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15.20: Helminthic Diseases of the Digestive System - Biology


15.20: Helminthic Diseases of the Digestive System

Nematode and Human Diseases | Helminths

The following points highlight the nine major human diseases caused due to infestation with the nematodes . The human diseases are: 1. Ascariasis 2. Ancylostomiasis 3. Enterobiasis 4. Trichuriasis 5. Trichinosis 6. Strongyloidiasis 7. Filariasis or Elephantiasis 8. Loiasis 9. Onchocerciasis.

Human Disease # 1. Ascariasis:

Ascariasis is a highly prevalent disease caused by the largest nematode (roundworm) Ascaris lumbricoides. It resembles an ordinary earthworm.

When fresh from the intestine, it is light brown or pink in colour but it gradually changes to white. It is most frequently seen in the stool of children. The male of A. lumbricoides measures about 15 to 25 cm in length, while the female is longer and stouter measuring 25 to 40 cm in length.

The egg-laying capacity of mature female Ascaris has been found to be enormous, liberating about 200,000 eggs daily.

The eggs liberated by a fertilised female pass Out of the human host with the faeces and may remain alive for several days. Infection is effected by swallowing ripe eggs (embryonated eggs) with raw vegetables cultivated on a soil fertilised by infected human excreta. Infection also occurs by drinking contaminated water.

Among children playing in the contaminated soil, there is also hand to mouth transfer of eggs by dirty fingers. Infection may also occur by inhalation of desiccated eggs in the dust reaching the pharynx and swallowed. A rhabditiform larva is developed from un-segmented ovum within the egg-shell in 10 to 40 days in the soil.

The ripe egg containing the coiled-up embryo is infective to man.

When ingested with food, drink or raw vegetables, the embryonated eggs pass down to the duodenum where the digestive juices weaken the egg-shell. Splitting of the egg-shell occurs and the rhabditiform larvae are liberated in the upper part of the small intestine. The newly hatched larvae burrow their way through the mucous membrane of the small intestine and are carried by the portal circulation to the liver.

Finally they pass out of the liver and via right heart enter the pulmonary circulation. Breaking through the capillary wall they reach the lung alveoli. From the lung alveoli the larvae crawl up the bronchi and trachea, they are propelled into larynx and pharynx and are once more swallowed.

The larvae pass down the oesophagus to the stomach and localize in the upper part of the intestine, their normal abode. The larvae on reaching habitat grow into adult worms and become sexually mature in about 6 to 10 weeks’ time. Four moultings of the larva occur-one outside while within the egg-shell, two in the lungs and one in the intestine.

The symptoms attributed to Ascaris infection may be divided into two groups:

(i) Those produced by migrating larvae, and

(ii) Those produced by the adult worms.

(i) Symptoms due to the migrating larvae:

In heavy infections typical symptoms of pneumonia such as fever, cough and dyspnoea may appear. Urticarial rash and eosinophilia are seen in such cases. Disturbances have been reported due to their presence in the brain, spinal cord, heart and kidneys.

(ii) Symptoms due to the adult worms:

With the adult worms inhabiting the intestine the patient complains of abdominal pains, vomiting, headache, irritability, dizziness and night terrors. Sometimes there is a diarrhoea and salivation. Often the patient grits his teeth in the sleep. When the adult worms migrate through the intestinal wall they cause severe peritonitis.

Wandering Ascaris may enter the lumen of the appendix, causing appendicitis. Obstructive jaundice and acute haemorrhagic pancreatitis have been known to occur when the worm has entered into the biliary passage. At times it penetrates high up in the liver causing one or more abscesses.

The treatment of human ascariasis has been fairly successful through the oral administration of piperazine citrate syrup (two spoonful twice a day for one week, followed by another course after a gap of one week) and hexyl-resorcinol tablets (10 mg taken at bed time with water).

Other drugs which are known to have specific action on Ascaris include the following tetramisole, pyrantel pamoate, bephanium hydroxynaphthoate, diethylcarbamazine (Hetrazan), thiobendazole and mebendazole.

Human Disease # 2. Ancylostomiasis:

Ancylostomiasis is caused by two hookworms Ancylostoma duodenale and Necator americanus. Both the hookworms are parasites within the intestine. The adult worms live in the small intestine of man particularly in jejunum, less often in duodenum and rarely in ileum.

They are most frequent in rural areas. Female hookworms produce 5000 to 10,000 eggs per day which pass out in the stools. Man acquires infection when the eggs hatch and the larvae penetrate through the skin of the hands and feet. Infection occurs when man walks bare-foot on the faecally contaminated soil. The filariform larvae penetrate directly through the skin with which they come in contact.

The most common sites of the entry are:

(i) The thin skin between the toes

(ii) The dorsum of the feet, and

(iii) The inner side of the soles.

Infection may also occur by accidental drinking of water contaminated with filariform larvae.

The filariform larvae enter the blood vessels and are carried to the lungs. Now they make their way to one of the bronchi, trachea and larynx, crawl over the epiglottis to the back of the pharynx and are ultimately swallowed. The growing larvae settle down in the small intestine, undergo moulting and develop into adult worms.

The characteristic symptoms of ancylostomiasis are ancylostome dermatitis or ground itch, and creeping eruption by ancylostome larvae, and gastro-intestinal disorders, and severe anaemia by adult worms. Gastro-intestinal manifestations produce dyspeptic troubles associated with epigastric tenderness stimulating duodenal ulcer.

Due to severe anaemia the skin becomes pale yellow in colour and the mucous membrane of the eyes, lips and tongue becomes extremely pale. The face appears puffy with swelling of lower eyelids and there is oedema of the feet and ankle. The general appearance of the patient is a pale plumpy individual with protruded abdomen and dry lustreless hair.

For the treatment of hookworm infection the following steps are to be taken:

(i) Expulsion of worms by antihelminthic drugs and

Human Disease # 3. Enterobiasis:

Enterobiasis is caused by Enterobius vermicularis commonly called pinworm, threadworm or seatworm.

These worms are small and white in colour. Male worm measures 2 to 4 mm and female worm measures 8 to 12 mm in length. Adult worms (gravid females) live in the caecum, colon and vermiform appendix of man. The females migrate out through the colon and rectum and enormous number of eggs in the skin folds about the anus, where they cause intense itching.

Each of the egg, newly laid in perianal skin, containing a tadpole-like larva completes its development in 24 to 36 hours time, in the presence of oxygen.

Infection occurs by the ingestion of these eggs. When the skin about the anus is scratched, eggs are easily picked upon the fingers and under the nails from where they find their way to food and are swallowed. The egg-shells are dissolved by digestive juices and the larvae escape in the small intestine where they develop into adult worms.

The pinworm infection is more frequent in children than in adults. The symptoms of enterobiasis include severe itching around the anus, loss of appetite, sleeplessness and sometimes inflammation of the vermiform appendix. Enterobiasis is treated with antihelminthics such as piperazine citrate, pyrevinium pamoate (Povan), pyrental pamoate, stibazium iodide, thiobendazole and mebendazole.

Human Disease # 4. Trichuriasis:

Trichuriasis is caused by Trichuris trichura, commonly known as whipworm. The adult worms live in the large intestine of man, particularly in the caecum also in vermiform appendix.

The worm resembles a whip in shape and general appearance. Male measures 3 to 4 cm and female measures 4 to 5 cm in length. The females lay enormous number of eggs daily that pass in the stool. Development proceeds slowly in water and damp soil.

A rhabditiform larva develops within the egg in the course of 3 to 4 weeks in tropical countries. The embryonated eggs are infective to man. Man is infected when the embryonated eggs are swallowed with food or water. The egg-shell is dissolved by the digestive juices and the larva emerges.

The liberated larvae pass down into the caecum, their site of localisation. They grow directly into adult worms and embed their anterior parts in the mucosa of the intestine. The worms become sexually mature within a month from the time of ingestion of the eggs and gravid females begin to lay eggs. The cycle is then repeated.

The patient suffering from trichuriasis (whipworm disease) shows the symptoms of acute appendicitis. In heavy infections the patient often complains of abdominal pain, mucous diarrhoea often with blood streaked stool and loss of weight. Prolapse of rectum has occasionally been observed in massive trichuriasis.

The drugs at present most commonly used for the treatment of trichuriasis are stibazium iodide, deftarsone, thiobendazole and mebendazole.

Human Disease # 5. Trichinosis:

Trichinosis is caused by Trichinella spiralis, the trichinia worm. It is one of the smallest nematodes infecting man. The male measures 1.4 to 1.6 mm and female measures 3.0 to 4.0 mm in length. This disease is common and widespread in Europe and America. Although it prevails in areas where pork is eaten. Humans become infected by eating undercooked or raw meat containing encysted larvae mainly pork.

The cysts, located in striated muscles, are digested liberating larvae that mature to adult worms that attach to the wall of small intestine. Female worms there liberate larvae that invade the intestinal wall, enter the circulation and penetrate the striated muscles, where they encyst and remain viable for years. Usually one larva is present in a single cyst.

The early symptoms of trichinosis is eosinophilia. The invasion of muscle by larvae is associated with muscle pain, swelling of the eyelids and facial oedema, eosinophilia and pronounced fever. Respiratory and neurologic manifestations may appear. On invasion of the muscle layer the larvae cause inflammation and destruction of muscle fibres.

The most frequently involved muscles are those of limbs, diaphragm, tongue, jaw, larynx, ribs and eyes. Larvae in other organs, including the heart and brain cause oedema and necrosis.

The diagnosis is made by identifying larvae in muscle biopsies or by serological tests. Antihelminthic drugs remove adult worms from the intestine. Promising results have been obtained in the treatment of trichinosis by thiobendazole (Botero, 1965). Corticosteroids have been found to be useful in alleviating clinical symptoms.

Human Disease # 6. Strongyloidiasis:

Strongyloidiasis is an infection caused by the nematode Strongyloides stercoralis, commonly called threadworm.

It is found worldwide but is most common in tropical countries. S. stercoralis is a complex organism that has three life cycles which are as follows:

(i) Parasitic pathogenic females live in the human small intestine and lay eggs that hatch in the mucosal epithelium, releasing rhabditiform larvae. These larvae become infective filariform larvae in the intestine or on the perianal skin and invade human host directly (the autoinfection cycle).

(ii) The rhabditiform larvae pass in the faeces, become infective filariform larvae in the soil and later penetrate human skin (direct development cycle).

(iii) The rhabditiform larvae passed in the faeces become free-living adults in the soil and eventually produce infective filariform larvae. These infective larvae penetrate the skin, enter blood vessels and pass to the lungs, where they invade alveoli. They ascend the trachea, descend the oesophagus and mature to become parthenogenic females in the small intestine.

Invading larvae cause dermatitis. Larvae migrating through lungs may provoke cough, haemoptysis and dyspnoea, severe infection of the intestine causes vomiting, diarrhoea, and constipation. Female worms and rhabditiform larvae living in jejunum crypts cause mild eosinophilia and chronic inflammation.

By contrast patients with hyperinfection may have ulceration, oedema, congestion fibrosis and severe inflammation of the intestine. The diagnosis is made by identifying larvae in the stool.

The most specific antihelminthic drug for treatment of strongyloidiasis is thiobendazole.

Human Disease # 7. Filariasis or Elephantiasis:

Filariasis is caused by Wuchereria bancrofti commonly called the filaria worm. The adult worms inhabit lymphatic vessels, most frequently those in the lymph nodes, testes and epididymis. The female worm discharges microfilariae that circulate in the blood. Humans are the only definitive host of these worms.

Insect vectors which serve also as intermediate hosts, include 80 species of mosquitoes of the genera Culex, Aedes, Anopheles and Mansonia. Filariasis is endemic in large regions of Africa, coastal areas of Asia, Western Pacific islands and coastal areas and islands of the Caribbean basis.

In India, it is distributed chiefly along the sea coast and along the banks of big rivers (except Indus) it has also been reported from Rajasthan, Punjab, Uttar Pradesh and Delhi. Following copulation the female worm delivers larvae called microfilariae. These, at night, get in the blood capillaries of the skin to be sucked up by the mosquito with blood meal.

When the infected mosquito bites a human being, the microfilariae are not directly injected into the blood but are deposited on the skin near the site of puncture. Later, attracted by the warmth of the skin, the microfilariae either enter through the puncture wound or penetrate through the skin on their own.

After penetrating the skin, microfilariae reach the lymphatic channels, settle down at some spot (inguinal, scrotal, or abdominal lymphatics) and begin to grow into adult forms.

Features of acute infection include fever, lymphangitis, lymphadenitis, orchitis, epididymitis, urticaria, eosinophilia and microfilaremia. Chronic infection is characterised by enlarged lymph nodes, lymphoedema, hydrocele and elephantiasis. Filariasis also causes tropical eosinophilia which is characterised by cough, wheezing, eosinophilia and diffuse pulmonary infiltrates.

The infection of the filaria worms also causes enlargement of the limbs, scrotum and mammae. The swelling takes place due to blockage of the lymph circulation by the parasitic worms resulting into the inflammation of lymph vessels and lymph glands. The diagnosis is usually made by identifying the microfilariae in the blood.

There is no effective drug for the eradication of the filaria worm. The drug of choice is diethylcarbamazine (Hetrazan) which kills microfilariae and possibly adult worms.

Human Disease # 8. Loiasis:

Loiasis is an infection caused by the filarial nematode Loa loa, the African eyeworm or loa- worm. It inhabits the rain forests of Central and West Africa. Humans and baboons are definitive hosts and infection is transmitted by mango flies (Chrysops species).

The adult L.loa migrates in the skin and occasionally crosses the eye beneath the conjunctiva, making the patient actually aware of his infection. Gravid worms discharge microfilariae that circulate in the blood stream during the day but reside in capillaries of the skin, lungs and other sense organs at night.

Most infections are symptomless but persist for years. Ocular symptoms include swelling of lids, congestion, itching and pain. Female worms, and rarely male worms may be extracted during their migration beneath the conjunctiva. Systemic reactions include fever, pain, itching, urticaria and eosinophilia.

The diagnosis is made by identifying microfilariae in the blood films taken during the day, by removal of adult worm from conjunctiva, or by identifying microfilariae or adult worms in biopsy specimen. Diethylcarbamazine (Hetrazan) is an effective remedy for loiasis, causing a quick disappearance of microfilariae from the peripheral blood and even death of adult worms in some cases.

Human Disease # 9. Onchocerciasis:

Onchocerciasis is the infection caused by the filarial nematode Onchocerca volvulus. It is one of the world’s major endemic diseases, afflicting an estimated 40 million people, of whom about 2 million are blind. Man is the only known definitive host. Onchocerciasis is transmitted by several species of black flies of the genus Simulium, which breeds in fast flowing streams.

There are endemic regions throughout the tropical Africa and in focal areas of Central and South America.

The adult worms live singly and as coiled entangled masses in the subcutaneous tissues of man. The gravid female worms produce millions of microfilariae which migrate from the nodule into the skin, eyes, lymph nodes and deep organs causing the onchocercal lesions. The diagnosis is made by identifying the microfilariae in tissue sections of skin and the adult worms in the subcutaneous nodules.

The cardinal manifestations are subcutaneous nodules, dermatitis and eye disease. Nodulectomy removes adult worms in palpable nodules. Suramin kills adult worms but has dangerous side effects. Oral diethylcarbamazine (Hetrazan) kills microfilariae. A new drug, ivermectin, kills microfilariae but with a lesser allergic reaction than diethylcarbamazine.


Microbial Diseases: Top 27 Things to Know About| Microbiology

Ans. They are Gram-positive pleomorphic rods known as diphtheroids (e.g., Propionibacterium acnes) which produce propionic acid that helps to maintain low pH of the skin ranging from 3 to 5. The acidic effect produced by these bacteria safeguards skin against many harmful microorganisms. The Corynebacterium xerosis, another diphtheroid is aerobic and inhabit the surface of the skin. The yeast Pityrosporum grows on oily skin secretions and causes scaling skin conditions known as dandruff.

Q.2. Give the main microbial diseases of the skin, causative agents, characteristics and treatment.

Ans. The common microbial diseases caused by bacteria, viruses, fungi and mites, and their cause, symptoms and treatment are listed in Table 16.1.

Q.3. Who was the last victim of small pox?

Ans. The last victim of small pox was an African in Somalia, who recovered from variola minor, in 1977.

Q.4. Which are the two main types of small pox?

Ans. Two main types of small pox are Variola major and Variola minor. Recovery from one type of disease provides immunity against both the types.

Q.5. Which are the two sites where the smallpox viruses are maintained?

Ans. One in USA and the second in Russia.

Q.6. What may be the after effect of use of aspirin to lower fevers in chicken pox and influenza?

Ans. Increases the chances of acquiring Reye’s syndrome.

Q.7. What is Reye’s syndrome?

Ans. Reye’s syndrome is an occasional complication after chickenpox, influenza and other viral infections. In it a few days after the initial infection recedes the patient persistently vomits and shows the signs of brain dis-function. It may follow coma, fatty degeneration of liver and death. Death and brain damage in those who survive is due to swelling in the brain that prevents the circulation of blood.

Q.8. What is a dermatophyte?

Ans. A fungus that colonizes on skin including hair and nail is called dermatophyte. Dermatophytes grow on the keratin, the skin protein found in dermis, hair and nails and cause infections called tinea or ringworms. Tinea capitis or ringworm of scalp results bald circular patches on the head of school children.

Q.9. List the bacterial, viral and protozoal diseases of the eye. Also give their causal organisms, symptoms and therapy.

Ans. These are given in Table 16.2:

Q.10. List the microbial diseases of the nervous system.

Ans. These are listed in Table 16.3.

Q.11. List the microbial diseases of cardiovascular and lymphatic systems. Also give their causal microorganism mode of transmission and therapy.

Ans. These are listed in Table 16.4.

Q.12. Name the bacterial diseases of upper respiratory system.

Ans. These are given in Table 16.5.

Q.13. Name a viral diseases of upper respiratory tract

Ans. Common cold is the viral disease of upper respiratory tract which is caused by coronaviruses or rhinoviruses from respiratory secretions. There is no therapy for it.

Q.14. Give bacterial diseases of lower respiratory system.

Ans. Bacterial diseases of lower respiratory system are given in Table 16.6.

Q.15. Give fungal diseases of the lower respiratory system.

Ans. See Table 16.7.

Q.16. Name a protozoal disease of lower respiratory system.

Ans. Pneumocystis pneumonia is caused by Pneumocystis carinii which is transmitted through respiratory route. Trimethoprim-sulphamethoxazole and pentamidine isethionate are used for treatment.

Q.17. Give food borne bacterial diseases of digestive system.

Ans. See Table 16.8.

Q.18. Give viral diseases of digestive system.

Ans. See Table 16.9

Q.19. Name the fungal diseases of the digestive system.

Ans. See Table 16.10

Q.20. Give the protozoal diseases of the digestive system.

Ans. See Table 16.11.

Q.21. Give the common helminthic diseases of digestive system. What are their causal organisms and how are they transmitted? Give their generally followed therapy.

Ans. See Table 16.12.

Q.22. How can Neisseria gonorrhoeae be microscopically recognized in the pus from a gonorrhoea patient?

Ans. A smear of the pus from a patient will show Neisseria gonorrhoeae as paired cocci contained within leukocytes which are Gram-negative.

Q.23. Give common bacterial diseases of the urinary system.

Q.24. Give bacterial diseases of the reproductive system in a tabulated form.

Ans. See Table 16.14 below.

Q.25. Give viral diseases of the reproductive system in tabular form.

Q.26. Name the most common fungal disease. Give its causative fungal species, transmission and therapy/treatment.

Ans. Candidiasis is caused by the fungus Candida albicans which is an opportunistic pathogen but may also be transmitted by sexual contact. Clotrimazole and miconazole are used.

Q.27. Name the disease caused by protozoan Trichomonas vaginalis.

Ans. It causes trichomoniasis (often vaginitis). The pathogen is usually transmitted by sexual contact and is generally treated with metronidazole.


Helminth infections: the great neglected tropical diseases

1 Department of Microbiology, Immunology, and Tropical Medicine, George Washington University, Washington, DC, USA. 2 Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. 3 Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 4 Bill and Melinda Gates Foundation, Seattle, Washington, USA.

Address correspondence to: Peter J. Hotez, Department of Microbiology, Immunology, and Tropical Medicine, George Washington University School of Medicine and Health Sciences, 2300 I Street NW, Washington, DC 20037, USA. Phone: (202) 994-3532 Fax: (202) 994-2913 E-mail: [email protected]

1 Department of Microbiology, Immunology, and Tropical Medicine, George Washington University, Washington, DC, USA. 2 Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. 3 Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 4 Bill and Melinda Gates Foundation, Seattle, Washington, USA.

Address correspondence to: Peter J. Hotez, Department of Microbiology, Immunology, and Tropical Medicine, George Washington University School of Medicine and Health Sciences, 2300 I Street NW, Washington, DC 20037, USA. Phone: (202) 994-3532 Fax: (202) 994-2913 E-mail: [email protected]

Find articles by Brindley, P. in: JCI | PubMed | Google Scholar

1 Department of Microbiology, Immunology, and Tropical Medicine, George Washington University, Washington, DC, USA. 2 Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. 3 Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 4 Bill and Melinda Gates Foundation, Seattle, Washington, USA.

Address correspondence to: Peter J. Hotez, Department of Microbiology, Immunology, and Tropical Medicine, George Washington University School of Medicine and Health Sciences, 2300 I Street NW, Washington, DC 20037, USA. Phone: (202) 994-3532 Fax: (202) 994-2913 E-mail: [email protected]

Find articles by Bethony, J. in: JCI | PubMed | Google Scholar

1 Department of Microbiology, Immunology, and Tropical Medicine, George Washington University, Washington, DC, USA. 2 Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. 3 Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 4 Bill and Melinda Gates Foundation, Seattle, Washington, USA.

Address correspondence to: Peter J. Hotez, Department of Microbiology, Immunology, and Tropical Medicine, George Washington University School of Medicine and Health Sciences, 2300 I Street NW, Washington, DC 20037, USA. Phone: (202) 994-3532 Fax: (202) 994-2913 E-mail: [email protected]

1 Department of Microbiology, Immunology, and Tropical Medicine, George Washington University, Washington, DC, USA. 2 Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. 3 Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 4 Bill and Melinda Gates Foundation, Seattle, Washington, USA.

Address correspondence to: Peter J. Hotez, Department of Microbiology, Immunology, and Tropical Medicine, George Washington University School of Medicine and Health Sciences, 2300 I Street NW, Washington, DC 20037, USA. Phone: (202) 994-3532 Fax: (202) 994-2913 E-mail: [email protected]

1 Department of Microbiology, Immunology, and Tropical Medicine, George Washington University, Washington, DC, USA. 2 Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA. 3 Department of Pathobiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. 4 Bill and Melinda Gates Foundation, Seattle, Washington, USA.

Address correspondence to: Peter J. Hotez, Department of Microbiology, Immunology, and Tropical Medicine, George Washington University School of Medicine and Health Sciences, 2300 I Street NW, Washington, DC 20037, USA. Phone: (202) 994-3532 Fax: (202) 994-2913 E-mail: [email protected]

Find articles by Jacobson, J. in: JCI | PubMed | Google Scholar

Helminths are parasitic worms. They are the most common infectious agents of humans in developing countries and produce a global burden of disease that exceeds better-known conditions, including malaria and tuberculosis. As we discuss here, new insights into fundamental helminth biology are accumulating through newly completed genome projects and the nascent application of transgenesis and RNA interference technologies. At the same time, our understanding of the dynamics of the transmission of helminths and the mechanisms of the Th2-type immune responses that are induced by infection with these parasitic worms has increased markedly. Ultimately, these advances in molecular and medical helminth biology should one day translate into a new and robust pipeline of drugs, diagnostics, and vaccines for targeting parasitic worms that infect humans.

Helminths (the word is derived from the Greek meaning “worms” ref. 1 ) have plagued humans since before the era of our earliest recorded history. The eggs of intestinal helminths can be found in the mummified feces of humans dating back thousands of years ( 2 – 4 ), and we can recognize many of the characteristic clinical features of helminth infections from the ancient writings of Hippocrates, Egyptian medical papyri, and the Bible ( 2 – 4 ). These same helminthiases markedly altered the course of modern twentieth century world history ( 2 , 4 – 7 ), especially in China during the Cold War, when the schistosome was known as “the blood-fluke that saved Formosa” ( 7 ) because acute schistosomiasis sickened Mao’s troops and aborted their amphibious assault of Taiwan (historically known as Formosa) just long enough for American ships to enter the Straits of Taiwan ( 5 – 7 ).

There are two major phyla of helminths. The nematodes (also known as roundworms) include the major intestinal worms (also known as soil-transmitted helminths) and the filarial worms that cause lymphatic filariasis (LF) and onchocerciasis, whereas the platyhelminths (also known as flatworms) include the flukes (also known as trematodes), such as the schistosomes, and the tapeworms (also known as the cestodes), such as the pork tapeworm that causes cysticercosis (Table 1). In 1947, Norman Stoll published a landmark paper entitled “This wormy world,” in which he set out to estimate the number of people infected with helminths worldwide ( 8 ). Over the last 60 years, several estimates have confirmed Stoll’s initial observation that hundreds of millions of people harbor parasitic worms ( 9 – 11 ). Today, it is estimated that approximately one-third of the almost three billion people that live on less than two US dollars per day in developing regions of sub-Saharan Africa, Asia, and the Americas are infected with one or more helminth ( 12 , 13 ). The most common helminthiases are those caused by infection with intestinal helminths, ascariasis, trichuriasis, and hookworm, followed by schistosomiasis and LF (Table 1). Practically speaking, this means that the inhabitants of thousands of rural, impoverished villages throughout the tropics and subtropics are often chronically infected with several different species of parasitic worm that is, they are polyparasitized ( 12 , 13 ).

The major human helminthiases and their global prevalence and distribution

For reasons not well understood, compared with any other age group, school-aged children (including adolescents) and preschool children tend to harbor the greatest numbers of intestinal worms and schistosomes and as a result experience growth stunting and diminished physical fitness as well as impaired memory and cognition ( 14 ). These adverse health consequences combine to impair childhood educational performance, reduce school attendance ( 15 ), and account for the observation that hookworm (and presumably other diseases caused by parasitic worms) reduces future wage-earning capacity ( 16 ). Hookworm and schistosomiasis are also important diseases during pregnancy, causing neonatal prematurity, reduced neonatal birth weight, and increased maternal morbidity and mortality ( 17 ). Among some adult populations living in impoverished areas of developing countries, onchocerciasis is a leading cause of blindness and skin disease, while LF is a major cause of limb and genital deformities. LF and onchocerciasis, together with hookworm and schistosomiasis, are also major determinants of reduced worker productivity ( 4 , 18 , 19 ). Such chronic, disabling, and often disfiguring effects of helminths translate into enormous poverty-promoting effects and represent a major reason why poor people remain mired in a downward cycle of destitution ( 19 ).

Adding to the global morbidity that results from human helminth infections are the observations that they have both direct and indirect effects on malaria and HIV/AIDS in developing countries. In sub-Saharan Africa and elsewhere, helminthiases are frequently coendemic with malaria ( 12 , 20 – 22 ) and HIV/AIDS ( 12 , 23 – 26 ). Indeed, it is not uncommon for an individual to be coinfected with the malaria-causing parasite and one or more parasitic worm ( 22 ), or HIV and one or more parasitic worm ( 25 , 26 ). Such coinfections have additive effects, such as severe anemia ( 21 ), and synergistic effects, such as increased transmission of the malaria-causing parasite, HIV, and/or increased susceptibility to infection with these pathogens as well as cause an exacerbated progression of these two killer diseases ( 12 , 20 – 26 ).

The high medical, educational, and economic burden of helminth infections, together with their coendemicity with malaria and AIDS, provides an important rationale for launching a global assault on parasitic worms ( 13 ). However, the tools we currently have for controlling worm infections are limited of the 1,556 new chemical entities marketed between 1975 and 2004, only four drugs — albendazole, oxamniquine, praziquantel, and ivermectin — were developed to treat helminthiases ( 4 , 27 ). Together with diethylcarbamazine (developed in the first half of the twentieth century) and mebendazole, these drugs represent almost our entire pharmacopeia for combating the most common infections in the world. The dearth of available anthelminthic agents partly reflects the very modest commercial markets for drugs targeting human helminth infections and partly reflects how remarkably little we know about the unique biochemical metabolism of parasitic worms and the mechanisms by which worms evade human host defenses, establish chronic infections, and cause adverse maternal and child health ( 14 ). Indeed, the diseases caused by infection with helminths are considered neglected tropical diseases, and the study of these diseases receives less than 1% of global research dollars ( 4 ). Despite this, as we discuss here, recent advances by molecular and immunological helminthologists have indicated that helminths are a rich source of interesting molecules that could lead to innovation for almost all aspects of biomedicine. We hope that such information might one day translate into the development of new drugs, diagnostics, and vaccines to combat infection with helminths as well as influence the development of new therapeutics for other human illnesses.

With the exception of Strongyloides stercoralis, helminths do not replicate within the human host. This fundamental aspect of helminth biology establishes a set of transmission dynamics quite different than those for viruses, bacteria, fungi, and protozoa. For example, prevalence, which is the proportion of persons in a defined population at a given time point infected with the helminth ( 28 ), is seldom used as the only measure to assess the epidemiological situation for that helminth infection, because morbidity is associated with the number of worms infecting the host (i.e., the worm burden) rather than the absence or presence of infection. Prevalence is commonly combined with worm burden (also referred to as the “intensity of infection”), which is commonly measured by the number of eggs per gram (EPGs) of feces for intestinal helminths and schistosomes ( 29 ). Based on EPGs and their association with morbidity, individuals are classified into categories of light, moderate, and heavy infection by the WHO ( 30 ). Furthermore, in the case of soil-transmitted helminths, the WHO recommends use of both prevalence and intensity of infection to classify communities into transmission categories — category I (high), category II (medium), and category III (low). These transmission categories are assigned according to both the number of heavily infected people in the community (greater or less than 10%) and the prevalence of infection (greater or less than 50%). For example, a community with greater than 50% prevalence but less than 10% heavy infection would be considered a category II transmission community. The WHO uses this information in algorithms to determine the type of mass treatment a community should receive. For filarial helminths, the transmission status in a community is determined by assessing the number of people with blood-circulating microfilariae or microfilarial antigen in the case of onchocerciasis, it is determined by counting the number of microfilariae in a skin biopsy or even counting the number of palpable nodules ( 30 ). It important to note that the quantitative assessment of worms provides no information on whether the infection represents either a recent or long-term infection nor does it indicate either the length or extent of exposure to infection (i.e., an individual residing near a source of transmission for many years may not necessarily have high egg count despite extensive exposure). There are several key determinants underlying the epidemiology of helminth infections.

Environment. Climate and topography are crucial determinants of the distribution of helminth infections ( 31 ). Helminths transmitted by vectors are limited to landscapes in which host and vector come together in the same habitat, resulting highly focal distribution. For example, the distribution of schistosomiasis reflects the biotic and abiotic features (i.e., climatic, physical, and chemical factors) that affect the survival and development of the snail vector ( 32 ). In the case of onchocerciasis, the distribution and incidence of the disease are limited by biogeographic variations favorable to exposure to the blackfly vectors ( 33 , 34 ). Soil-transmitted helminths are highly affected by surface temperature ( 35 ), altitude, soil type, and rainfall ( 36 , 37 ).

Heterogeneity. Heterogeneity in the worm burden among different individuals infected with the same helminth is a hallmark feature of helminth epidemiology ( 38 ). A consequence of such heterogeneity is the aggregated distribution of helminth infection in endemic communities, such that a small proportion of hosts are rapidly, frequently, and/or heavily infected ( 38 , 39 ). For example, 70% of the worm burden occurs in 15% of the infected individuals at a given time point ( 40 ). The aggregated distribution of helminth infection has led some to hypothesize that certain “wormy” people are “predisposed” to heavy infection from as yet undefined genetic, immunogenetic, ecological, behavioral, and social factors ( 41 ). Predisposition refers to studies in which intensity of infection prior to anthelminthic treatment positively correlates with intensity of reinfection 12–24 months after treatment ( 41 ). The bases of both heterogeneity and predisposition to helminth infection have yet to be fully elucidated. However, among the major factors under consideration are age, household clustering, and genetics.

Age dependency. Much epidemiologic research has focused on heterogeneity in the intensity of helminth infection by age ( 42 ). Changes with age in the average intensity of infection tend to be convex, rising in childhood and declining in adulthood. For Ascarislumbricoides and Trichuristrichiura, the heaviest and most frequent infections are in children aged 5–15 years, with a decline in intensity and frequency in adulthood ( 43 ). Similarly, for all the major schistosomes, the heaviest and most frequent infections are in older children aged 10–15 years ( 44 ). In contrast, hookworm frequently exhibits a steady rise in intensity of infection with age, peaking in adulthood ( 45 ). Similarly, the pathologic events that occur with filarial infections also predominate in adulthood.

Some of the strongest evidence for protective immunity to human helminth infection has come from epidemiological observations of a “peak shift” in prevalence and intensity of infection with age ( 46 ). Briefly, if age-infection data are compared across host populations, the peak level of infection intensity (e.g., EPGs for intestinal helminths) is higher and occurs in younger individuals when transmission is also higher, but the peak intensity of infection is lower and occurs in older individuals when transmission is lower ( 46 ). This shift in the peak level of infection intensity and the age at which this peak occurs is consistent with mathematical models that assume a gradually acquired protective immunity, an interpretation supported by experimental studies in animals ( 46 ).

Household clustering. Evidence for household clustering of infected individuals exists for most diseases caused by infection with a helminth, including ascariasis ( 47 ), trichuriasis ( 47 ), and strongyloidiasis ( 48 , 49 ). This clustering can persist through time, as shown by familial predisposition to heavy infection with Ascarislumbricoides and Trichuristrichiura in Mexico ( 50 ). Household aggregation of lymphatic filarial infection (individuals with LF and/or microfilaraemia) has been described in India and Polynesia ( 51 , 52 ). In one study of schistosomiasis, shared household accounted for 22% of the variance in S. mansoni egg counts ( 53 ). There is also some evidence for a similarity in antibody isotype level among family members for crude schistosome antigen extracts, reflecting the degree to which this phenotype might be influenced by genetic factors ( 54 ).

Genetics. For a number of species of parasitic worms, it has been established that the intensity of infection is a heritable phenotype ( 55 ). The most advanced research program investigating the identity of host genes that influence helminth infection involves schistosomiasis. The first genome scan for a helminth infection identified linkage of intensity of infection with S. mansoni in a Brazilian population to the chromosomal region 5q31–q33 ( 56 ), and subsequent confirmation of this link was established in a Senegalese population ( 57 ). The 5q31–q33 region includes loci for numerous immune response genes, including those encoding the Th2 cytokines IL-3, IL-4, IL-5, IL-9, and IL-13, interferon regulatory factor 1, colony-stimulating factor 2, colony-stimulating factor 1 receptor, and the IL-12/IL-23 p40 subunit ( 55 ). Genes controlling IgE production, asthma, malaria parasitaemia, and inflammatory bowel disease, among others, have also been mapped to this region of chromosome 5, although the causative polymorphisms have not yet been identified.

Polyparasitism. Finally, an increasing number of studies of helminth epidemiology have shown that it is common for individuals to be infected with more than one species of helminth ( 21 , 58 – 63 ). There is also evidence suggesting synergism and antagonism in concurrent intestinal nematode and schistosome infections ( 62 – 64 ) as well as filarial nematode infection and soil-transmitted helminth infections ( 65 ). A number of epidemiological studies have indicated that individuals infected with multiple species of helminth often harbor heavier infections than individuals infected with a single helminth species ( 58 – 61 ). An important consequence of simultaneous infection with the parasites that cause hookworm, schistosomiasis, and malaria is severe anemia ( 21 , 66 ). It has also been speculated that helminth infections may adversely influence host immune responses to the malaria-causing parasite and other pathogens ( 20 ).

Most helminth infections, if left untreated, result in multi-year, chronic inflammatory disorders that cause both concurrent and delayed-onset pathology to the afflicted human host ( 67 – 69 ). In addition to the overt and dramatic effects of blindness and elephantiasis in individuals with onchocerciasis and LF, respectively, it is now appreciated that chronic helminth infections are also linked to more insidious persistent health conditions such as anemia, growth stunting, protein-calorie undernutrition, fatigue, and poor cognitive development ( 68 ). These seemingly subtle and often overlooked morbidities are very important because of the high prevalence of helminthiases in the rural developing world, in which any health impairment is substantially magnified in terms of degradation of individual patient performance status ( 70 ).

Initially, in childhood, it is the presence of helminth infection and the intensity of infection that determine the risk for disease formation. It is also true that for many of the tissue-invasive helminths, such as the schistosomes and filariae, tissue damage can continue into later adult life, with disease persisting and even increasing long after the infection is cleared. As such, measures of infection prevalence do not capture the prevalence of infection-associated disease, particularly in adult life. Conditions such as elephantiasis, which occurs in individuals with LF visual impairment, which occurs in individuals with onchocerciasis periportal fibrosis and hypertension, which occur in individuals with intestinal schistosomiasis biliary obstruction, cholangitis, and cholangiocarcinoma, which occur in individuals with food-borne trematodiasis and urinary obstruction and bladder cancer, which occur in individuals with urinary schistosomiasis, are potentially the most life-threatening consequences of helminth infections. Although most likely to contribute to hospitalization and to cause mortality, these advanced outcomes are rare when compared to the disease burden of the average patient, which is characterized by the subacute morbidities detailed earlier.

The temporal lag between initial high-intensity childhood infection and the delayed onset of “classical” parasite-associated pathologic findings have led to a serious underappreciation of the day-to-day burden of helminthic diseases. In international health assessments based on the disability-adjusted life year (DALY) metric ( 71 ), DALY calculations are weighted to stress diseases prevalent among adults in the 20–40 age group, and therefore diseases arising primarily in childhood carry far less weight ( 72 ). In the current Global Burden of Disease (GBD) assessments by the WHO, it is not clear whether prevalence of infection per se was used to gauge the disease burden of helminths or the more appropriate duration of infection-associated pathology, which is often irreversible. The DALY disability weights assigned to specific helminth infections were developed by nonpatient committees based on disease scenarios that did not reflect what we now appreciate as the full spectrum of helminth infection–associated pathology ( 71 ). Although efforts are underway to revise the GBD assessments ( 73 ), it is important that we do not underestimate the substantial disease burden of more than one billion individuals worldwide who are affected by helminth infections.

A new focus for assessing the health burden related to helminthic diseases has been the adoption of patient-based quality-of-life (QoL) interview techniques for assessing disease burden across many international settings ( 74 , 75 ). Although health-related QoL is in some sense a cultural construct, and subjective adaptation to physical impairments is likely to vary from region to region, certain universal features of disease impact can be identified. Implementation of QoL assessment for most prevalent diseases, and the subsequent use of quality-adjusted life years (QALYs) for comparison of disease impacts ( 76 ), is likely to provide the most useful comparison of disease burdens across different societies and their economies.

The reduction in the intensity of some human helminth infections with age might be indicative of host immunity. Immune responses to helminths are intriguing not only from the perspectives of understanding protective immunity and immunopathology, but also because a major branch of the mammalian immune system, type 2 immunity, seems to have evolved specifically to deal with this class of pathogens. Type 2 immunity involves the rapid activation and engagement of cells of both the innate (eosinophils and basophils) and adaptive (CD4 + T cells that commit to the Th2 pathway) immune systems ( 77 ). Cells of both the innate and adaptive immune systems that are involved in type 2 immunity share the ability to synthesize the core type 2 cytokine IL-4, which mediates (both directly and indirectly) the reactions that historically have been considered to be symptomatic of helminth infection such as IgE production, eosinophilia, and changes in the physiology of target organs (e.g., the intestine and lungs) that are associated with goblet cell hyperplasia and smooth muscle contraction ( 78 ).

Based on findings from studies of infections in humans and mouse models of helminth infections, we know that, depending on the infection in question, type 2 immune responses can prevent the survival of infecting parasites during a homologous secondary infection ( 79 ), expel adult parasites from the gut ( 78 ), allow host survival in a setting where the immune response cannot clear the parasites ( 80 ), and/or mediate pathological fibrotic responses ( 81 ). Fibrosis has its origins in the wound-healing responses that must be required on an ongoing basis in animals chronically infected with pathogens that cause large amounts of tissue damage, such as most helminths ( 82 ).

In key ways, our understanding of type 2 immunity has lagged behind that of type 1 immunity (which encompasses Th1 cells) and even of the more recently defined Th17 cells and Tregs. In each of these cases, a set of cytokines made by cells of the innate immune system, often in response to the ligation of TLRs by a component of a pathogen, strongly promotes the development of defined CD4 + T cell lineages that in productive immune responses are appropriate to the particular situation. Thus, we know that IFN-γ and IL-12 can promote Th1 responses TGF-β, IL-6, and IL-23 can promote Th17 cell development and TGF-β alone plays a role in driving Treg development ( 83 , 84 ). Although we know that IL-4 and IL-13 are important for Th2 cell development, the production of these cytokines by innate immune cells seems to play little part in promoting the initiation of Th2 responses, and it has been clear that other crucial, yet ill-defined, conditions are important in this process. Recent work in type 2 immunity, largely involving excellent mouse models of human helminthiases and studies of allergy and asthma, which share with helminth infections an association with type 2 immune responses, has begun to shed light on some of these issues. For example, it is now clear that in addition to IL-4, IL-13, IL-5, IL-9, and IL-10, Th2 cells can make IL-25 and IL-31, and that these two cytokines can have crucial roles in promoting and/or regulating Th2 immune responses ( 85 , 86 ). There have also been substantial developments in understanding how the induction of type 2 immune responses is influenced by other cells, specifically through the recognition that thymic stromal lymphopoietin (TSLP), synthesized by epithelial cells, can condition dendritic cells to promote Th2 cell development ( 87 ). Lastly, there has been considerable progress in identifying genes that are expressed in response to stimulation by cytokines produced by Th2 cells and in defining the roles of the products of these genes as effectors of Th2 immunity as well as inducers and regulators of Th2 immune responses. Among these gene products are intelectins, arginases, resistin-like molecules (RELMs), and chitinases ( 88 ). Indeed, the coordinated production of members of the latter three classes of molecules by macrophages exposed to IL-4 and/or IL-13 is a feature of the “alternative activation” pathway executed by these cells during helminth infections. This is an area of great current interest ( 89 ), especially since recent reports have highlighted the protective effects of these cells during helminth infections ( 80 , 90 ).

How more recently discovered components of type 2 immune responses, such as IL-25 and IL-31, participate in host protective and immunopathologic processes is only just beginning to be examined using helminth infections in the mouse ( 91 – 94 ), and little has been done as of yet to explore these pathways in humans infected with helminths. This is a target area for emphasis in immunologic research on helminths in the near future, both in terms of increasing our understanding of the basic immunobiology of infections with these parasites, but also and more importantly, as a means to improve attempts directed toward the rational development of vaccines and immunotherapeutics.

Many helminthiases are chronic diseases, and it remains unclear how the Th2 immune response is regulated during the course of these long-term infections, during which antigen loads remain high and pathology is, at least in part, immune mediated ( 95 ). There is great interest in the possibility that Tregs play a role in these processes, perhaps in combination with unusual immunoregulatory helminth-derived products ( 96 ), and that such regulation underlies the reverse correlations between infection with a helminth and asthma, allergy, and certain autoimmune diseases that have been reported in a growing number of studies (something that is known as the hygiene hypothesis) ( 97 , 98 ). This remains a key area for further exploration, not only in the hope that understanding the regulatory response will allow intervention to enhance immune responses and decrease infection, but also because of the potential therapeutic use of helminth regulatory strategies for other disorders. Indeed, understanding how helminth infections regulate inflammation could promote new approaches for the development of therapeutics for a wide variety of inflammatory conditions.

Deciphering the genetic code of helminth parasites will allow us to understand the fundamental nature of these pathogens and the pathogenesis of the diseases that they cause. Genetic manipulation of helminth genomes, including transgenesis approaches, offers a means to determine the importance of specific helminth genes in disease pathogenesis, including those that could be targeted by novel therapeutic interventions.

Genomics. Helminth parasites have large complex genomes. In general, for both nematodes and platyhelminths, genome size ranges from approximately 50 to 500 Mb, with up to 20,000 protein-encoding genes. This genome size is comparable to that of insects. Several helminth parasites have become the focus of endeavors aiming to determine entire genome sequences. Information from these sequencing projects will facilitate determination of function and importance of genes or groups of genes in cellular and biochemical pathways and their role in the host-parasite relationship.

It is anticipated the complete genomes of Schistosoma mansoni and Schistosoma japonicum will be reported within the next year ( 99 ), following the release recently of reasonably comprehensive descriptions of their transcriptomes ( 100 , 101 ) and the proteome of S. japonicum ( 102 ). Schistosomes have sizeable genomes. The haploid genome of S. mansoi is estimated to be approximately 300 Mb, arrayed on seven pairs of autosomes and one pair of sex chromosomes ( 103 ). For comparison, this genome size is about ten times that of the genome of the malaria-causing parasite Plasmodium falciparum and one-tenth the size of the human genome. Schistosoma haematobium and S. japonicum, the other major schistosome species that parasitize humans probably have a genome size similar to that of S. mansoni, based on the similarity of their karyotypes ( 103 ). The S. mansoni genome is AT-rich (60%–70% AT in the euchromatin), replete with repetitive sequences. The approximately 13,000 protein-encoding genes include several, sometimes numerous, introns ranging in size from small to very large. The complexity of the proteome is expanded by the presence of single nucleotide polymorphisms, trans-splicing of a subset of the transcriptome, and alternative splicing of some genes (reviewed in ref. 104 ).

The draft genome sequence of the filarial nematode parasite Brugia malayi was reported recently ( 105 ). This was a landmark in human parasitology as it represented the first genome sequence of a parasitic helminth to be deciphered. B. malayi has a genome of 90 Mb, with a compliment of 14,500–17,800 protein-encoding genes. As in the free-living nematode Caenorhabditis elegans and many bacteria, a number of the B. malayi genes are organized into operons — units of transcription wherein several genes are regulated by the same promoter, thereby enabling the cell or organism to facilitate global gene expression in response to stimuli and environmental conditions.

The genome sequence of no parasitic nematode other than B. malayi has been completed. However, the draft genome sequence for B. malayi offers a broad foundation for rational intervention for both filariae and parasitic nematodes at large. Comprehensive analyses of the transcriptomes and genomes of a number of other medically important parasites, including hookworms and Trichinellaspiralis, are in progress ( 106 , 107 ). Through both genomics and more conventional biochemical methodologies, bioactive proteins with remarkable therapeutic potential have been identified and isolated from hookworms and other nematodes (reviewed in ref. 108 ). These include a novel factor VIIa/tissue factor inhibitor and a neutrophil inhibitory factor, which have undergone clinical trials with beneficial and promising outcomes for human thrombotic disease ( 109 – 112 ). These successes serve to emphasize that genomic studies of the parasitic helminths are likely to lead to new treatments for disease, including diseases not directly caused by helminth pathogens.

Gene manipulation by RNA interference. Until recently, gene manipulation approaches had not been seriously considered as tools to learn more about helminth-encoded proteins that might be intervention targets. This situation is now changing in response to the availability of genome sequences and other advances. RNAi technology has revolutionized investigation of the role and importance of genes in model organisms such as C. elegans. Methods developed for RNAi in C. elegans are now being deployed in schistosomes and some parasitic nematodes. Skelly and coworkers established the feasibility of experimental RNAi in S. mansoni by describing knockdown of the gut-associated cysteine protease cathepsin B by soaking larval schistosomes in dsRNA that effects RNAi ( 113 ). Krautz-Peterson et al. extended these studies by comparing and optimizing RNAi methodology ( 114 ). They reported that square-wave electroporation was dramatically more efficient than either soaking the parasites in an equivalent dsRNA dose or soaking them in an equivalent dsRNA dose in the presence of liposomes. They also demonstrated that small, interfering RNAs were as effective as longer dsRNAs. Other reports have confirmed the utility of RNAi in schistosomes to address gene function and importance ( 115 – 117 ). Indeed, RNAi has been used to demonstrate a crucial role for S. mansoni inhibin/activin (SmInAct a member of the TGF-β receptor family) in embryogenesis knockdown of SmInAct expression in eggs aborts their development ( 118 ). Given that eggs are responsible for the pathology of schistosomiasis, this protein is a potential therapeutic intervention target. As gene silencing by RNAi in schistosomes has been reported to deliver a specific effect, with no obvious or widespread nonspecific effects on nontarget genes, gene manipulation by RNAi might have wide applicability and promote functional schistosome genomics. The latter are expected to improve our knowledge of the function of schistosome gene products and lead to new interventions for treatment and control.

In contrast to work with schistosomes, RNAi in parasitic nematodes has had limited success or has been unsuccessful ( 119 , 120 ). Given the importance of RNAi in revolutionizing our understanding of the biology of the C. elegans, this overall lack of success for parasitic nematodes has so far been a disappointment for the molecular helminthology community. The physiological basis for the poor performance of RNAi in parasitic nematodes might relate to an absence of pivotal RNAi pathway components, as evidenced by the absence in B. malayi of the gene encoding the Sid-1 membrane channel that is involved in dsRNA uptake ( 105 , 121 ).

Transgenesis. Gain-of-function approaches with reporter transgenes, for example transgenes encoding either jellyfish GFP or firefly luciferase, have also been investigated in parasitic worms. Monitoring the expression of the reporter protein provides information on the progress of the transgenesis procedures. In parasitic nematodes, reporter gene activity driven by exogenous and endogenous gene promoters has been demonstrated in B. malayi, S. stercoralis, and Parastrongyloides trichosuri ( 122 – 124 ). In addition, heritable transmission of plasmid-based transgenes has been reported ( 123 , 124 ). Similar findings have been described in schistosomes, and stage- and tissue-specific expression of schistosome genes has been investigated using reporter transgenes driven by the promoters of schistosome genes, including cathepsin L ( 125 ). Recently, Brindley and coworkers have described somatic transgenesis of S. mansoni facilitated by either the piggyBac transposon ( 126 ) or the murine leukemia retrovirus ( 127 ), including the first demonstration of integration of reporter genes into the chromosomes of a parasitic worm.

Proteomics, glycomics, and metabolomics. Proteomic analyses in parasitic helminths are not as advanced as genomic or transcriptomic studies, but these aspects, along with glycomics and metabolomics, have now begun to be addressed. For example, proteomic analysis of the tegument of adults, the excreted and secreted products of adults, and the egg shells of S. japonicum and S. mansoni have yielded several thousand proteins, many of which have been putatively identified and many of which are much more closely related to the orthologous host proteins than to orthologs of invertebrates ( 102 , 128 ). Proteomic investigations have also revealed differences between the secretome of Trichinella spiralis and that of Trichinella pseudospiralis ( 129 ) as well as the plasticity of the proteome of gut-dwelling nematodes in response to immunological pressure ( 130 ). Glycomics will provide information about the glycan structures of helminths that are known to mediate and modulate host immunological responses to these parasites ( 131 , 132 ). Moreover, techniques from developmental biology and other disciplines, such as whole mount in situ hybridization (WISH) and gene microarrays, have now been established as crucial tools for investigating the function of helminth genes and proteins ( 133 – 135 ).

Beginning with the widespread use of the drug diethylcarbamazine for the treatment of LF in China during the 1970s, the mass treatment of human populations with anthelminthic drugs, known as mass drug administration (MDA), has been a major approach to controlling human helminthiases in developing countries ( 13 ). During the late 1980s, the first public-private partnership was formed to provide MDA of ivermectin to African populations at risk for onchocerciasis ( 13 ), and since then the mainstay of global worm control has been MDA of anthelminthic drugs through the activities of public-private partnerships, using either drugs donated by multinational corporations or low-cost generic drugs (Table 2). An important stimulus for these partnerships has been a series of resolutions adopted at the World Health Assembly — the major decision-making body for the WHO, which meets annually and is attended by delegates from each member nation — calling for MDA to control or eliminate one or more helminth infections of global importance. Since 2006, several partnerships committed to MDA have formed an alliance, which is known as the Global Network for Neglected Tropical Diseases and aims to increase efficiencies and produce economies of scale by delivering a package of drugs that simultaneously targets the six most common human helminthiases (ascariasis, trichuriasis, hookworm, schistosomiasis, LF, and onchocerciasis) as well as trachoma ( 13 ). Because of its low cost and cost savings, integrated helminth control has become highly attractive to both global policy makers and donors.

Major global helminthic disease control initiatives

In resource-poor settings with a substantial burden of helminthiases, it has become a common practice during MDA to treat individuals regardless of whether or not they are currently infected with the disease-causing parasitic worm. However, based on a mixed legacy of relying on drugs to control or eliminate a widespread infectious disease, such as malaria, there are concerns that emerging drug resistance or other factors could derail global efforts to implement MDA, integrated or otherwise ( 13 ). These concerns, together with a need to better understand a number of fundamental clinical and epidemiological aspects of human helminth infections as well as their interactions with geographically overlapping coinfections (e.g., malaria and HIV/AIDS) have created an urgency for stepped up clinical research activities as they relate to large-scale helminth control. Such activities have focused around three major areas: first, a reexamination of the health impact of human helminthic infections, with particular interest in the effects of mono- and polyparasitism on childhood growth and development as well as their effects on pregnancy and birth outcomes ( 63 , 136 – 140 ) second, large-scale monitoring and evaluation of MDA and integrated control, along with operational research with goals to improve the access of populations to anthelminthic drugs and to monitor for possible drug resistance ( 141 – 145 ) and third, the development of new tools to control helminth infections, that is, drugs, diagnostics, and vaccines ( 19 , 146 ).

For purposes of MDA and integrated control efforts, current synthesis of the available study data has culminated in a recently issued set of WHO guidelines ( 147 ). Parallel studies are examining the added benefits of micronutrient supplementation, particularly in combating the anemias associated with hookworm and schistosomiasis ( 148 , 149 ). Other studies are specifically examining the impact of infection among women who are pregnant and women of child-bearing age, risk groups who are often excluded from MDA because of fears of fetal toxicity ( 136 , 150 , 151 ), or they are examining the early developmental effects of helminthic infections among preschool children ( 152 ). Despite the evident success of MDA, limitations have been observed in the effectiveness of treatment in some field settings, and concern has been raised about the potential for emergence of resistance to the mainstay drugs of MDA programs, including the benzimidazole anthelminthic, used predominantly to combat soil-transmitted helminth infections, and ivermectin, which is used to combat filarial infections ( 146 , 153 – 158 ). However, with the exceptions of β-tubulin as a biomarker to determine nematode resistance to the benzimidazoles mebendazole and albendazole ( 159 ) and possibly ABC transporters and β-tubulin as biomarkers for determining resistance to ivermectin and other macrocyclic lactones ( 160 ), we lack robust biomarkers for detecting resistance to most anthelminthic drugs.

Despite the remarkable successes of MDA programs, disease elimination is often not obtained in highly endemic areas, and research on new drugs (and means for their successful implementation) is clearly needed to maintain and expand effective control. In the coming decade, the mining of newly completed helminth genomes should help to facilitate the discovery of new anthelminthic drugs. In the meantime, recent animal and clinical studies have documented the efficacy of artemether compounds for treating the early phases of schistosome infection ( 161 ) and a new broad-spectrum agent known as tribendimidine for treating soil-transmitted helminth infections ( 162 ). New classes of cysteine protease inhibitors are being developed as anthelminthic and antiprotozoal drugs ( 163 ), and other studies have indicated the efficacy of triclabendazole for infection with the difficult to treat liver fluke Fasciola hepatica ( 164 , 165 ). Human and animal studies also suggest that tribendimidine will prove effective against food-borne flukes ( 166 ) and the drug moxidectin might become an alternative to ivermectin for the treatment of filarial infections ( 167 ). Finally, based on the observation that the filarial parasites Wuchereria bancrofti and Onchocerca volvulus harbor bacterial endosymbionts of the genus Wolbachia and depend on these endosymbionts for normal metabolic and reproductive activities, there is excitement about the development and use of antibiotics to target adult filarial worms ( 168 ). This is of particular importance because to date there is no effective drug that targets the adult stage of these parasitic worms.

In parallel with drug discovery efforts are two anthelminthic vaccine development efforts, each conducted by a dedicated product-development partnership. For hookworm, the high rate of drug failure for single-dose mebendazole as well as rapid reinfection and the possible emergence of drug-resistant parasites have stimulated efforts by the Human Hookworm Vaccine Initiative to develop a bivalent vaccine comprised of recombinant hookworm vaccine antigens that target the infective larval stages and adult blood-feeding stages ( 146 , 169 , 170 ). Currently, one larval antigen is being evaluated in a phase 1 clinical trial in a region of Brazil that is endemic for hookworm and a second adult hookworm antigen is about to enter into clinical trials ( 170 ). Related antigens are also being used to develop recombinant onchocerciasis vaccines ( 171 ). In addition, the Institut Pasteur is conducting clinical trials in sub-Saharan Africa using a recombinant vaccine (encoding a glutathione S-transferase) to protect against infection with S. haematobium ( 172 ). A surface protein encoding a novel tetraspanin is also awaiting early development as a vaccine to protect against infection with S. mansoni ( 173 ). Ultimately, it is anticipated that anthelminthic vaccines are likely to be used alongside drugs in an integrated program linking vaccination with chemotherapy ( 146 , 174 ).

The recent developments in molecular and medical helminthology could relatively soon be translated into a new generation of anthelminthic therapeutics. Based on advances in schistosome genomics, a family of promising schistosome vaccine antigens has already been identified ( 173 ) and ultimately could be formulated into a schistosomiasis vaccine. Such a vaccine could be used together with a hookworm vaccine. At the same time, the recently revealed importance of Wolbachia endosymbionts is helping to launch new drug discovery efforts for the treatment of LF and onchocerciasis as well as treatment programs based on either existing or new antibiotics ( 168 ). The recent completion of the filarial genome might soon yield additional drug targets ( 105 ). Revelations within the last five years about the impact of helminthiases on the transmission of the pathogens that cause malaria and HIV/AIDS and on the progression of these diseases ( 12 ), suggest that deworming and other large-scale anthelminthic measures might promote important “back-door” approaches for controlling them ( 12 , 13 ).

At the same time, our enthusiasm for seeing helminthological science translate into new interventions needs to be tempered because of some sobering elements. First, despite these new advances, overall, we are still at a relatively nascent stage of helminth translational research and development. The development of in vitro methodologies and high throughput technologies for studying helminths has not, for the most part, kept up with the generation of parasitic helminth genomic and other bioinformatic databases. Until there is greater investment of scientific horsepower and funds into fundamental helminthology research, we are still a way off using the reverse genomic and vaccinology approaches that have benefited modern bacteriology. Second, because worm infections occur almost exclusively among the poorest people of the world, there are no market incentives for mining bioinformatic databases for anthelminthic drug and vaccine discovery. Therefore, unless there is financial innovation for the poor or a paradigm shift by the multinationals in orphan drug development for developing countries, we must either rely on the existing veterinary pipeline of new anthelminthics feeding into the human pipeline or we need to expand the role of nonprofit product-development partnerships ( 4 , 13 , 146 ). Critical to the success of new anthelminthic interventions is likely be North-South partnerships with so-called “innovative developing countries,” i.e., economically disadvantaged nations endemic for neglected tropical diseases such as Brazil, China, and India, which have nonetheless achieved a high level of biotechnological sophistication ( 175 ). Third, until vaccines or new drugs are developed for human helminthiases, we must rely on a tiny pharmacopeia of existing drugs. Currently, integrated control of the six most common human helminthiases, which affect approximately one billion people in developing countries, depends on the availability and effectiveness of just four drugs — albendazole, mebendazole, praziquantel, and ivermectin. Adequate resources need to be set aside for the development of genetic resistance markers and for careful monitoring and evaluation of large scale programs if we are to preserve these agents as public health control tools. Finally, in the absence adequate of new support for helminthology training, we risk losing a generation of whole-organism scientists who have the skills to study both the parasites and the diseases they cause. Because of the enormous benefits in human capital that would result from investing in the study of fundamental and translational helminthology and because access to anthelminthic interventions has now been recognized as a fundamental human right ( 176 ), we believe that now, more than ever, the scientific and global public health communities should address the neglected status of the helminthiases and prioritize their study.

The authors acknowledge with gratitude the editorial assistance of Sophia Raff and Julie Ost. The authors are supported by grants from the Sabin Vaccine Institute and the Bill and Melinda Gates Foundation (P.J. Hotez and J.M. Bethony), Geneva Global (P.J. Hotez), and National Institute of Allergy and Infectious Diseases, NIH (P.J. Hotez, P.J. Brindley, C.H. King, E.J. Pearce, and J.M. Bethony).

Nonstandard abbreviations used: LF, lymphatic filariasis MDA, mass drug administration.

Conflict of interest: P.J. Hotez is an inventor on two international patent applications for a hookworm vaccine. P.J. Hotez and J.M. Bethony received funding from the Bill and Melinda Gates Foundation through the Sabin Vaccine Institute. The remaining authors have declared that no conflict of interest exists.

Reference information: J. Clin. Invest.118:1311–1321 (2008). doi:10.1172/JCI34261.


15.20: Helminthic Diseases of the Digestive System - Biology

Digestive System Infections

  • The digestive system is often divided into two sections: gastrointestinal (GI) system is the tubular path from the mouth to the anus.
  • The second section is referred to as the accessory digestive organs. The accessory digestive organs are responsible for either grinding the food (teeth) or injecting digestive secretions (pancreas).
  • The internal surface of the small intestine has millions of hair like projections called villi.
  • Intestinal peristalsis moves undigested and unabsorbed food from the small intestine into the large intestine and colon.
  • The colon finishes the absorption of nutrients and water.
  • Feces is the remaining undigested material which is eliminated via the anus. As much as 40% of the fecal volume is bacteria.
  • Antigenic drift and antigenic shift primary mechanism for production of new strains of flu.
  • The membrane covering most of the GI tract and protects it is called the peritoneum.
  • Accessory digestive organs include tongue, teeth, liver, gallbladder and pancreas.
  • The esophagus, stomach and small intestine (duodenum) are almost free of microbes.
  • Gastroenteritis is an inflammation or irritation of the lining in the: stomach or intestines.
  • Bacteria growing on the tooth’s surface make acid which then destroys the enamel.
  • Gingivitis is an inflammation of the gums surrounding the teeth.
  • Bacterial gastroenteritis is an inflammation of the stomach and intestines caused by bacteria or bacterial toxins.
  • Bacterial pathogens of the gastrointestinal tract, attach and bind to the surface, proliferate and transmit disease. These microbes develop mechanisms that optimize these characteristics while minimizing the host’s ability to destroy them.
  • Viral gastroenteritis is an intestinal infection caused by several different viruses.
  • Hand washing is the single most important way to avoid infection of the digestive system
  • Fecal Oral route is a major cause of digestive diseases due to infection.
  • The human heart is a muscle with four chambers.

The digestive system is made up of a series of hollow organs that are joined together by a flexible tube that extends from the mouth to the anus. The tube has a lining called the mucosa. In the mouth, stomach, and small intestine, the mucosa has small glands that make digestive juices used to break down foodstuffs. The mucosa is a target of many infectious agents. It is the site that bacteria, viruses, protozoa and worms attach to in order to replicate and invade the rest of the body.
The liver and the pancreas also contribute digestive juices that are secreted to the intestine.
The digestive system will be presented in order to better understand how infections occur within it and how symptoms arise from specific diseases. Bacteria and virus are prokaryote organisms that can infect the digestive system and a select few will be presented that represent a significant impact on human health. Heminthic (worms) and protozoan infections will be presented that represent eukaryote infectious agents of the digestive system.

  • The structure of the digestive system is schematically outlined.
  • Pathogenic bacteria, viruses, protozoa, helminthics and toxins in the digestive system.
  • Animations of pathogen Life Cycles
  • Concept map showing inter-connections of new concepts in this tutorial and those previously introduced.
  • Definition slides introduce terms as they are needed.
  • Visual representation of concepts
  • Animated examples—of concepts are used to step wise breakdown a concepts.
  • A concise summary is given at the conclusion of the tutorial.

Structure and function of the gastrointestinal tract.
Structure and function of the accessory Digestive Organs.
Bacterial, viral and protozoan diseases of the digestive system.
Helminthic infestations of the intestinal tract.
The microbiota of the digestive system is not spread evenly throughout.

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Teach Yourself Microbiology Visually in 24 Hours

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Digestive Phases

The response to food begins even before food enters the mouth. The first phase of ingestion, called the cephalic phas, is controlled by the neural response to the stimulus provided by food. All aspects—such as sight, sense, and smell—trigger the neural responses resulting in salivation and secretion of gastric juices. The gastric and salivary secretion in the cephalic phase can also take place due to the thought of food. Right now, if you think about a piece of chocolate or a crispy potato chip, the increase in salivation is a cephalic phase response to the thought. The central nervous system prepares the stomach to receive food.


Critical Thinking

Two periods of acute disease are the periods of illness and period of decline. (a) In what way are both of these periods similar? (b) In terms of quantity of pathogen, in what way are these periods different? (c) What initiates the period of decline?

In July 2015, a report (C. Owens. “P. aeruginosa survives in sinks 10 years after hospital outbreak.” 2015. http://www.healio.com/infectious-disease/nosocomial-infections/news/online/%7B5afba909-56d9-48cc-a9b0-ffe4568161e8%7D/p-aeruginosa-survives-in-sinks-10-years-after-hospital-outbreak) was released indicating the gram-negative bacterium Pseudomonas aeruginosa was found on hospital sinks 10 years after the initial outbreak in a neonatal intensive care unit. P. aeruginosa usually causes localized ear and eye infections but can cause pneumonia or septicemia in vulnerable individuals like newborn babies. Explain how the current discovery of the presence of this reported P. aeruginosa could lead to a recurrence of nosocomial disease.

Diseases that involve biofilm-producing bacteria are of serious concern. They are not as easily treated compared with those involving free-floating (or planktonic) bacteria. Explain three reasons why biofilm formers are more pathogenic.

A microbiologist has identified a new gram-negative pathogen that causes liver disease in rats. She suspects that the bacterium’s fimbriae are a virulence factor. Describe how molecular Koch’s postulates could be used to test this hypothesis.

Acupuncture is a form of alternative medicine that is used for pain relief. Explain how acupuncture could facilitate exposure to pathogens.

Two types of toxins are hemolysins and leukocidins. (a) How are these toxins similar? (b) How do they differ?

Imagine that a mutation in the gene encoding the cholera toxin was made. This mutation affects the A-subunit, preventing it from interacting with any host protein. (a) Would the toxin be able to enter into the intestinal epithelial cell? (b) Would the toxin be able to cause diarrhea?

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    • 2021 Jun 13 Could hosting parasitic worms prevent ageing? Dr Tom Mules interviewed for Sunday Morning on Radio New Zealand. (Also see, Could there be dog hookworm larvae in NA doses from providers?)
    • 2021 May 5 Hookworms to Heal Dr Tom Mules interviewed for Sunday Morning on Radio New Zealand. (Also see, Could there be dog hookworm larvae in NA doses from providers?)
    • 2019 Jul 24 Professor Graham Le Gros: Hookworms could have huge potential for health - Simon Barnett and Phil Gifford, NewstalkZB. (Also see Graham Le Gros and helminthic therapy.)
    • 2019 Jul 22 Human hookworms: potential to help inflammatory diseases - Jesse Mulligan, Radio New Zealand. (Also see Graham Le Gros and helminthic therapy.)
    • 2018 Mar Guidelines for Self-Administering Helminth Therapy (using HDC) - Michael Ruscio interviews Dr Nancy O'Hara, Dr. Ruscio Radio
    • 2018 Jan 27 Lessons from parasitic worms Kim Hill interviews Dr Kara Filbey for Saturday Morning, Radio New Zealand
    • 2018 Jan 8 Worm Therapy with Dr. William Parker: Rational Wellness Podcast 038 - Ben Weitz DC interviews William Parker
    • 2018 Jan Healthy Worms to Repair the Gut & Immune System - Michael Ruscio interviews Garin Aglietti, Dr. Ruscio Radio
    • 2017 Dec Are Worms the Next Probiotic? - Michael Ruscio interviews William Parker, Dr. Ruscio Radio
    • 2017 Oct 13 Can We Worm Our Way Into Better Health? Crowd Science, BBC World Service
    • 2017 June 5 Hookworms against diabetes! - Norman Swan interviews Robyn McDermott on Health Report, Radio National
    • 2016 Dec 28 Undark Podcast #10: The Helminth Hackers - David Corcoran interviews Leah Shaffer
    • 2016 Oct 6 Hookworms to treat coeliac disease? - Nights, Radio New Zealand
    • 2016 July 1 The Re-education of the Immune System - (9.00 to 42.00 minutes) To the Point, KCRW, with Moises Velazquez-Manoff, Dave Elliot, Mikael Knip and Shabaana Khader. Click on the Mini-Player button at top right, to jump straight in at 9.00 minutes.
    • 2015 Nov 2 The Enemy of my Enemy, Part 2: A Can of Worms - Sam Ancona Esselmann interviews Moises Velasquez Manoff for Carry the One Radio
    • 2015 Jun 19 The Future of Healing the Immune System: Biome Reconstitution - Neil Nathan interviews William Parker for The Cutting Edge of Health, and Wellness Today
    • 2012 Jan 25 Got Bugs! - William Parker, AutismOne
    • 2010 Apr 2 An update on hookworms - Pat Walters, Radiolab
    • 2010 Apr 2 Enemy Camp 2012: Act Three. As The Worm Turns - This American Life
    • 2009 Sept Sculptors of Monumental Narrative - Dickson Despommier and Pat Walters, Radiolab
    • 2020 Nov 3 The Probiotic Planet: Using Life to Manage Life - Jamie Lorimer
    • 2018 Dec 1 Hookworms for Autoimmune Disease: Parabiotics and the Rise of Antifragile Medicine - Steve Nenninger
    • 2017 Worm Booklet: Treating Autoimmune Diseases with Hookworms - Steve Nenninger
    • 2017 Mar 11 The Worms Inside Me: My experiment with helminthic therapy - Beth Anderson
    • 2016 Evolutionary Thinking in Medicine: From Research to Policy and Practice. Ed: Alvergne, Jenkinson and Faurie. This book, which is available from Amazon, contains a chapter by Jorge Correale (“Helminth Immunoregulation and Multiple Sclerosis Treatment”) and one by Gabriele Sorci, et al., entitled, “ Microbes , Parasites and Immune Diseases” (page 211 in Part VI: Immunology). This latter chapter is available, in full, as a FREE download via a link in the Table of Contents on this page.
    • 2015 Dec 1 Body by Darwin: How Evolution Shapes Our Health and Transforms Medicine - Jeremy Taylor. There’s an extended excerpt of this book on Live Science, here.
    • 2012 Sept 4 An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases - Moises Velasquez-Manoff. This book has been reviewed by Donna Beales.
    • 2011 Jun 21 The Wild Life of Our Bodies: Predators, Parasites, and Partners That Shape Who We Are Today - Rob Dunn
    • 2009 Sept 18 The Hygiene Hypothesis and Darwinian Medicine (Progress in Inflammation Research) Edited by Graham Rook
    • 2007 Apr 2 Riddled with Life: Friendly Worms, Ladybug Sex, and the Parasites That Make Us Who We Are - Marlene Zuk

    Microbiology > Gutsy: The Gut Microbiome Card Game

    Download Cards & Instructions

    Each of us has a community of microbes that lives in our digestive system. Scientists call this community our gut microbiome. It plays many important roles in our bodies, like helping to digest food, regulating our immune system, preventing diseases, and even affecting our appetites and our emotions.

    Many things, like what we eat and drink, who we interact with, and the medicines that we take, influence the kinds of microbes that live in our gut. A diverse microbiome is good for our health!


    15.20: Helminthic Diseases of the Digestive System - Biology

    Digestive System Infections

    • The digestive system is often divided into two sections: gastrointestinal (GI) system is the tubular path from the mouth to the anus.
    • The second section is referred to as the accessory digestive organs. The accessory digestive organs are responsible for either grinding the food (teeth) or injecting digestive secretions (pancreas).
    • The internal surface of the small intestine has millions of hair like projections called villi.
    • Intestinal peristalsis moves undigested and unabsorbed food from the small intestine into the large intestine and colon.
    • The colon finishes the absorption of nutrients and water.
    • Feces is the remaining undigested material which is eliminated via the anus. As much as 40% of the fecal volume is bacteria.
    • Antigenic drift and antigenic shift primary mechanism for production of new strains of flu.
    • The membrane covering most of the GI tract and protects it is called the peritoneum.
    • Accessory digestive organs include tongue, teeth, liver, gallbladder and pancreas.
    • The esophagus, stomach and small intestine (duodenum) are almost free of microbes.
    • Gastroenteritis is an inflammation or irritation of the lining in the: stomach or intestines.
    • Bacteria growing on the tooth’s surface make acid which then destroys the enamel.
    • Gingivitis is an inflammation of the gums surrounding the teeth.
    • Bacterial gastroenteritis is an inflammation of the stomach and intestines caused by bacteria or bacterial toxins.
    • Bacterial pathogens of the gastrointestinal tract, attach and bind to the surface, proliferate and transmit disease. These microbes develop mechanisms that optimize these characteristics while minimizing the host’s ability to destroy them.
    • Viral gastroenteritis is an intestinal infection caused by several different viruses.
    • Hand washing is the single most important way to avoid infection of the digestive system
    • Fecal Oral route is a major cause of digestive diseases due to infection.
    • The human heart is a muscle with four chambers.

    The digestive system is made up of a series of hollow organs that are joined together by a flexible tube that extends from the mouth to the anus. The tube has a lining called the mucosa. In the mouth, stomach, and small intestine, the mucosa has small glands that make digestive juices used to break down foodstuffs. The mucosa is a target of many infectious agents. It is the site that bacteria, viruses, protozoa and worms attach to in order to replicate and invade the rest of the body.
    The liver and the pancreas also contribute digestive juices that are secreted to the intestine.
    The digestive system will be presented in order to better understand how infections occur within it and how symptoms arise from specific diseases. Bacteria and virus are prokaryote organisms that can infect the digestive system and a select few will be presented that represent a significant impact on human health. Heminthic (worms) and protozoan infections will be presented that represent eukaryote infectious agents of the digestive system.

    • The structure of the digestive system is schematically outlined.
    • Pathogenic bacteria, viruses, protozoa, helminthics and toxins in the digestive system.
    • Animations of pathogen Life Cycles
    • Concept map showing inter-connections of new concepts in this tutorial and those previously introduced.
    • Definition slides introduce terms as they are needed.
    • Visual representation of concepts
    • Animated examples—of concepts are used to step wise breakdown a concepts.
    • A concise summary is given at the conclusion of the tutorial.

    Structure and function of the gastrointestinal tract.
    Structure and function of the accessory Digestive Organs.
    Bacterial, viral and protozoan diseases of the digestive system.
    Helminthic infestations of the intestinal tract.
    The microbiota of the digestive system is not spread evenly throughout.

    See all 24 lessons in Anatomy and Physiology, including concept tutorials, problem drills and cheat sheets: Teach Yourself Microbiology Visually in 24 Hours


    Watch the video: L4 Digestive System Diseases Part 2 (January 2022).