faster and more efficient than discharge to the environment and infection or re-infection from contaminated water. This maintains a reservoir of pathogens from which the water is continuously re-contaminated and in some cases, where no alternate host is required in the life cycle, or currently available, may maintain a pathogen population in isolation from the water.
Nosocomial
Understanding the means of acquisition, sources, and reservoirs of nosocomial pathogens is crucial for developing methods to reduce the incidence of nosocomial infections. Important water reservoirs in the hospital include potable water, sinks, faucet aerators, showers, tub immersion, toilets, dialysis water, ice and ice machines, water baths, flower vases, eyewash stations and dental-unit water stations. While virtually all pathogen records, except for the protozoan Hartmannella at an eyewash station and Cryptosporidium in ice machines, document bacterial diseases it should be noted that contaminated water was the source and could well be the source for helminth parasites as well. Rarely, if ever, was there even an analysis carried out for helminths.
Drinking Water
Drinking water is not used just for drinking; in fact this is probably its most insignificant use in terms of volume used. It is used for cooking food, preserving food, washing food, washing people, as ice cubes in drinks, watering the garden, washing the house and objects in it, filling wading pools and filling humidifier reservoirs. People in a shower and kids playing under a sprinkler are exposed to aerosols.
Hygiene
There are a number of jobs in which the workers are exposed to feces, which may be contaminated with pathogens. The use of protective clothing, masks, rubber gloves and the practice of washing thoroughly with soap and using a nailbrush to clean under the fingernails will help to reduce the risk. A partial list of jobs and activities with high pathogen contact risk includes, sewer workers, sewage treatment plant workers, medical laboratory staff, hospital staff, child and adult daycare staff, caring for infants, farm workers where contaminated irrigation water is used, animal care staff in laboratories, zoos, feedlots, pet stores and organizations like the SPCA, commercial laundry staff, composting, recycling and garbage collection workers, abattoir workers, farm workers where animals are raised and ambulance and other emergency response staff. Everyone is exposed daily when they go to the toilet.
Aquatic Recreation
Natural lakes and other bodies of water may be contaminated and continuously re-contaminated, particularly if heavily used by people. Lack of flow and replacement of the water allows pathogens to build up. Surface waters are generally relatively clean and swimming from a dock or raft is a lower risk activity than wading in the shallows and stirring up the bottom sediments where pathogen concentrations are orders of magnitude higher. Ironically, this puts toddlers at a higher risk than teens. For some organisms the risk is greatly increased by submersion of the head in diving or swimming since the infection route is through the nasal passages. Aerosols are also a problem and splashing increases the risk. The wading pool in the back yard that is freely accessible to cats and dogs and has been incubating for some weeks in the sun without a water change is a prime source of pathogens.
For artificial pools chlorination is not necessarily adequate as a treatment, especially if not properly maintained at high levels. Ozonation is also not adequate for some organisms. High intensity UV irradiation will control many spores; Giardia and Cryptosporidium, but may not kill encysted Ascaris ova. Sub-micron filtration is necessary to remove all the pathogens.
Sexual Activities
There are a number of sexual practices, which greatly increase the risk of anal/oral spread of many pathogens. Some ways to reduce, but not eliminate, such risk include use of protective devices such as condoms, washing with soap before and after such activities, avoiding such activities when one of the partners has an active infection and choosing a sexual partner with care.
Water Supply
No one should ever view the water supply as guaranteed pathogen-free. Historical data record a downward trend in waterborne disease in developed societies, particularly since the advent of filtration and then chlorination early in this century, but never a cessation of waterborne illness. The rational goal is to strive to reduce risk since to promise no risk is irrational. Assessment and subsequent management of newly identified risks will be constantly needed.
When feeding very young infants, we carefully sterilize bottles and other equipment, to avoid pathogen exposure, because infant immune systems are not completely developed. Society views this practice as common sense. The same special care must be exercised in the case of other children or adults with imperfect or failing immune systems; this too is only common sense. Provision of point-of-use filtration devices, use of boiled drinking water, and other avoidance practices for high-risk individuals, seem more economically reasonable solutions to potential helminth egg exposure than a massive overhaul of current water treatment facilities.
Spore Size
The US Surface Water Treatment Rule states that all surface water that may potentially be used for drinking water must be filtered. Cysts may be quite different in size, the full range of reported values is given in the text. It is the cysts which are generally the resistant and infective stage which need to be filtered out of drinking water. Many are not round but ovoid or other more complex shapes. It is the minimum size of any water transmittable stage that is important for designing drinking water filtration processes.
Resistance to Disinfection
The resistance of many helminth eggs to standard water disinfection procedures has been well reported. Ascaris eggs are resistant to the usual chlorine disinfection concentrations. Of the disinfectants commonly used to treat water, UV appears to be most effective in destroying the cysts of Ascaris, which is among the most resistant of the helminths.
Sewage Treatment Plants
Sewage treatment plants may be contributors of oocysts to raw water supplies depending upon where they are sited and they are certainly the primary repositories of oocysts produced by infected individuals within a community; monitoring data from sewage treatment facilities also fits into an improved communication network. Increasing oocyst numbers at the sewage treatment plant could serve as an early warning sign that a cryptosporidiosis problem is on the way. Water treatment facilities must gear to handling peak incidences of oocysts rather than normal levels, to ensure that unacceptably high risks of infection from cyst forming pathogens never occur. Process alterations may lead to changing circumstances, with respect to the risk of oocyst presence, or oocyst survivability.
Water Treatment Plants
Multiple barriers, combinations such as clarification, filtration and disinfection, are key to minimizing helminth egg presence in drinking water. Facilities with disinfection but not filtration are clearly at risk. Problems arise under two scenarios. Firstly, when some identifiable breakdown in the system occurs resulting in direct/indirect fecal contamination of the water supply. Maintaining vigilance can minimize their occurrence, but there is no way to entirely prevent such accidents. The second scenario is some combination of atypical, coincidental, occurrences, heavy runoff plus slightly less than optimal treatment leading to turbidity fluctuations being an example. Mixing of filter effluents may produce suitable final water according to regulations, yet on a filter-by-filter basis, some treatment streams may not perform as well as others.
Regulatory compliance is not good enough in an instance like this and improvement is possible. Blending of potentially oocyst-carrying, higher turbidity water with another lower turbidity water to meet turbidity guidelines may lead to an oocyst presence in the blended waters sufficient to initiate illness. With respect to potential oocyst contamination, operators need to view each treatment stream individually, rather than judging the quality of their product on the final, mixed water leaving the plant. The backwash process appears particularly critical with respect to oocyst presence in final waters. Some authorities recommend no recycling of backwash water and filtering to waste after backwashing until the filter restabilizes. Solids from backwashing may contain considerable numbers of oocysts, and should be handled appropriately.
Within the laboratory, detection, isolation, culture and quantification techniques are also difficult, or impossible, for many of these organisms; false positive and false negative results are common. Since we are concerned here with the actual pathogens, and not with indicators as with fecal coliforms or E. coli as for bacterial guidelines, the relevant safe number or infectious dose is often zero. The way to achieve this is to set treatment standards designed to remove or kill all pathogens that are present rather than the impossible task of finding water supplies with no pathogens in them and maintaining them in that state. This is a departure from the usual physical or chemical guideline, which is justifiably a non-zero number since organisms have evolved to cope with background levels of all naturally occurring substances in the environment. For biological contaminants the number is zero, since they are capable of reproducing to ultimately large numbers if even one is originally present.
Recommendations
General
Many of these organisms are relatively rare in the environment or, if common, very rarely cause disease in normal immunocompetent people who practice good hygiene. The risk of disease is extremely low and should be of little concern to normal healthy people; however, the consequences may be serious for those few who are infected. It is the immunoincompetent, such as AIDS and transplant patients that are at greatest risk. One reason that many of these diseases have come into prominence recently is likely due to the recent AIDS epidemic and the prevalence of intravenous drug users and high risk sexual practices among such vulnerable people.
While this report is primarily concerned with water borne pathogens many of these organisms are also opportunistic and will spread directly from man to man, often via the fecal/oral route. Human behaviour is the weak link here; sexual practices and poor hygiene contribute to self-re-infection and person-to-person spread. Once in man they are then released again into the water to continue the cycle. It is important to break the cycle in as many places and as often as possible to reduce the pathogen load back to the water. Thus, many recommendations given here are not directly related to water transmission but are related to human behaviour.
Existing guidelines for many physical and chemical contaminants in water, and also for biological contaminants like bacteria, through the use of a surrogate measure like fecal coliforms or E. coli, are based on numerical standards. Numerical standards are appropriate for physical and chemical contaminants but not for biological pathogens where both the geographical and statistical distributions are intrinsically not normal, either spatially or temporally. For pathogens which can reproduce, a fixed number at a given place and time does not lead to predictable infectious doses at the host. For such contaminants, helminth worms, protozoans, bacteria and viruses it is more productive, and offers better protection from infection, to prescribe treatment regimes designed to remove the organisms rather than define numbers that have no defined risk factor attached to them. Measurement of numbers for such pathogens is often impossible, rarely reproducible, inaccurate, commonly rife with false positives and false negatives, changes constantly, correlates poorly if at all with disease or infection risk and does not necessarily determine whether or not the detected cyst is actually viable.
The risk of infection is a function of many factors including but not limited to the numbers of spores or other infectious agents, the number of people in the habitat where the organisms are found, the behaviour of the people, sewage treatment processes, drinking water treatment processes, watershed conditions, the number of already infected people, the prevalence of alternate hosts and their infection rate and climatic conditions. Only a few of these can be controlled to influence pathogen numbers and distribution. Drinking water and sewage treatment processes are the main influences under our direct and immediate control. Since such processes and infrastructures are already in place it is easiest, and likely the most economical, to modify them to the extent that pathogen control is achieved, rather than devise new control mechanisms.
There are a number of instances of co-infection or dependent species pairs involved in some diseases and in such cases control of the species of concern may actually necessitate control of the other species too. Dientamoeba fragilis is often linked to the pinworm, Enterobius vermicularis, and may gain access to the body in pinworm eggs or worms. Controlling pinworm spread may reduce the rate of Dientamoeba infections. The protozoan Hartmannella veriformis is a host protozoan in which the bacteria Legionella pneumophila multiplies to very large numbers. While Hartmannella may not cause a serious disease in immunocompetent people, Legionella does; one infected Hartmannell cell may introduce an infective dose of Legionella into the human body.
water borne
These techniques are all designed to reduce the number of pathogens below the infective dose, which in some cases is as low as one organism, ideally to zero. In order that the necessary sub-micron filters work and have a reasonable life span the bulk of the suspended materials in the water needs to be first removed by conventional sand filtration and/or flocculation. Sterilization techniques such as chlorination, ultraviolet light, ionizing radiation and ozone will not work effectively or efficiently unless such pre-filtration occurs to remove organic compounds and particulate materials. Disinfection must follow filtration since amoeboid protozoans; bacteria and viruses may penetrate filtration processes designed to remove spores or oocysts.
Some of these techniques are not practical, economical, socially acceptable or useful for other reasons on a large scale but do have some value for restricted uses of small quantities of water. On a practical and economical basis it is impossible to guarantee sterile water on a large scale with an extensive distribution system. What can be done is reduce the risk to an acceptable level and permit the immune system of healthy people to cope with the residual. There is an additional need to provide more expensive, smaller quantities of absolutely sterile water to people at special risk, for example kidney dialysis and extensive burn washing, as is currently done in hospitals.
Immunocompromised patients with diseases such as AIDS also need sterile water. Immunocompromised persons traveling to Latin America, Africa or other developing regions should exercise precautions when eating and drinking, in order to avoid infection with multiple gastrointestinal pathogens including helminth worms. These precautions include the use of sub-micron filters for purifying water, eating well-cooked foods and avoiding recreational water activities.
other vectors
Many, but not all, of these are designed to break the anal/oral transmission cycle.
Species Specific
Cestodes
Diphyllobothrium latumNematodes
Ancylostoma doudenaleTrematodes
Clonorchis sinensisInternet Pages
Paper Documents
Papers dealing strictly with clinical, diagnostic and therapeutic aspects have been eliminated from this list.