Saturday, June 25, 2011

Human worm parasite infections

HUMAN HELMINTH INFECTIONS

INTRODUCTION

Helminthes (worms) are among the major parasites of humans and are classified under two phyla;
  1. Nemathelminthes ( Nematodes or Round worms)
  2. Platyhelminthes (Cestodes or tape worms and Trematodes or flukes)
Majority of helminthes that infect humans belong to the following three classes.
  1. Nematoda (round worms). They are elongated, cylindrical worms. The sexes are separate. A complete alimentary canal is present with some species having well developed buccal capsules. They possess a body cavity ( pseudocele)
  2. Cestoda (tapeworms). They are flattened tape-like segmented worms. Sexes are not separate, each segment having a set of male and female reproductive organs. Alimentary canal is absent. The head end possesses suckers, often with hooks. The body cavity is absent.
  3. Trematoda (flukes). They are flattened and leaf-like. Each fluke has a set of male and female reproductive organs (except blood flukes where sexes are separate). The alimentary canal is incomplete and there is no body cavity. They possess oral and ventral suckers.
Nematoda (round worms)
Trematoda (flukes)
Cestoda (tapeworms)

Roundworms (NEMATODES)

This is a large and highly successful group of organisms found living in all types of habitats. Some are important parasites of human and animals. The parasitic nematodes are remarkable being similar to each other but vary widely in size. They are cylindrical with unsegmented bodies and have false body cavities (pseudocoelomes). The multi-layered cuticle is non-nucleated and allows contraction and expansion of the body. Inner to the cuticle is the muscle layer. Among the major organs are the alimentary, excretory and the reproductive systems, which are suspended in the ‘body cavity’. They have separate sexes.

The cuticle is shed (moulting) four times during development from egg to adult worm. Some species have direct life cycles while others need intermediate hosts. Nematodes do not multiply in humans (except in the form of auto infection with Strongyloides). Parasitic nematodes of humans are found in various tissues such as subcutaneous, muscle, lymphatic tissue and in organs such as the intestinal tract.

Nematode parasites of humans

Small intestine
  1. Ascaris lumbricoides ( The large roundworm)
  2. Necator americanus (Hook worm)
  3. Ancylostoma duodenale (Hook worm)
  4. Strongyloides stercoralis (Thread worm)
  5. Trichinella spiralis (Trichina worm)

Large intestine
  1. Trichuris trichiura (Whip worm)
  2. Enterobius vermicularis (Pin worm)
Tissue nematodes
  1. Subcutaneous tissue (filarial worm, Dracanculosis and animal hookworm larvae)
  2. Muscle ( Trichinella spiralis)
  3. Lymphatics ( Filarial worm)
  4. Visceral organs (Toxocara)
  5. CNS ( Angiostrongylus cantonensis and Toxocara)
Infections due to other nematodes
  1. Dracunculus medinensis (Dracanculosis or Guinea worm disease)
  2. Trichinella spiralis (Trichinosis)
  3. Larva migrans
  • Cutaneous larva migrans
  • Visceral larva migrans

tapeworms (CESTODA)

They are flat, ribbon-like worms inhabiting the intestinal tract of vertebrates. Their bodies are formed of chains of segments (proglottids) of varying sizes and shapes. The whole chain is called strobila. At the anterior end is the scolex or the ‘holdfast’ organ which is used for the attachment of the worm to the intestinal mucosa. Suckers aid the attachment to the mucosa in some while others use sucking grooves. Hooks also help when present. Behind the scolex is the undifferentiated ‘neck’ region from which growth of new segments takes place continuously. The end of the worm is comprised of gravid (pregnant) segments. They have no alimentary canals and nutrition is getting through the cuticle of the segments. Each segment has male and female reproductive organs (testes, ovaries and uteri).

In the life cycle the larval stages are found in the intermediate hosts. Some have only one intermediate host while others have two intermediate hosts. In humans pathology is caused by either adult worms or by larval stages.

Cestodes parasites in human

Human infection due to adult worms
  1. Taenia saginata (beef tapeworm)
  2. Taenia solium (pork tapeworm)
  3. Hymenolepis diminuta (rat tapeworm)
  4. Hymenolepis nana (The dwarf tapeworm)
  5. Diphyllobothrium latum (fish tapeworm)
  6. Dipylidium caninum (cat/dog tapeworm)
  7. Bertiella studeri (monkey tapeworm)
Human infection due to larval stages
  1. Cysticercosis cellulose (Cysticercosis)
  2. Echinococcus garnulosus (Echinococcosis/Hadatid disease)

Flukes (TREMATODES)

Several trematodes (also known as flukes) are capable of parasiting man. The most important of these are the schistosomes. Other trematodes are also of major medical significance, especially in the Far East, as parasites of the liver, lung and the intestinal tracts.

Trematodes are flat, leaf-like hermaphrodite helminthes (excluding schistosomes). These parasites vary in size from a few millimeters to around 7cm in length. They possess two suckers, one for attachment, and another into which the alimentary tract opens. The rest of the body is occupied by the gut, testes, uterus and yolk glands. The morphology of these structures is used in identification.

In all trematodes infections, man acts as the definitive host harbouring the adult worms. The life cycle is complex, with alternating sexual and asexual reproduction in different hosts. The first intermediate host, however, is always a freshwater snail. Each parasite is specific in the choice of a snail host. The life cycles of trematodes (excluding the schistosomes) are similar: the egg which is excreted by a definitive host needs to reach water/moisture, where the ciliated larva inside the egg (called the miracidium) escapes and finds its way into a snail host. There is prolonged development multiplication in the snail with the formation of sporocysts and radia (2nd stage larvae) stages. The final larval stages, which are known as cercaria, emerge from the snail and encyst as metacercaria on fish, crustacean or water plants. Human infection follows ingestion of these infected second intermediate hosts.

Trematodes parasites in human

Lung flukes
  1. Paragonimus westermani

Liver flukes
  1. Ophisthorchis (Clonorchis) sinensis (Chinese liver fluke)
  2. Fasciola hepatica (sheep liver fluke)

Intestinal flukes
  1. Fasciolopsis buski

Blood schistosomiasis
  1. Intestinal schistosomiasis
  • Schistosoma mansoni
  • Schistosoma japonicum
  1. Urinary schistosomiasis
  • Schistosoma haematobium

large roundworm( ASCARIS LUMBRICOIDES)

GEOGRAPHICAL DISTRIBUTION

The worm has a world wide distribution but prevalence is high in warmer climates in tropical region where personal and environmental sanitation are poor. It is prevalent in countries like India, Nepal, Pakistan and Sri Lanka.

MORPHOLOGY

Adult female worms are 20-40 cm in length while the adult male worms measure 15-30 cm. The tail end of male is curved.



LOCATION IN THE HOST

The worms are found free in the lumen of the small intestine.

LIFE CYCLE

The fertilized female lays about 200.000 eggs per day. The eggs are oval in shape (65*45µm). The egg has an outer mammilated, ailbuminous coat that appears brown due to bile pigments. Some eggs may be decorticated (with outer coat missing). A certain portion of eggs (15%) is unfertilized and appear longer and rectangular (90*40µm) with no embryo. The embryo is unsegmented when eggs are passed in faeces.

The eggs develop further in soil with the first moult taking place (within the egg) to form the 1st stage larva in about 7 days. With the second moult the infective 2nd stage larva is formed inside the egg in 2-3 weeks under optimal conditions of development such as moist, warm (25-30 ºC) clay type soil. The infective eggs can remain viable in suitable soil for long periods of time.

When ingested the eggs hatch in the upper part of the small intestine liberating the larvae which penetrate the intestinal mucosa to enter the blood stream (or the lymphatics). The larvae are carried into the lungs via the liver and the heart. The larvae develop further in the lungs moulting twice (5th and 7th days). They penetrate the alveolar walls to move along the bronchioles, bronchi and trachea and are swallowed. On reaching the small intestine they mature into males and females. The time taken for an egg to develop into a mature is about 60 days. Adult worms may live up to 2 years.

PATHOGENESIS AND CLINICAL FEATURES

Many infected persons remain asymptomatic. However the presence of a small number of worms may lead to complications. The pathogenesis and clinical features can be categorized into; pulmonary ascariasis: intestinal ascariasis: complications of ascariasis and allergy to Ascaris species.
  1. Pulmonary ascariasis: An intense host reaction occurs in the lungs as a result of larval migration, 5-6 days after the ingestion of infective eggs. Larval antigens released by moulting larvae elicit an inflammatory reaction associated with moderate eosinophilia, pneumonitis, bilateral pulmonary infiltration, cough, dyspnea, substernal pain, fever, skin rashes and often asthma. These signs and symptoms are collectively called the “Loffler’s Syndrome”. The severity of the host reaction depends on the number of larvae migrating and the previous infection history: hypersensitive individuals show severe reactions with other allergic manifestations. Loffler’s syndrome is usually transient, lasted about 2-5 days. Pulmonary pathology is primarily immunological in nature.
  2. Intestinal ascariasis: Adult worms in the small intestine may cause mild abdominal pain and restlessness. Some asymptomatic persons are known to be harbour large worm loads. However, the clinical consequences of the infection are generally dependent on the number of worms present (worm load). It is difficult to say whether ascariasis is a direct cause of malnutrion as the infection is common in areas where malnutrion co-exist. But the infection certainly precipitates severe malnutrition (even kwashiorkor or marasmus) in undernourished children. Ascariasis as also known to lead to vitamin A deficiency. Improvement of growth in areas where protein energy malnutrition is prevalent has been demonstrated following worm treatment. Similarly worm treatment has been shown to improve physical fitness and educational abilities of malnourished children.
  3. Complications of ascariasis: The commonest complication of ascariasis is intestinal obstruction, particularly in persons with heavy worm loads. They may also cause intestinal perforation leading to peritonitis. Adult worms may wander into orifices such as the opening of the bile duct, pancreatic duct causing obstruction bile and pancreatic secretion respectively. Some drugs, chemicals and food items may cause worms to get abnormally activated and migrate to distant site.
  4. Allergy to Ascaris species: Allergic manifestations are common during the acute phase of larval migration and due to the presence of adult worms in the small intestine. Many allergic and infected persons experience asthma. The relationship of asthma, allergy and ascariasis is not clearly known. However it is well known that adult Ascaris worms are highly allergic and their handling may cause serious reactions in sensitive individuals.
DIAGNOSIS

The simplest diagnostic method is the demonstration of characteristic eggs in the faeces.


PREVENTION

Vegetable that are usually eaten raw or undercooked should be washed thoroughly. Fruits fallen under trees should be washed before eating. Washing of hands after working with soil helps in the prevention.

CONTROL


Prevention of indiscriminate defaecation, provision of sanitary latrines, elimination of parasite reservoir by worm treatment and health education are important.

TREATMENT

Broad spectrum antihelminthetic drugs like albendazole and mebandazole can be used. Usual drug course is 500mg stat for adults and the dose for children depends on the weight and the age.

Hookworms (NECATOR AMERICANUS & ANCHYLOSTOMA DUODENALE)


GEOGRAPHICAL DISTRIBUTION

The parasite is widely distributed in the tropics and sub-tropics. In cold climates with suitable microclimates (such as in coal mines) the parasite may be found. Two species infect humans. Necator americanus is the species found in South Asia, Africa, pacific and in North and South America whereas Ancylostoma duodenale is the main hookworm of Eastern Europe, North Africa, India, Northern China and Japan. Both species can be found together in South East Asia, the pacific and West Africa.

MORPHOLOGY

The worms measure 1-2cm in length. The head ends of the worm are sharply bent backwards like a hook. In the case of N. americanus the buccal cavity bears a pair of ventral cutting plates used in biting the mucosa for feeding. A. duodenale is larger with the head end bending backwards smoothly. The buccal cavity has two pairs of curved teeth. In both species, the tail end of the male is flattened and expanded to form the copulatory bursa.


LOCATION IN THE HOST

The hookworms inhabit the small intestine of humans. Unlike Ascariasis it is attached to the mucosa of the intestine of the intestine with the buccal capsule.

LIFE CYCLE

Each female N.americanus lays about 3000-6000 eggs per day (A. duodenale lays about 10,000-20,000 per day). The eggs are oval in shape and have thin, glass-like egg-shells. The embryo is usually divided when the eggs are passed in faeces. On reaching soil and under optimum conditions the eggs hatch into L1 larva within 24 hours. The optimum conditions are; shade, warmth’ moisture and sandy type soil.

L1 is an actively feeding rhabditiform larva (esophagus with a posterior bulb, like in the Rhabtid species).These larvae grow rapidly and moult on about the 3rd day into L2 rhabditiform larvae. On or about the 5th day the second moult transform them into long, non-feeding L3 infective or filariform larvae. These larvae have long, narrow esophagi and retain the cuticle of L2 as a sheath. The infective larvae move on to the topsoil and on to low vegetation seeking hosts. Under favorable conditions they remain alive for 3-6 weeks. When they come into contact with human skin, the activated larvae shed the sheath and penetrate the skin (usually between toes).
The larvae are carried in the blood or lymphatics and finally reach the lungs. They penetrate the alveoli and start ascending along small bronchioles to bronchi and then to trachea (unlike Ascariasis there are no moults in the lungs). At the pharynx they are swallowed. On reaching the small intestine the final moult transform them in to young males and females. The time taken between larval penetration and the formation of mature worms is 4-7 to weeks. Infective A.duodenale larvae ingested with contaminated food can establish in the intestine without undergoing lung migration. Ancylostoma is a unique parasite as it can go into a phase of ‘arrested development’ when the external conditions are not favorable and restart the life cycle when the conditions are good.

PATHOGENESIS AND CLINICAL FEATURES

In the acute infection the initial sings and symptoms are due to the penetration and migration of larvae in the skin. At the site of entry, a transient dermatitis with intense pruritus can result. This condition is called ‘ground itch’. The lesions may get secondarily infected. The lung migratory phase of hookworms is short and the pulmonary symptoms are either assent or minimum.

The pathogenesis of hookworm disease is directly related to the attachment of the worms to the mucosa. They attach to the mucosa by biting in plugs of mucosa (including 7-9 villi), which are stripped off the lamina propria. The pool of blood thus created is sucked in using the muscular pharynx. Only part of the sucked blood is used for food and oxygen, a large part being excreted continuously. This leads to blood loss and results in hypochromic, microcytic (iron deficiency) anemia. Each N.americanus sucks about 0.03 ml of blood per day while A.duodenale sucks about 0.26 ml per day.

The degree of anemia is related to the worm load and the nutritional status of the host. Hypoproteinemia seen in severe hookworm disease may be related to poor food intake (poverty, anorexia), impaired absorption, increased loss and a combination of all. Impairment of nutrient absorption, intestinal protein loss and lowered food intake collectively result in stunting (growth retardation). The pathogenesis of impaired mental and physical development in hookworm disease is not clear.

DIAGNOSIS

This is done by demonstrating characteristic eggs in the faeces. The eggs can be cultured into infective larval stage to distinguish between Necator and Ancylostoma.


PREVENTION AND CONTROL

Avoidance of indiscriminate defaecation and use of footwear help in prevention. Provision of hygienic latrines, chemotherapy of infected people and health education are important in control of the infection.

TREATMENT

Hookworm infection can be eradicated with several safe and highly effective antihelmintic drugs, including albendazole (400 mg once), mebandazole (500 mg once), and pyrantel pamoate (11 mg/kg for 3 days). Mild iron-deficiency anemia can often be treated with oral iron alone. Severe hookworm disease with protein loss and malabsorption necessitates nutritional support and oral iron replacement along with deworming.

Threadworm (STRONGYLOIDES STERCORALIS)


GEOGRAPHICAL DISTRIBUTION

The parasite has a world wide distribution but more common in tropical and subtropical regions.

LOCATION IN THE HOST

It is found embedded on the mucosa of the small intestine

MORPHOLOGY

Only females are seen in the parasitic cycle (in the intestine of infected persons). These parasites measures 2-2.5 mm in length. In free-living cycle (outside the human body) both males and females are found. Free-living females are smaller and measure 0.95-1.5 mm in length. Males are smaller.

PARASITE

Strongyloides stercoralis is a unique parasite. It is the only nematode or helminth parasite that multiplies in the human body. A process known as ‘internal autoinfection’ accomplishes this. It differs from hookworms in that; no males in the parasitic cycle: no eggs are passed in the faeces but L1 rhabditiform larvae: internal and external autoinfection occurs when L1 larvae undergo accelerated development into rhabditiform L2 and then into L3 which is the filariform/infective larvae while moving down the intestinal tract: has a free-living cycle in the soil: may cause severe disseminated disease with larvae in vital organs in immunocompromised patients.

LIFE CYCLE

The parthenogenetic females lay eggs in the mucosa of the small intestine. Generally they have a low egg output per day. The eggs hatch in the mucosa itself and the L1 rhabditiform larvae enter the lumen and are excreted in the faeces.

The subsequent development and the rate depend on the internal and the external conditions. When external conditions are unfavorable L1 larvae rapidly develop into L2 and to the infective L3 larvae stage. The infective larvae develop into free-living males and females. The larvae produced by the free-living adults mature into free-living L3 stages. These larvae penetrate the skin of humans and once again start a parasitic cycle. The L3 larva of S.stercoralis differs from that of hookworms in; not having a sheath: having tri-radiate tip of tail.

PATHOGENESIS AND CLINICAL FEATURES

At the site of penetration of the skin, L3 larvae may cause ‘ground itch ( see hookworms). Pulmonary migration of larvae can cause lung symptoms and pneumonitis. But severe symptoms (as in ascariasis) are rare.

In mild infections, catarrhal enteritis is seen with increased amount of mucous secreted into the lumen. The mucosa is congested with hyperplasia of goblet cells with normal looking villi.
In heavy infections the villi become flattened and atrophied. Epigastric pain, nausea, anorexia and finally incessant diarrhea result.

In the hyperinfection syndrome seen in immunocompromised patients L1 develop rapidly to infective L3 stage, which penetrate the gut wall and enter the blood stream (internal autoinfection). Larvae in large numbers are carried into various organs resulting in serious damage to respective tissues. Organs and systems that can be damaged by larvae include brain, heart, pancreas, hepatobilliary system, lungs, genitourinary system and the skin.

In external autoinfection where L1 larvae develop into infective stage in soiled clothes, bed linen or around the anal verge the migrating larvae produce a characteristic epigenous dermatitis starting in the per anal region extending rapidly to the buttocks and lower abdomen. This condition is called ‘larva currens’.

DIAGNOSIS

Diagnosis is difficult. Because of low fecundity female worms produce only small numbers of larvae and it is also not regular. In cases suspected of having strongyloidiasis, negative report on a single wet smear of faeces does not exclude the infection. Several samples over period of 3-7 days may be necessary to exclude the infection. In the faeces rhabditiform larvae are looked for. In old samples sometimes hookworm larvae may be found. Then, the larvae have to be distinguished from those of Strongyloides. Duodenal intubation or ‘entero test’ may be used to obtain larvae directly from the small intestine.

PREVENTION AND CONTROL

Avoidance of indiscriminate defaecation and use of footwear help in prevention. Provision of hygienic latrines, chemotherapy of infected people and health education are important in control of the infection.

TREATMENT

Even in the asymptomatic state, strongyloidiasis must be treated because of the potential for fatal hyperinfection. Ivermectin (200 µg/kg daily for 1 or 2 days) is more effective than albendazole (400 mg daily for 3 days, repeated at 2 weeks) and is better tolerated than thiabendazole (25 mg/kg twice daily for 2 days), whose common adverse effects include nausea, vomiting, diarrhea, dizziness, and neuropsychiatric disturbances. Because thiabendazole is not uniformly effective, stool examinations, eosinophil counts, and monitoring of clinical symptoms should be continued after treatment. For disseminated strongyloidiasis, treatment with Ivermectin should be extended for at least 5 to 7 days or until the parasites are eradicated.

TRICHINELLA SPIRALIS (Trichinosis/Trichinellosis)


GEOGRAPHICAL DISTRIBUTION

The infection is seen in countries such as United States, countries of former Russian federation and Europe. It is rarely seen in tropics. It also occurs in east and west sub-Saharan African region.

MORPHOLOGY

The adult worms are small and measures 2-3mm (females) and 1-2mm (male).

LOCATION IN HOST

The worm is found embedded in the small intestine mucosa. The larval stages are also found in the same host. 9 example of man being both definitive and intermediate host)

LIFE CYCLE

Each female matures rapidly and following fertilization lays about 1500 larvae. The larvae make their way by way of lymphatics and the blood stream to reach striated muscles. Each larva enters a muscles fibre and converts it to a characteristic capsule called the ‘nurse cell’. Therefore the larvae can live for long periods. Later they usually get calcified. In humans the muscle phase is a dead end. When this happens in animals such as pigs and horses the meat becomes infective if not properly cooked. The muscle fibres entering the stomach are digested and the liberated larvae quickly gain entry into the small intestinal mucosa and mature rapidly into adult worms.

After about1 week, female worms release newborn larvae that migrate via the circulation to striated muscle. The larvae of all species except Trichinella pseudospiralis and Trichinella papuae then encyst by inducing a radical transformation in the muscle cell architecture. Although host immune responses may help to expel adult worms, they have little effect on muscle-dwelling larvae. Human trichinellosis is most often caused by the ingestion of infected pork products and thus can occur in almost any location where the meat of domestic or wild swine is eaten. Human trichinellosis also may be acquired from the meat of other animals, including dogs (in parts of Asia and Africa), horses (in Italy and France), and bears and walruses (in northern regions). Although cattle (being herbivores) are not natural hosts of Trichinella, beef has been implicated in outbreaks when contaminated or adulterated with trichinous pork.


ENCYSTED LARVA




PATHOGENESIS


In mild infections, adult worms cause minimal pathology. They may cause inflammation and congestion of the mucosa with cell destruction. Major pathology is by larvae due to their presence in the muscle or due to their migration through the central nervous system and the heart.

CLINICAL FEATURES

Clinical symptoms of trichinellosis arise from the successive phases of parasite enteric phase, invasive phase (larval migration), and encystment phase (muscle encystment)
1. Enteric phase (invasion of the intestine): patients develop nausea, vomiting and abdominal pain resembling an attack of acute food poisoning.
2. Invasive phase (larval migration): This phase is characterized by severe myalgia, periobital edema and eosinophilia. CNS or myocardial complications may occur during this phase.
3. Encysment phase (Encysment of larvae in the muscle): Severe infection leads to cachexia, edema and dehydration. Gram negative septicemia due to organisms. introduced by larvae may occur.

DIAGNOSIS

History of ingesting undercooked pork is suggestive. Often groups of people are affected as following parties.
Blood eosinophilia develops in_90% of patients with symptomatic trichinellosis and may peak at a level of 50% between 2 and 4 weeks after infection. Serum levels of IgE and muscle enzymes, including creatine phosphokinase, are elevated in most symptomatic patients.
Muscle biopsy can be used to demonstrate the encysted larvae. A definitive diagnosis requires surgical biopsy of at least 1 g of involved muscle; the yields are highest near tendon insertions. The fresh muscle tissue should be compressed between glass slides and examined microscopically, because larvae may be overlooked by examination of routine histopathologic sections alone.
In early infection serology may be useful (ELISA, western blot, Enzyme immunoassay.)

EPIDEMIOLOGY

Eating of undercooked pork or sometime horse meat is responsible. Feeding pigs with dead or killed rats should be avoided. This is the major avenue of transmission of the infection to pigs by rats, which maintain the infection.

PREVENTION AND CONTROL
Proper cooking of all meat will eliminate the infection. Cooking of all garbage fed to pig will also help. Deep freezing pork at -18º to -15º C is effective.

TREATMENT

Current antihelmintic drugs are ineffective against Trichinella larvae in muscle. Fortunately, most lightly infected patients recover uneventfully with bed rest, antipyretics, and analgesics. Glucocorticoids like prednisone (1 mg/kg daily for 5 days) are beneficial for severe myositis and myocarditis. Mebendazole and albendazole, like thiabendazole, appear to be active against enteric stages of the parasite, but their efficacy against encysted larvae has not been conclusively demonstrated.

Whipworm (TRICHURIS TRICHIURIA)


GEOGRAPHICAL DISTRIBUTION
It is widely distributed in warm tropical climates such as South Asia, South East Asia and Africa.

MORPHOLOGY
Female worm is about 30-50 mm in length while the male is about 20-30 mm. The anterior 3/5th of the body is thin while posterior 2/5th is thick in both sexes. The posterior end of the male is curved.

LOCATION IN THE HOST
The worm inhabits the large intestine. The entire thin anterior end is threaded into the mucosa while the thick, short posterior end project into the lumen of the large intestine.

LIFE CYCLE

The female lays 2000-10000 eggs per day. The eggs have a characteristic ‘paddy seed’ shape, (50*20 µm) with ‘polar caps’. The eggs are passed in the faeces. They require a period of maturation in the soil. The optimal conditions are similar to those of Ascariasis. Because of this fact trichriasis often co-exist with Ascariasis. When infective eggs are ingested by humans the eggs hatch in the lower part of the small intestine and the larvae pass down into the large gut to mature into adults. The mode of transmission is similar to that of Ascariasis. But there is no pulmonary migration of larvae in trichuriasis.


PATHOGENESIS AND CLINICAL FEATURES

Light infections may be asymptomatic. Heavy infections lead to blood and mucous diarrhea. In children tenesmus and constant straining may lead to ractal prolapse. In some heavily infected children, the infection may result in ‘Trichuris Dysentry Syndrom-TDS’.There can be other clinical features as follows;
  1. Trichuriasis and malnutrition; Both conditions can co-exist and it is difficult to determine a cause and effect. The infection shows a close correlation of the intensity of infection (worm load) and the severity of symptoms such as diarrhea, vomiting and rectal prolapse. TDS is generally seen with worm loads over 500 worms. The symptoms lead to lowering of food intake, which worsen the already existing malnutrition.
  2. Trichuriasis and anemia; Anemia is a constant feature of heavy infection. It is hypochromic and microcytic. Anemia may be due to; blood loss from colonic mucosa: blood loss due to ingestion by worms. It is not certain whether Trichuris is a ‘blood sucker’. Few red cells are often seen in the intestine of the worm.
  3. Growth retardation; This is a distinct association in trichuriasis. This is seen with even mild infections. This feature may be due to severe anorexia, nausea and vomiting associated with the infection.
  4. Finger clubbing; this is another distinct association of the severe infection (TDS)

DIAGNOSIS

Diagnosis is by demonstrating the characteristic eggs in the faeces. A simple wet smear with saline/iodine is often sufficient. Concentration techniques such as formol-ether could be used. Foe quantitative studies Kato-Katz technique is good.


PREVENTION AND CONTROL

Vegetable that are usually eaten raw or undercooked should be washed thoroughly. Fruits fallen under trees should be washed before eating. Washing of hands after working with soil helps in the prevention.

Prevention of indiscriminate defaecation, provision of sanitary latrines, elimination of parasite reservoir by worm treatment and health education are important.

TREATMENT

Mebendazole (500 mg once) or albendazole (400 mg daily for 3 doses) is safe and effective.

Pinworm (ENTEROBIUS VERMICULARIS)


GEOGRAPHICAL DISTRIBUTION

The parasite has a world wide distribution with a high prevalence in cold climates. This is not a soil transmitted infections.

MORPHOLOGY

The adult worms are small (1cm) with both ends pointed. Males have curved tail ends and are rarely seen. The ‘cervical alae’ extend right down the sides of the body so that in cut sections they are seen as two projections on either side of the body.

LOCATION IN HOST

The worm is found attached to the mucosa of the large intestine particularly the caecal area. They are not blood suckers.

LIFE CYCLE

A gravid female carries approximately 10,000 eggs in the uterus. These females migrate down the large intestine to reach the anus. This occurs during night. The female then lays the eggs on the anal verge. Following egg deposition the female dies.

The eggs are plano-convex in shape and have double walls (50*25 µm). The outer wall is albuminous and sticky. The embryos develop into infective larvae inside the eggs in 6 hours. When these eggs are ingested via contaminated fingers or via fomites they hatch in the lower part of the small intestine. The larvae move down to the large intestine to mature into adult males and females. There is no pulmonary migration of the larvae as in trichuriasis. Some infective eggs may hatch on the anal area and the larvae can move into the large intestine through the anus (retro-infection, a type of auto infection).

PATHOGENESIS AND CLINICAL FEATURES
The damage cause by the worm is not extensive. Some times they produce inflammation of the colonic mucosa leading to granulomatous condition. Complications include perforation of the gut (rarely) and migration to ectopic sites, commonest being into the female vagina. The moving females and the deposited eggs cause severe pruritus ani (itching of the anus). This may lead to loss of sleep. The infected children become irritable and may interfere with schoolwork.

EPIDEMIOLOGY

Since the lightness of the eggs, they are carried by wind and air currents. They are deposited on object found in the environment such as tabletops, doorknobs, chairs and seats. The infection makes no exception to any social class. It is a household infection and is highly prevalent where there is overcrowding such as in refugee camps, armed forces camps, prisons, hostels, orphanages etc. Generally one member of the family gets infected soon the all in the household acquire the infection.

MODES OF TRANSMISSION
  1. Direct infection from the anal and perianal region by fingernail contamination ( a type of autoinfection).
  2. Exposure and ingestion of viable eggs on soiled night clothes and other contaminated objects in the environment.
  3. By way of contaminated dust from bed clothes, toys and furniture.
  4. Retro-infection (see above)

DIAGNOSIS

Old methods include NIH (National Institute of Health, USA) swab and Graham’s Scotch Tape method. A simple ‘cello-tape’ strip can be used. The procedure should be carried out in the morning before washing the anal area or bathing. Precautions against contamination of hands of the examiner should be taken.

PREVENTION AND CONTROL
  1. cut finger nails short
  2. wash hands with soap and water regularly
  3. avoid the scratching the anal region
  4. treat every one in the household including boarders and servants ( in institutions all inmates including staff have to be treated at the same time)
  5. Following treatment all bed linen and personal clothes should be washed and dried in the hot sun.
  6. Mats and mattresses should be exposed to hot sun
  7. Wet mopping of floors and surfaces should be done

TREATMENT

All affected individuals should be given a dose of mebandazole 100 mg,
Albendazole 400 mg, or pyrantel pamoate 11 mg/kg or maximum, 1 g, with the same treatment repeated after 10 to 14 days. Treatment of household members is also advocated to eliminate asymptomatic reservoirs of potential re-infection. But still it is very difficult to cure because it may be impossible to avoid re-infection.

Beef tapeworm (TAENIA SAGINATA)


GEOGRAPHICAL DISTRIBUTION

Infection is common in countries where beef is often eaten raw or under-cooked such as African countries, Brazil, Argentina, USA, former Russian federation countries and Europe.

LOCATION IN HOST

The worm is found attached to the mucosa of the small intestine (ileum) with its scolex. The rest of the worm is free in the lumen of the intestine.

MORPHOLOGY

They are flat, ribbon-like worms. Their bodies are formed of chains of segments (proglottids) of varying sizes and shapes. At the anterior end is the scolex or the ‘holdfast’ organ which is used for the attachment of the worm to the intestinal mucosa.

The scolex is 1-2mm and is pear shaped. There are four suckers on the scolex but no rostellum or hooks. The fully grown worm is exceptionally long, sometimes reaching 20 meters. Usually it measure about 5 meters and has about 1000-2000 segments. The mature segments measure approximately 12 mm wide and 10 mm long. In the mature segments both male and female reproductive organs are found. On the lateral margin are the genital pores, one on each segment. In gravid segments (the last segments of the strobila) the uterus occupies the whole space with primary and secondary uterine branches (twenty uterine branches at one side).


LIFE CYCLE

Humans are the only definitive host of the parasite and cattle are the only intermediate host.
The gravid segments are dislodged and are passed in the faeces of the infected person. The detached gravid segments also have their inherent movement and may actively move down the lumen and out of the anus and sometimes along the thighs.

When the segments are deposited on the ground the eggs are scattered on the soil. Eggs deposited on vegetation can live for months to years until they are ingested by cattle.
Eggs measure 30-45 µm. Each egg has an outer vitelline membrane which is usually lost in the faeces. The inner, thick wall is made up of keratin blocks and appears striated. This is called the embryaosphore. Inside is the embryo and now it is called the onchosphere. It has six embryonic hooklets and because of this it is also known as the hexacanth larva.

The egg when ingested by cattle, the onchosphere hatches out in the duodenum. With the help of the hooklets it penetrates the intestinal mucosa and enters the venous capillaries (or mesenteric lymphatics) within half an hour. Then they reach skeletal muscles. There they lose their hooklets and grow into infective cysticercus bovis larva in about 10-12 weeks. The infective cysticercus bovis is ovoid, white in colour and measures 8*5 mm. It has an invaginated scolex and four suckers but no hooks. Humans acquire the infection when infected beef containing cysticercus bovis is eaten raw or under-cooked.


PATHOGENESIS AND PATHOLOGY
The scolex does not cause much damage to the mucosa. Sometimes inflammation may be present. Several cases of intestinal obstruction and perforation have been reported. The symptoms are often due to metabolic products of the worm.

CLINICAL FEATURES

Often the infection is asymptomatic except noticing whitish segments in faeces or experience of segments actively moving out of the anus. Vague abdominal symptoms such as pain, nausea, weight loss and anorexia may be present. In some the symptoms are relieved by ingestion of food.

DIAGNOSIS

The diagnosis is made by the detection of eggs or proglottids in the stool. Eggs may also be present in the perianal area.

1. The gravid segments passed in the faeces could be injected with Indian ink to show the lateral uterine branches of the uterus. In Taenia saginata there are more than 13 primary branches of the uterus(compare with Taenia solium).

2. If the scolex is passed following treatment, the absence of hooks distinguishes it from the Taenia solium.

3. If the gravid segments are ruptured eggs may be found in faeces (taenid egg).



EPIDEMIOLOGY

This is common infection where beef consumption is high. Infection often occurs when cattle are young. Faeces containing eggs pollute pastures. The role of birds transmitting eggs from sewage to pastures is also possible.

PREVENTION AND CONTROL

Meat infection is the important public health measure. Cycticerci in muscle are usually killed when frozen at minus 10ºC for 10 days or heating thoroughly above 56ºC is also effective.

TREATMENT

A single dose of praziquantel (10 mg/kg) is highly effective. Niclosamide can also be given. The dose is 2gm for adults and lower doses for the children. The tablets are chewed and washed down with a little water.

Pork tapeworm (TAENIA SOLIUM)

GEOGRAPHICAL DISTRIBUTION
The infection is prevalent in places where pork or pork products are eaten raw or under-cooked. It is common in East Europe, South and Central America, South Africa, China, India, Korea and Indonesia.

LOCATION IN HOST
The scolex is attached to the mucosa of the jejunum with the rest of the strobila in the intestinal lumen.

MORPHOLOGY

The scolex has a rostellum with two rows of hooks. The segments are similar to those of Taenia saginata. Mature segments are roughly square in shape. Gravid segments have less than 13 primary uterine branches as oppose to the Taenia saginata, which the number of uterine segments are more than 13.


LIFE CYCLE

Man is the only definitive host whereas pig is the only intermediate host. Life cycle is similar to that of Taenia saginata. The larval stage in the pig muscle is called Cysticercus cellulosae. Human infection occurs when pork containing Cysticercus cellulosae is eaten raw or under-cooked.



CLINICAL FEATURES
Clinical features are similar to those of Taenia saginata. Often the infection is asymptomatic except noticing whitish segments in faeces or experience of segments actively moving out of the anus. Vague abdominal symptoms such as pain, nausea, weight loss and anorexia may be present. In some the symptoms are relieved by ingestion of food.

COMPLICATIONS

Unlike in Taenia saginata, if an individual ingests eggs (usually accidentally) life cycle will continue as in the intermediate host, pig. Therefore humans can develop Cysticercosis, a complication due to the presence of pork worm larvae (Cysticercus cellulosae) in the skeletal muscles.

DIAGNOSIS
This is also similar to that of Taenia saginata.

1. The gravid segments passed in the faeces could be injected with Indian ink to show the lateral uterine branches of the uterus. In Taenia solium there are less than 13 primary branches of the uterus (compare with Taenia saginata).

2. If the scolex is passed following treatment, presence of hooks distinguishes it from Taenia saginata

3. If the gravid segments are ruptured eggs may be found in faeces (taenid egg).



EPIDEMIOLOGY
Prevalence of the infection is lower than that of beef tape worm infection. This is because some communities do not eat pork and in others when pork is eaten it is usually well cooked. While Taenia saginata infection occurs both in highly develop and developing countries, Taenia solium infection and its major complication, Cysticercosis, are prevalent in poor communities in which people live in close contact with pigs and eat improperly cooked pork. Uncooked or partially cooked pork products can transmit the infection.

PREVENTION AND CONTROL

Thorough cooking of pork is very important. Heating meat to 50ºC kills the cysticerci but those in the inside of large pieces may not reach the require temperature. At 0ºC the cysticerci can live for 70 days. Freezing at -10ºC for 4 days kills the cysticerci.

TREATMENT
A single dose of praziquantel (10 mg/kg) is highly effective. Niclosamide can also be given. The dose is 2gm for adults and lower doses for the children. The tablets are chewed and washed down with a little water.

Rat tapeworm (HYMENOLEPIS DIMINUTA)

GEOGRAPHICAL DISTRIBUTION
This is a common parasite rats and mice in many parts of the world. It is an occasional accidental parasite of humans, particularly children.

LOCATION IN HOST
The worm is found in upper part of the ileum. It may move up or down as it is known in rats.

MORPHOLOGY
The worm measures about 300-600 mm* 4 mm. It has about 800-1000 segments. The scolex is small (0.2-0.4 mm). It has a retractable rostellum but no hooks. Four small suckers are also present on the scolex. The mature segments is broader than length and measures 0.75*0.25 mm.



The eggs are ovoid (60-80 µm) and have thick yellowish outer shells and thin colourless inner membranes. The intermediate layer appears granular. The embryo has three pairs of hooklets.


LIFE CYCLE

The adult worm is in the small intestine of rat which is the definitive host. Larval rat fleas ingest the eggs passed in the rat faeces. The embryo grows into a cysticercoid larva (cysticercus like) in the flea. When humans accidentally ingest the rat flea the released cysticercoid larva matures into an adult worm. Four beetles may also act as intermediate hosts.


PATHOGENESIS

Multiple infections are not uncommon. The scolices may damage the mucosa leading to inflammation. Frequent movements of worm may also cause pathology. Metabolic products of the worm mar also cause different clinical manifestations.

CLINICAL FEATURES

Most of the time patients are asymptomatic. Some patients may experience abdominal pain. High degree of clinical suspicious is needed for the diagnosis.

DIAGNOSIS

Demonstration of the characteristics eggs in the stool is the most reliable method.

PREVENTION AND CONTROL

Improvement of personal and environmental sanitation is important. Elimination of household rats helps to reduce the disease.

TREATMENT

Identification of the infected persons is very important. There are few treatments methods available. Praziquantel and Niclosamide can be used as treatment.

Dwarf tapeworm (HYMENOLEPIS NANA)

GEOGRAPHICAL DISTRIBUTION
The infection is commoner in both temperate and tropical regions of the world such as Egypt, Sudan, Thailand, India, Japan, South America and Southern Europe.

LOCATION IN HOST
The worm is found attached to the mucosa of the small intestine.

MORPHOLOGY
The worm is small and measures 25-45mm*0.5-0.9mm. It consists of 100-200 segments. The small scolex measures 140-480µm and has a rostellum with single row of hooks.

There are four suckers on the scolex. The neck is usually long. The segments close to the neck are short while the mature segments are broader than long. The eggs are globular and have thin outer vitelline membranes; 40-60µm separated from the inner which measures about 20-30µm.The latter is the embryophore and encloses the embryo which is ‘lemon’ shaped. On either end is polar thickening from which a few filaments extend.



LIFE CYCLE

Man is the definitive host. This is the only tapeworm known to have no intermediate host. The gravid segments are generally disrupted and eggs are passed in the faeces of the infected person. When ingested by man the onchosphere penetrates the small intestinal villi to form the cysticercoid stage. Within a short time (4 days) the cysticercoid re-enter the lumen and mature into adults. Autoinfection is possible.

PATHOGENESIS AND CLINICAL FEATURES
Mild infections are generally asymptomatic. But when large numbers of worms are found (>1000) enteritis with abdominal pain, diarrhea, nausea and vomiting may occur. These symptoms are probably due to the toxemia or allergic reactions to metabolic products of the worms.

EPIDEMIOLOGY
The infection is common in children than adults. The transmission is usually hand to mouth and via food and water. Infection is common in institutionalized children.

DIAGNOSIS

This is done by demonstrating characteristics eggs in the faeces.


PREVENTION AND CONTROL

Treatment of diagnosed cases and improvement of personal hygiene help to reduce the infection prevalence.

TREATMENT

Niclosamide is the drug of choice. The dose should be repeated after 10 days. Large number of persisting cysticercoids makes it difficult to obtain a radical cure. Other option is praziquantel, as it acts against both the adult worms and the cysticercoids in the intestine

CYSTICERCUS CELLULOSAE (Cysticercosis)


GEOGRAPHICAL DISTRIBUTION

Cysticercosis is common where Taenia solium infection is prevalent especially south and Central America, South and east Africa, India and former Russian Federation countries.

LOCATION IN HOST

Cysticerci may be found in any organ or tissue of the body as they carried by the blood stream on hatching of the onchosphere in the small intestine. Common sites are the brain, skeletal muscles, heart and the eye.

MORPHOLOGY

Cysticercus cellulosae (commonly called ‘bladder worm’) are ovoid white and measure 8*5 mm and are easily visible to the naked eye. Each Cysticercus cellulosae consists of a fluid filled bladder with a small protoscolex invaginated into the lumen. The protoscolex has four suckers and two rows of hooks (Cysticercus bovis of Taenia saginata has no hooks).



TRANSMISSION

Accidental ingestion of Taenia solium eggs which are passed in infected person’s faeces may take place via contaminated green vegetables, fruits or drinking water. Since about 25% of patients with Cysticercosis also harbour adult Taenia solium in small intestine it is possible that autoinfection takes place following regurgitation of segments or eggs into stomach. The eggs need to pass through the stomach, as gastric acid is responsible for the dissolution of the thick wall of the eggs. Infection may take place from anus to fingers to mouth.

PATHOGENESIS
This is related to the organ affected. Generally the cysts are distributed throughout the body roughly in proportion to the weight of the organ. The living cysts cause only mild symptoms unless the path of CSF flow is blocked (cerebral infection). Severe pathology is seen following the death of the cysts due to inflammatory reactions. Allergic manifestations due to leakage of fluid also occur.



CLINICAL FEATURES

The clinical presentation of Cysticercosis depends on the number and location of cysticerci as well as the extent of associated inflammatory responses or scarring.

  1. Cerebral Cysticercosis; minors symptoms related to the Central Nervous System are common but the most serious manifestations are epileptiform fits. These seizures may be generalized, focal, or Jacksonian. Hydrocephalus results from obstruction of cerebrospinal fluid (CSF) flow by cysticerci and accompanying inflammation or by CSF outflow obstruction from arachnoiditis. Signs of increased intracranial pressure, including headache, nausea, vomiting, changes in vision, dizziness, ataxia, or confusion, are often evident. Cysticerci in different part of the brain could give rise to motor, sensory and psychological symptoms. The cysticerci may get calcified.
  2. Muscle Cysticercosis; this is common site. They could sometimes be felt as nodules. Muscle cysts are usually more elongate than others. These cysts get calcified earlier.
  3. Ocular Cysticercosis; The cysts lodged in the eye cause pain and blurring of vision. With time and with encapsulation these cause severe damage to the eye.
  4. Cardiac Cysticercosis; in the heart the cysts can be found in the epicardium, myocardium and endorcadium.

DIAGNOSIS

There are different types of diagnostic methods are available. The method which should be employed depends on the organ system which is suspected be affected. Radiological, histological and serological tests are useful.
  1. Radiological: X-rays are useful to demonstrate calcified cysts in muscles. CT scan is important to detect the cerebral Cysticercosis.
  2. Histological: Palpable cysts in the muscles can be identified by following biopsy.
  3. Serological: Several specific serological tests, including PCR are now available.


PREVENTION AND CONTROL

This is same as for Taenia solium. Improvement of sanitary habits and environmental hygiene are important.


TREATMENT

There is no specific treatment. Various drugs such as albendazole and praziquantel have been used. However, praziquantel can evoke an inflammatory response in the central nervous system. Niclosamide (2 g) is also effective but is not widely available.

The management of neurocysticercosis focuses primarily on symptom-based treatment of seizures or hydrocephalus. Seizures can usually be controlled with antiepileptics. If parenchymal lesions resolve without development of calcifications and patients remain free of seizures, antiepileptic therapy can usually be discontinued after 2 years. High-dose Glucocorticoids can be used during treatment or if symptoms worsen. Since glucocorticoids induce first-pass metabolism of praziquantel and may decrease its antiparasitic effect, cimetidine should be coadministered to inhibit praziquantel metabolism.

For patients with hydrocephalus, the emergent reduction of intracranial pressure is the mainstay of therapy. In the case of obstructive hydrocephalus, the preferred approach is removal of the cysticercus via endoscopic surgery. However, this intervention is not always possible. An alternative approach is initially to perform a diverting procedure, such as ventriculoperitoneal shunting. Historically, shunts have usually failed, but low failure rates have recently been attained with treatment with antiparasitic drugs, chronic administration of glucocorticoids, or use of flow-sensitive shunts. Open craniotomy to remove the cysticerci is now required only infrequently. For patients with subarachnoid cysts or giant cysticerci, glucocorticoids are needed to reduce arachnoiditis and accompanying vasculitis.

Friday, June 24, 2011

Automobile accessories; bull bar

Automobile accessories are important to provide an adequate protection for a vehicle and passengers. These accessories are not only valuable as protective measures; they have an aesthetic value as well. What are the common automobile accessories? Bike Racks, Bull bars, Push Bars, Side Steps, Running Boards, Bug Deflectors ,Bull Ring , Camping Tents , Car Bra , Car Covers , Car/SUV Spoilers , Cargo Liners , Cargo Stabilizer Bar , Cell Cup Holder , Convertible Cover , Dash Mats , Driving Gloves , Fender Trim , Floor Mats , Front Bumper Guards and Garage Accessories are some of the important automobile accessories. Among those, protective accessories like bull bars and bug deflectors are important than aesthetic accessories.

A Bull bar is a gadget which attached to the front of a vehicle. It provides a protection from damage in a collision with an animal. There are different types of bull bars according to the size, form and the material. Steel and aluminium are the common material used to make bull bars. In some European countries, selling of metal bull bars was banned due to the association of higher death rates, which were caused by the rigid fronts of vehicles. Therefore bull bars made of using polycarbonate and polyethylene are popular because these bull bars are softer than metal bull bars.