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Cosmopolitan but much more common in the tropics. The eggs pass on to the ground via the faeces. Fertilised eggs require 10 to 40 days in the outside world to mature before they become infectious. Direct self-infection is thus ruled out. Once they are mature the eggs are taken up once more (faeco-oral transmission) via infected food, drink, dirty hands or fingernails. In the intestine small larvae emerge from the eggs, and these bore through the intestinal wall. In this way they reach the blood (portal vein system). They are carried with the blood, through the liver to the lungs (lung passage occurs 3 to 14 days after ingestion). In the lungs the larvae make their way to the bronchial lumen and climb via the respiratory branches into the throat. They are swallowed, and in this way they again reach the intestine. They grow into adult worms in the jejunum. They do not damage the intestinal wall. Egg laying begins two months after infection. The adult worm survives on average for 1 year. The creatures reach 15 to 40 cm. There is no animal reservoir. Occasionally infections with Ascaris suum occur (parasite of pigs). This worm resembles Ascaris lumbricoides very closely and some think the parasites are identical.
This is the most common worm infection in humans. It has a cosmopolitan distribution. Children are most often infected. The eggs are very resistant, which makes it possible in certain circumstances for them to survive for a long time in the outside world. The number of eggs which can be found in the soil is a measure of the hygiene standard and degree of sanitation of an area (faecal pollution of the ground).
The vast majority are asymptomatic. Some people have various forms of intestinal discomfort or allergic symptoms. Serious complications are rare. Nevertheless, in view of the large number of infected persons, the morbidity and mortality should not be disregarded.
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Lung passage symptoms
The larvae undergo lung passage. This produces symptoms of mild to severe cough, dyspnoea, thoracic pain, some fever. The clinical picture is similar to asthma or pneumonia. On chest X-ray migratory infiltrates are observed. Eosinophilia is present. This whole phenomenon is called Loeffler's syndrome. The sputum contains many eosinophils, Charcot-Leyden crystals and sometimes also larvae. The symptoms last for some days or weeks.
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Obstruction of hollow organs
When numerous adult worms are present, they may form a tangle and cause mechanical intestinal obstruction manifested by a bloated abdomen, increased peristalsis with clangour, colicky pain, vomiting (bile, faecaloid) and dilated intestinal lumen on an abdominal X-ray. Migration into the biliary tract may lead to biliary obstruction (cholestasis) with possibly infection (cholangitis, liver abscess, pancreatitis). Sometimes there is migration to the appendix with inflammation (appendicitis). Sometimes an adult Ascaris is present in vomitus. Occasionally, an adult can penetrate the lacrimal duct. Recent surgical intestinal sutures can be breached by an inquisiting adult Ascaris, leading to bowel perforation and peritonitis. Infection with Ascaris lumbricoides also plays a role in the development of pigbel (necrotising enteritis, see chapter on diarrhoea).
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Malnutrition
Ascaris itself does not cause malnutrition. In borderline malnutrition the presence of numerous worms can have a negative effect, however. It is also important to know that many patients suffer from anorexia. Humans infected with Ascaris are best treated before they undergo intestinal surgery. Migration of an Ascaris through an intestinal suture line is a serious event. Pre-operative deworming is advised in endemic areas.
Since an adult female lays up to 200,000 eggs per day, as a rule no concentration technique is necessary to detect eggs in the faeces. If infection is solely with one or more male worms, then of course no eggs will be detected. During lung passage there is significant eosinophilia. After lung passage there is no longer appreciable eosinophilia. X-ray of the intestine may show one or more adult worms. The worm forms a long, thin dark area if using barium contrast. Sometimes a central longitudinal radio-opaque line can be seen; this is the intestinal tract of the worm. Such a line is absent in tapeworms. An ultrasound of the pancreas (Wirsung duct) or of the biliary tract and gallbladder, sometimes shows an ectopic migrating adult Ascaris.
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Cosmopolitan. The eggs are eliminated with the faeces. Infection is via the oral route (direct anus-hand-mouth as in Enterobius or after maturation in the outside world). In one week it becomes an adult worm measuring 3 to 5 cm. Egg laying begins 2 months after infection. The adult worm has a thin whip-like head with which it buries itself in the mucosa of the large intestine. The worm survives for several years. The parasite is possibly the same as Trichuris suis, a parasite of pigs.
Most infected humans remain asymptomatic. Only in severe infections (> 1000 worms; >10,000 eggs per gram of faeces) do symptoms occur: these include diarrhoea (dysentery type), malnutrition or anaemia. In undernourished children with chronic diarrhoea and tenesmus there is sometimes prolapse of the rectum, in which the worms can be seen on the prolapsed mucosa.
Diagnosis is based on faecal examination. No concentration technique is necessary for clinically relevant infections. Sometimes the worms can be seen on the rectal mucosa (rectoscopy or during anal prolapse).
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This parasite is cosmopolitan. There is no intermediate host. Infection is via ingestion of eggs. They accumulate in the ileocaecal region. After copulation the males die. The females migrate via the colon to the anus and lay their eggs chiefly at night, as they creep over the peri-anal skin. This explains the nightly itching. In rare cases there is vaginal itch because the females can also hide there. Sometimes the parasites are found in the appendix. The eggs must be sought not only in the faeces, but also on the peri-anal skin (using Scotch tape or other transparent sticky tape). In women the eggs may be found in the urine, due to contamination. Sometimes a small number of adult worms are found in the vagina. Apart from the itch there are few problems. There is a possible association between infection with Enterobius and infection with the pathogenic amoeboflagellate, Dientamoeba fragilis. Enterobius gregorii is also a parasite of humans. Infections with this nematode follow the same course as Enterobius vermicularis.
Mebendazole 100 mg (Vermox®), to be repeated after 1 and 2 weeks. Albendazole is also effective. Since the eggs can adhere to all objects e.g. underclothing, sheets and so on, these should be changed. In a family it is best to treat all the family members, even those without symptoms. Vanquin® (pyrvinium) may also be used as an alternative to mebendazole. The faeces may discolour red.
There are two important hookworms: Necator americanus and Ancylostoma duodenale. [L. necator = murderer; Gr. ancylo = hook , stoma = mouth]. [There are a few minor hookworms which are of much less clinical importance and seldom cause infections with adult worms (e.g. Ancylostoma ceylanicum, A. caninum, A. malayanum, Cyclodontostomum purvisi). The status of Ancylostoma japonica, A. tubaeforme, Bunostomum phlebotomum and Necator argentinus is doubtful. Necator suillus and Uncinaria stenocephala can infect humans]. The adult worms are found in the small intestine. They measure approximately 1 cm. Adult hookworms survive for several years, Necator longer than Ancylostoma. A few weeks or months after infection eggs can be found in the faeces. Once the eggs arrive in the outside world with the faeces, they take one week to mature to infectious larvae. At first they are rod-shaped = rhabditiform, later thread-shaped = filariform. They may survive for weeks or months (at an optimal temperature and humidity for as much as 2 years). A soil with neutral pH is optimal for their development, as is shade and a sufficiently high temperature (23°C to 30°C is ideal). If the faeces mix with urine the eggs die. Frost, direct sunlight and a soil saturated with salt or water, are unfavourable for the development of the young parasites. Infection occurs via the mouth (A. duodenale) or via the skin (A. duodenale and N. americanus). If they enter through the skin, the young parasites have to pass through the lungs. A new dimension in the epidemiology of hookworm disease emerged when it was found that insufficiently cooked meat from paratenic hosts such as pigs, cattle, rabbits and sheep can be responsible for transmission. The adult hookworms bore a hole in the mucosa of the duodenum and the small intestine and suck blood. They adhere with hooked teeth in their mouth (Ancylostoma) or with two buccal cutting plates (Necator). A. duodenale sucks 5 to 10 times more blood than N. americanus (approximately 30 µl per day for Necator and 260 µl for Ancylostoma). It is estimated that the life span of adult worms is 5 to 15 years.
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Hypobiosis can occur in ancylostomiasis, although its importance is not clear. In hypobiosis, there is arrested development of migrating Ancylostoma duodenale larvae which migrate to the mammary glands and are secreted with the breast milk and infect the child. This is similar to that seen in Ancylostoma caninum which infects puppies in the same way.
8.5.3 Intestinal nematodes: hookworms, symptomsAt the site where the hookworms penetrate, the skin develops a rash and itch. This is shortlived and rarely noticed. Lung passage also rarely produces symptoms, but may be accompanied by Loeffler’s syndrome. There are few intestinal symptoms. Significant infections (>1000 worms) may result in pronounced anaemia. The haemoglobin level may sometimes be very low. Children and pregnant women in whom the iron supplies are already low, are particularly affected. Hypoproteinaemia may also occur and results in oedema. Protein deficiency also has consequences for the production of immunoglobulines. Some patients exhibit geophagia. In history, certain regions in the USA were famed for their "quality" clay and people would cover great distances to eat this iron-containing soil. In 1920 someone even began a mail order business to send clay to people with hookworms. * 8.5.4 Intestinal nematodes: hookworms, diagnosisThe eggs are found in fresh faeces. In an old stool (>24 hrs), the eggs will have hatched and rhabditiform larvae can be seen (Gr. rhabdos = rod). There is mild eosinophilia. Since an adult hookworm lays approximately 25,000 eggs per day, as a very rough estimate 100 eggs per gram of faeces corresponds to 1 adult worm.
8.5.5 Intestinal nematodes: hookworms, differential diagnosisDifferentiation from Strongyloides larvae is based chiefly on the difference in morphology of the "head" end. The mouth is elongated in ancylostomes and shorter in Strongyloides. Sometimes, if intestinal transit has been swift, eggs of Strongyloides stercoralis may be found in the faeces. These too should be differentiated from hookworm eggs. Ternidens deminutus is a nematode which is generally non-pathogenic, and which strongly resembles the hookworm (although Ternidens eggs are somewhat larger). Eggs of Oesophagostomum are morphologically identical to those of hookworms. Identification of the latter parasite can only be made by coproculture (identification of the typical stage 3 larvae).
8.5.6 Intestinal nematodes: hookworms, treatment
8.5.7 Intestinal nematodes: hookworms, preventionMass chemotherapy, together with health education and sanitary provisions are strategies which are often used. The most heavily infected individuals are the chief target group. Wearing footwear only partly prevents infection because oral infection is also important for Ancylostoma duodenale. Children are the main victims, rarely wear shoes and their whole skin is a portal of entry. *
Note 1: iron Iron is essential to humans for the transport of oxygen by haemoglobin, for myoglobin, for oxidative metabolism and for normal cell growth. Humans have three important proteins in connection with iron: transferrin, transferrin receptor and ferritin. A normal Western diet contains approximately 15 mg of iron per day, but only approximately 1 mg is taken up in the intestines. Chronic blood loss of 10-20 ml per day (contains 5-10 mg iron) leads to a negative iron balance. The iron status of humans can be determined in various ways: haemoglobin concentration, serum ferritin, serum iron and transferring, total iron binding capacity. The bone marrow may be stained for iron (gold standard). In modern centres it is also possible to determine soluble transferrin receptors which are increased in iron deficiency. The latter tests are sometimes used when there is confusion between the anaemia of chronic disease and iron deficiency anaemia. * Note 2: anaemia There is no single international definition of anaemia which applies world-wide. According to WHO anaemia must be considered in men if Hb is below 13 g%, in women and children between 6-12 years old if Hb is below 12 g% and in children younger than 6 years if it is below 11 g%. If the haemoglobin concentration falls moderately below this level, there is an increase in the intra-erythrocytic production of 2,3 diphosphoglycerate. This substance displaces the oxygen dissociation curve and increases oxygen release by up to 40%. The venous oxygen pressure will then be lower. If the haemoglobin falls below 7-8 g%, other adaptive factors begin to come into play. The cardiac output increases, both at rest and during exertion. There is tachycardia and hyperkinetic circulation with arterial and capillary pulsations and heart murmurs. If the myocardium is healthy and the onset of anaemia is slow, the combination of the 2,3 DPG effect and increased cardiac output permit adaptation to quite low haemoglobin concentrations. If the haemoglobin falls even further, this will result in symptoms such as pronounced tiredness, dyspnoea during exercise, palpitations, angina or claudication and finally high output heart failure. * Note 3: Hookworms in the New World Hookworms were found in the intestines of a 2800-year-old Peruvian mummy and thus were present before the time of European colonisation. It is rather puzzling how hookworms came to America. It is assumed that humans came to America via the Bering Strait between Siberia and Alaska during the Ice Age in the Pleistocene epoch. The worms would certainly have found it very difficult to maintain transmission in that cold climate. There must have been ‘cold sterilisation’. The eggs and larvae in the faeces would not have been able to survive in the frozen tundra. Possible explanations are the long life span of the worms, the ability of humans to cover long distances in a relatively short time, and possibly warm years during the Ice Age. * Note 4: Hookworms and Rockefeller In view of the enormous problem of hookworm disease in the South of the USA, in 1909 the American zoologist Charles W. Stilles was able to convince the millionaire John D. Rockefeller to give 1 million US$ to set up the Rockefeller Sanitary Commission for the Eradication of Hookworm Disease. These activities later led to the Rockefeller Foundation and the Rockefeller University.
8.6 Intestinal nematodes: oesophagostomiasis
Nematodes of the genus Oesophagostomum (O. bifurcum, O. aculeatum, O. stephanostomum) are widely distributed intestinal worms of monkeys. In some regions humans are accidental final hosts. The eggs are morphologically identical to those of hookworms. The larvae develop when the eggs land on the ground, progressing through stages 1-3 in 5 to 7 days. Probably a number of stage 3 larvae can resist long periods of dehydration. Stage 3 larvae are swallowed with food or water and penetrate the human intestinal wall. They then develop further, inducing abscesses with a necrotic content (helminthoma). These abscesses occur in the intestinal wall and mesenterium. As soon as the worms become adult, they return to the intestinal lumen where they attach to the mucosa and mate. Adult worms in the intestinal lumen do not cause illness. In veterinary medicine the illness is known as "pimply gut", which refers to countless abscesses under the serosa. In humans the worms cause severe intestinal lesions, including eosinophilic granulomas in the intestinal wall, abscesses and peritonitis. Epigastric or periumbilical masses may result. Foci of Oesophagostomum bifurcum infections occur commonly in a small part of West Africa (Northern Ghana and Togo). * Note: eosinophilic intestinal granulomata Sometimes during laparotomy a part of the intestine has to be removed, in which a worm or worm fragments are subsequently observed. There are several pathogens which can be present under these circumstances. In Central and South America Angiostrongylus costaricensis (syn. Parastrongylus costaricensis) causes eosinophilic granulomas in the ileocaecal area, but the eggs never appear in the faeces. Anisakiasis or herring-worm disease and Macracanthorhynchus infections (caused by a thorny-headed worm which normally has pigs as its final host, and which is transmitted by dung beetles) are other causes of eosinophilic gastro-intestinal granuloma. Gongylonema pulchrum may cause eosinophilic lesions of the mouth, gums or tongue. Dung beetles and cockroaches are the intermediate hosts of this nematode. Eustrongylides is a genus of pinkish red nematodes (25-150 mm long and 2 mm in diameter) which are transmitted via fish. The larvae can easily be observed with the naked eye during visual inspection of the fish, and this is one reason why infections are not common. Birds such as flamingos and herons are the usual final hosts. There is a significant risk of scepticaemia.
8.7 Intestinal nematodes: Strongyloides stercoralis8.7.1 Intestinal nematodes: Strongyloides stercoralis, summary
8.7.2 Intestinal nematodes: Strongyloides stercoralis, life cycleThe adult female worm, (average 2.7 mm) is found in the mucosa of the small intestine. Males cannot penetrate the intestinal mucosa and perish. Reproduction is asexual via parthenogenesis. The females lay eggs after 2-3 weeks, from which larvae are quickly produced. Initially the larvae are described as rhabditiform. These quickly develop into filariform (infectious) larvae. These larvae may:
* Some related parasites which seldom cause infections in humans:
* 8.7.3 Intestinal nematodes: Strongyloides stercoralis, symptomsMild infection is generally asymptomatic. In severe infections there may be intestinal discomfort or diarrhoea. During lung passage symptoms may occur, depending on the number of larvae. Auto re-infection via the skin may give rise to significant itching, chiefly peri-anal. Migration of the larvae in the skin leads to itching red swollen lines (on the rump, arms, face, etc.). These lines may occur anywhere and progress swiftly (up to 10 cm per hour). The swelling is the result of an urticarial reaction to the migrating larva (the larva itself is only 0.5 mm long). These lesion disappear spontaneously a few hours later, to reappear once more at a different site. * Immune suppression (especially HTLV-1 infection), achlorhydria, haematological malignancies including lymphoma, cytotoxic medication, nephrosis, burns and especially the long-term use of systemic corticoids, all increase the risk of hyperinfection. In such cases there is extensive multiplication with spread of the larvae to all organs. Symptoms include purpura-like skin lesions (initially often peri-umbilical), severe diarrhoea, pulmonary symptoms (dyspnoea, bronchospasms, bloody sputum) and meningo-encephalitis. Hyperinfection with Strongyloides stercoralis may be accompanied by bacterial septicaemia. Usually Gram-negative bacteria are involved. Mixed infection may occur. This probably depends on mechanical damage to the colon wall, adhesion of intestinal bacteria to the outside of migrating larvae and excretion of bacteria from the intestinal system of the parasite. Hyperinfection has a high mortality (75%). In chronic and persistent infection, an underlying infection with HTLV-1 or use of glucocorticoids should be considered. There have been fewer hyperinfections in AIDS patients than one would expect at first sight. * 8.7.4 Intestinal nematodes: Strongyloides stercoralis, diagnosis
The eggs hatch very rapidly in the intestine and are often not found in a faecal specimen. Larvae are found in the faeces. Often the numbers are not so high and a concentration technique, called the Baermann method, needs to be used. Larvae can also be detected via duodenal intubation. Differentiation from hookworm larvae is necessary. Eosinophilia is almost always present, except when immune suppression exists. A history of larva currens is suggestive of strongyloidosis and is enough to start treatment even if no larvae are found in the faeces. In hyperinfection larvae may be found in the sputum or in broncho-alveolar lavage fluid. The sputum must be regarded as infectious. If this sputum is cultured on blood agar, bacterial colonies can be seen which form a curvilinear pattern, reminiscent of a pearl necklace. This follows the migration of a larva on the agar plate, with translocation of the bacteria. * 8.7.5 Intestinal nematodes: Strongyloides stercoralis, therapyThiabendazole was used in the past, but had many side effects. Albendazole is only moderately effective. Mebendazole is not active. Ivermectin is easy to use and effective and at present is the first line treatment. If immunosuppression is present, the cure rate with ivermectin is lower, certainly if cortisone has been taken. It should be mentioned that there are parenteral ivermectin formulations for veterinary use. They are not (as yet) registered for use in humans, but anecdotal case reports mention success with them. Cyclosporin A is an immunosuppressive agent, which among other indications is used for transplant patients. It has an anthelmintic action on Strongyloides stercoralis. Transplant patients who take cyclosporin A have a greatly reduced risk of Strongyloides hyperinfection. In hyperinfection it is important not to forget to use antibiotics, in view of the risk of severe septicaemia. * 8.8 Pruritus caused by worms
8.9 Intestinal nematodes: Capillaria philippinensis8.9.1 Intestinal nematodes: Capillaria philippinensis, summary
8.9.2 Intestinal nematodes: Capillaria philippinensis, life cycleCapillaria philippinensis (synonym Calodium philippinensis, Aonchotheca philippinensis) is a nematode which causes severe infections. The parasite was discovered in 1960 in Luzon, an island in the Philippines. Subsequently is was also found in Thailand, Indonesia, Egypt, Japan, Taiwan, Korea and Iran. It is a parasite of fish-eating waterbirds. The infection occurs due to eating infected fish which live in fresh or brackish water. The larvae are found in the muscles of the fish. It is an intestinal nematode which has an intermediate host (most nematodes don’t). After developing to adult forms the parasites, which are 2 to 4 mm long, live in the mucosa of the small intestine. The worm is capable of multiplication in the human intestine (cf. Strongyloides). This phenomenon may lead to severe infection (high worm load) with chronic watery diarrhoea, malabsorption and cachexia. Ascites, pleural fluid and severe electrolyte imbalance including hypokalaemia may occur. The infection may sometimes be fatal.Do not confuse Capillaria philippinenisis with Capillaria hepatica.
8.10 Capillaria philippinensis, diagnosis, treatmentDiagnosis is made by means of faecal examination. Every infection must be treated promptly with mebendazole, 200 mg x 2 per day for 20 days. Albendazole may also be used. Cooking fish prevents the infection. Eating raw fish, however, is a culinary habit in many Asiatic countries and this is difficult to change.
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