Habitat:

• The adult tape worms are located affixed to the wall of intestinal mucosa of dogs and wild canines.
• The larval stage (hydatid cyst) is present in humans and other herbivorous animals.

Morphology of Echinococcus granulosus:

• Adult worm:
  • It is small tapeworm measuring 3-6 mm in length. It constitutes of scolex (head), neck and body or strobili.
  • Scolex:
    • Scolex is pyriform, 300 mm in diameter. It bears four suckers and a protrusible rostellum with two circular rows of hooks.
  • Neck:
    • It is short and thick.
  • Strobili or body:
    • It consists of 3 segments (occasionally 4).
    • The segment is immature, the second one is mature.
    • The last one (as well as fourth one, when present) is gravid.
    • The terminal segment being the biggest, measures 2-3 mm in length and 0.6 mm in breadth.
    • The terminal gravid segment lacks uterine openings. The segment, thus always bursts open before or after passage into the stool, releasing hundreds of eggs.
• Eggs:
  • The eggs are the infective stage of parasite.
  • It is ovoid in shape and appears similar to other eggs of Taenia.
  • It measures 32-36 mm in length by 25-32 mm in breadth.
  • The egg has two layers- outer thin wall and inner embryophore.
  • It consists a hexacanth embryo with 3 pairs of hooks.

• Larva (Hydatid cyst):
  • The larval stage of dog tapeworm is known as the hydatid cyst.
  • It is present in various organs of man and other intermediate hosts.
  • It depicts the scolex of the future adult worm and remains invaginated with a vesicular body.
  • On entry to the definite host, the scolex with 4 suckers and rostellar hooklets, becomes evaginated and develops into an adult-worm.
  • The hydatid cyst in man is particularly unilocular, subspherical in shape and filed with third.
  • The mature cysts measure around 5 cm in diameter.
  • The cyst wall is made up of two layers.
  • The outer cuticular layer called the ectocyst is hyaline, milky, opaque, laminated and non-nucleated. It is tough elastic layer and is 1 mm thick.
  • The inner or germinal layers, endocyst is cellular, nucleated and is extremely thin (22-25 mm in thickness). It is the vital layer of the cyst and gives rise to broad capsules with scolices. It secretes the specific hydatid fluid and gives rise to outer layers.
• Hydatid fluid:
  • The inner of the cyst is filled with a clear, colorless fluid, may be pale yellow in color known as the hydatid fluid.
  • The third is nutritive and provides nourishment for growing brood capsule and scolices. The third is slightly acidic, pH 6.7.
  • It consists of NaCl, Na2SO4, Na3PO4 and Na and Ca salts of succinic acid.
  • A large number of brood capsule, free scolices and loose hooklets resembling sand grains float in the fluid called the hydatid sand.
  • The hydatid fluid is antigenic and highly toxic when absorbed, it gives rise to anaphylactic symptoms.

Life cycle of Echinococcus granulosus:

-The life cycle of E. granulosus is completed in two hosts:

• Definitive host- dogs and wild canines
• Intermediate hosts– man, sheep, cattle, goat etc.
• The eggs are discharged with the feces of the definitive hosts.
• These are swallowed by the intermediate hosts sheep and other domestic animals while grazing in the field and also by man, especially by children due to intimate handling of infected dogs.
•  In the duodenum, the hexacanth embryo are hatched out.
• In about 8 hours after ingestion the embryo bore their way through the intestinal wall and are carried by the blood stream to various internal organs especially the liver and lungs are the most common sites.
• In these organs, the embryos get through the initial inflammatory response of the host and undergo dramatic changes.
•  It increases in size up to 5-8 cm in few months and is finally transformed into a fluid filled hollow bladder, hydatid cyst.
•  The cyst has an inner germinal layer that contains a large number of nuclei from which buds of tissue develop into hollow fluid filled brood capsules.
• These brood capsules may remain affixed to the cyst wall by means of their peduncle or may float in the hydatid fluid.
• Eventually many larvae are produced in large numbers from the germinal layer within the brood capsule.
•  As the cyst grows older, a larger number of brood capsules and free protoscolices float free inside the hydatid fluid.
• Dogs and other canid host gain infection by ingestion of hydatid cyst containing protoscolices (fertile cyst), present in the viscera of sheep, cattle or other intermediate hosts.
•  In the small intestine, protoscolices evaginate, penetrate deep between villi and enter the cyst of Lieberkuhn.
•  It develops into a mature adult worm and began to produce infective eggs within 41-76 days of ingestion of the hydatid cysts.
• The life cycle of parasite comes to a dead end in man as dog have no access to infected viscera of man containing hydatid cyst. The natural cycle is maintained between dog and sheep.

Mode of transmission of Echinococcus granulosus:

• The disease caused by E. granulosus is zoonotic.
• Human being an accidental host, acquires the infection through ingestion of the eggs in following ways:
• Direct contact with infected dogs.
• Indirectly through food, water and other materials contaminated with eggs of the parasite.
• Less commonly, by coprophagic flies which may aid as mechanical vector of eggs.

Pathogenesis of Echinococcus granulosus:

• Mainly mechanical damage is produced.
• The young cyst that develops embryos lodged in vital centers may soon infected with functions of the organ with damaging, even fatal results.
•  Benign cyst may be asymptomatic or it may produce physical burden to the patient.
• The severity relies on the type of tumor and organ or tissue where it first becomes implanted and Anaphylactic reactions develop.

Clinical manifestation of Echinococcus granulosus :

• The parasite gives rise to cystic echinococcosis earlier known as hydatid disease or hydatidosis. The hydatid cyst is primarily responsible for the pathogenesis of the disease.
• The condition persists as asymptomatic for a long period after infection in a majority of cases.
• The clinical symptoms in CE in symptomatic cases, relies upon the organ involved, interaction between the expanding cyst and adjacent organ and complications occurred by rupture of cyst.
• The cyst in vital organs interfere with the function of affected organs with the risk of fatality in certain cases.
• Hepatic hydatid:
  • It is seen in 66% of cases. It may appear as hepatomegaly, with or without palpable abdominal man.
  • The condition is linked with pain, nausea and vomiting, portal hypertension and biliary peritonitis.
  • Cyst may rupture into bile ducts, leading to intermittent jaundice, fever and eosinophilia.
  • Allergic exhibition up to anaphylactic shock may occur in case of sudden rupture.
• Pulmonary Hydatid:
  • Pulmonary cyst may be present in 22% of patients.
  • Cyst occurring within the lung tissue cause hemoptysis transient thoracic pain and shortness of breath.
  •  In case the rupture is incomplete, cyst may transform into chronic pulmonary abscess.
  • The patient reports of sudden attack of cough with sputum containing frothy blood, mucus and hydatid sand.
• Brain cyst (up to 1%)
  • A large cyst may lead to symptoms of increased intracranial tension (headache, vomiting and poor vision) up to epilepsy.
• Renal cyst (about 3%)
  • It causes intermittent pain and hematuria.
  • The hydatid sand may be present in urine.
  • Hydatid cyst of the spleen, heart may present as tumor like condition or an abscess.
• Osseous cyst (about 2%)
  • Osseous cyst wall has only 1 layer the germinal layer which develops first in the narrow cavity, then extend to the osseous tissue leading to:
  • Erosion of large men of bone
  • Destruction of bone trabecular
  • Spontaneous (pathological) fractures

Complications:

• The cyst may rupture due to the trauma and during surgery into the pericardium, the bile ducts and the GI tract leads to severe clinical outcomes such as pleural effusion, pneumothorax and secondary echinococcosis of peritoneal or pleural cavity.
•  A ruptured hydatid cyst leads to two risks:
• The released hydatid fluid if absorbed in the circulation bronchi, peritoneum or pleura produces a sudden anaphylactic shock which may be fatal.
• This may result in the formation of secondary echinococcosis in various parts of body due to dissemination of scolices by the circulation.

Epidemiology

• E. granulosus is cosmopolitan in distribution.
• Infection is endemic to East and South Africa, central and South America, South east and central Europe and Middle East, Russia and China.
• Annual incidence of CE per 100000 rates vary largely among these countries.

Echinococcus granulosus (Dog tapeworm)

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The post Difference between Ancyclostoma duodenale and Necator americanus appeared first on Online Biology Notes.

• Hookworms are parasitic nematode that lives in the small intestine of mammalian host such as dog, cat or humans.
• They are characterized by their presence of well-defined buccal capsules bearing clotting plates and teeth.
• Two species of hookworms, commonly infect humans:
  • Ancylostoma duodenale
  • Necator americanus
• Ancylostoma duodenale, also known as the old hookworm is a common hookworm of human.
•  It causes ancylostomiasis in humans, characterized by non-deficiency anemia and hypoalbuminemia.
• Necator americanus also known as the New World hookworm is another cause of hookworm disease in humans.
•  Necatoriasis is the term for the condition of being host to an infestation of a species of Necator.

Habitat:

• The adult worm lives in the small intestine of a man particularly in the jejunum, less often in the duodenum and rarely in the ileum.

Morphology: Ancyclostoma duodenale

Adult worm:

• It is small greyish white, cylindrical worm.
• When freshly passed the worm has a reddish-brown color due to the ingested blood in intestinal tract.
• The anterior end of the worm is bent slightly in the same direction of the body curve resembling a hook, hence they are called hookworms.
• The large and conspicuous buccal capsule is lined with a hard substance
• The buccal capsule is provided with 6 teeth, 4-hook like on the ventral surface and had a pair of knob-like (triangular plates) on the dorsal surface.
• There are five glands connected with the digestive system:
  • one of them called the esophageal gland, secretes a ferment which prevents the clotting of blood.
• The sexes are easily differentiated by their size, the shape of the tail and position of the genital opening.
• Male:
  • shorter, measuring 8mm in length, the posterior end is expanded in an umbrella like fashion (copulatory bursa).
  • -Genital opening is present posteriorly and opens with the cloaca.
• Female:
  • longer than males, measuring 12.5 mm in length.
  • The posterior end is tapering and possess no bursa.
  • The genital pore is present at the junction of posterior and middle third of the body.
  • Owing to the position of the genital opening, the worm assumes the Y-shaped figure during copulation.
• Copulatory bursa in males is characteristic bell shaped used to catch and hold the female nematode during mating.
• – It is membranous, asymmetrical and consists of 13 fingers like rays in 3 lobes: 1 dorsal and 2 lateral.
• -Dorsal lobe consists 3 (1 single dorsal ray and 2 external dorsal rays: the two lateral lobes contain 1/3 pairs of lateral rays and 2 pairs of ventral rays).

Eggs:

• Eggs are oval in shape.
• 60 mm in length and 40 mm in breadth colorless.
• They are surrounded by a transparent hyaline shell-membrane.
• Eggs contain an un-segmented ovum usually with 4 blastomeres.
• A clear space is present between the egg shell and segmented ovum.
• These eggs floats in saturated solution of common salt.
• The eggs of Necator is slightly smaller than Ancylostoma.
• The female Ancylostoma produces 10,000-20,000 eggs per day whereas N. americanus produce less eggs i.e. 3000-6000 per day.

Filariform larva:

• It is the non-feeding form of the worm and is the infective form of the parasite.

Life cycle:

• The life cycle of the two species of hook worm are same.
• The only difference is the morphology of filariform larva.
• Life cycle is completed in a single host, the man. No other intermediate host is required.
• The following are the various stages of the life cycle:
• Stage 1: Passage of eggs from the infected host
  • The eggs containing segmented oval with 4 blastomeres, are passed out in the feces of human host.
• Stage 2: Development in soil
  • Eggs under the favorable conditions (damp, warm, well-oxygenated soil) hatch to rhabditiform larva (250mm in length) i.e. L1 larva within 48 hours.
  • The rhabditiform larva moults twice, on the 3^rd and 5^th day to develop into a filariform larva (500—600 mm in length), the infective stage of the parasite.
  • The time taken for development from eggs to filariform larva is on an average 8-10 days.
• Stage 3: Entrance to new host
  • The L3 larva cast of their sheath and gain entrance into the body by penetrating the skin, through the epidermis to dermis and subcutaneous tissue.
• Stage4: Migration
  • On reaching the subcutaneous tissue, the larva enters into the lymphatic small vessels.
  • They pass through the lymph-vascular system into the venom circulation and carried via the right heart into the pulmonary capillaries.
  • They break the lung capillaries and enter into the alveolar spaces.
  • They then ascend upward the bronchial tree to trachea and larynx, crawl up over the epiglottis to the back of pharynx and ultimately swallowed.
  • During migration or entering the esophagus, the larva undergoes a third moult to form fourth stage (L4 larva) equipped with a buccal capsule allowing adherence to the gut wall.
• Stage5:  Localization and laying of eggs
  • The growing larva settle down in the small intestine, undergo a fourth moult to develop into an adolescent worm.
  •  At this stage, the provisional toothless buccal capsule formed is cast off and definitive buccal capsule complete with teeth is formed.
  •  During 4-5 weeks, the adults who remain attached to mucosa of the small intestine becomes sexually mature.
  • The fertilized females begin to lay eggs which are excreted out in the feces.
  • The cycle is thus repeated.
  • The interval between the time of skin infection and the first appearance of eggs in feces is about 6 weeks.

Mode of transmission:

• Human feces are the only source of infection.
•  The route of infection transmission:
  • Cutaneous route: Penetration of the skin by infective filariform larva
  • Oral route: Ingestion of L3 larva present in the soil, occurs less frequency. Larva in mouth develops directly into adult worms.
  • Transmammary transmission: Breast feeding by mothers to infants.
  • Very rarely, trans-parental transmission.

Pathogenesis:

Pathogenicity of adult worm:

• The major pathological changes in ancyclostomiasis are caused by the attachment of adult worms to the intestinal walls by their buccal capsule.
• The common site of infection is the upper small intestine.
• The attachment of parasite leads to mechanical disruption of intestinal mucosa of the resulting ‘mucosal plug’ lodged within the worm’s buccal capsule.
• These parasites penetrate the blood vessels with their mouth parts and suck the blood to get the nutrition.
• These worms cause considerable loss of blood and tissue.
• The adult Ancylostoma can suck about 0.2 ml blood a day while smaller Necator suck about 0.03 ml per day.
• The secretions of the site may continue for sometimes, this add to blood loss.
• Excessive blood loss caused by heavy and prolonged worm infection leads to hypochromic microcytic anemia.

Pathogenicity of infective larva:

• The infective filariform larva at the site of the penetration of the skin, produce a local reaction called ground itch.
•  This allergic manifestation is more severe in Necator infection
•  In previously sensitized host, it can lead to secondary bacterial infections.
• The migration of large no. of larva, through the lung produces minute hemorrhage and infiltration of leucocytes resulting in the entrapment of the larva in lung tissue.
• Both eosinophilia and leukocytosis occur at this stage.

Clinical manifestation:

The clinical symptoms depend on the site where the worms are present and their burden.

1. Skin infection:

• Hookworm related cutaneous larva migrans (HrCLM) is a parasitic skin disease caused by migration of hookworm larva in the epidermis.
• Ground itch is the early clinical manifestation during the penetration of L3 larva on the skin. It is believed to be due to allergic components of the larva.
• Lesions are characteristically seen in and around feet particularly between the toes.
• It is associated with intense itching, edema and erythema and rash.
• The associated secondary bacterial infection is more common during this stage.

2. Pulmonary infection:

• It is associated with low grade fever, mild cough dizziness and hemolysis.
• Pneumonia with pulmonary consolidation is seen in persons with severe infection.

3. Intestinal infection:

• Acute intestinal symptoms such as abdominal pain, nausea, vomiting and hemorrhagic diarrhea are observed.
• Chronic hook worm disease is characterized by blood loss and Ion-deficiency anemia and is associated with fatigue, pallor, tachycardia and dyspnea on exertion.
• Hypoproteinemia may cause edema and there can be sign of malabsorption and malnutrition.
• In children there may also be adverse effects on physical growth and intellectual growth.
• The severity of the disease varies with the worm burden and the amount of blood lost heavy infections can be fatal, particularly in infants.

Laboratory diagnosis:

• Specimen:
  • Stool, duodenal content obtained by the duodenal intubation (Ryles tube) may sometimes reveal either egg or the adult worms.

 1. Stool microscopy:

• A specific diagnosis of hookworm infection is based on the microscopic identification of eggs.
• This is carried out by examination of a direct wet mount of the stool.
• In case of light hook worm infection, detection of eggs can be done using concentration methods-formalin ether concentration technique or simple salt floatation technique.
• Kato-Katz is a useful method for quantitation estimation of hook worm eggs present in the stool.
• The intensity of the infection is determined by counting the no. of eggs in a measured volume of feces.

2. Stool culture:

• Harada- mori method of culture of stool is carried out to demonstrate L3 larva.
• The eggs present in the stool are smeared in moist filter paper, after an incubation of 5-7 days at room temperature, L3 larva hatch out of eggs.

3. Imaging methods:

• On chest X-ray a patchy infiltrate may be demonstrated in the migratory phase of larva in the lungs.

4. Blood test:

• This is carried out to ascertain the nature of anemia and the presence of eosinophilia.

5. Occult blood test:

• occult blood in the stool gives a position reaction in case of hookworm infection
• Charcot-Leyden crystals are often found in the stool.

Treatment:

• Mebendazole is a drug of choice- oral, 100 mg twice daily for 3 days
• Others anti parasitic drugs are- pyrantel pamoate, thiabendazole, Albendazole, levamisole
• Treatment of iron deficiency anemia with replacement iron therapy.

Prevention:

• Sanitary disposal of human feces
• Treatment of infected persons.
• Use of sanitary latrines, use of foot wears.
• Health education with improved nutrition supplemented with the dietary iron.

Epidemiology:

• Hookworm infections are the second most common helminthic infection next to ascariasis.
• The infection in worldwide is distribution more commonly in areas with warm and moist climate.
•  Approx. 1200 million people are infected worldwide.
• Ancylostoma is found in Europe around the Mediterranean, on the west of South America and in parts of China, India and Nepal.
• Necator is found much over of the western Hemisphere, Africa and South East Asia.

Hookworm infection: life cycle, transmission, pathogenesis, diagnosis and treatment

The post Hookworm infection: life cycle, transmission, pathogenesis, diagnosis and treatment appeared first on Online Biology Notes.

• Dracunuculus medinensis is among the longest nematodes affecting humans.
• It is also known as Guinea worm, Medina worm, serpent worm or dragon worm.
• It causes dracunculiasis or dracontiasis, a nodular dermatosis produced by the development of Dracunculus parasite in the subcutaneous tissue.

Habitat:

• The adult females inhabit the subcutaneous tissue usually of the foot or lower limbs.
•  Less frequently they also inhabit other parts of the body including the head and neck.

Morphology:

Adult worms

• Male:
  • Male worms are difficult to demonstrate as they are immediately after fertilizing the females.  Hence, it has not yet been recovered from man.
  • The male measures 12-30 mm in length and 0.4 mm in breadth.
• Female:
  • It is slender long worm and is one of the longest nematodes known to cause infection in man.
  • It measures 60 cm to 1 mm or more in length and 1.5 to 1.7 mm in diameter, resembling a piece of long twine thread.
  • The body is cylindrical, smooth and milk white in color.
  • The posterior end is extremely tapering and is bent to form a hook.
  • A minute triangular mouth is present in an anterior end.
  • An inner layer of 4 papillae-6 papillae and outer layer of 4 pairs of papillae surrounded the mouth.
  • A pair of uteri, oviducts and tubules and a single unpaired vagina constitutes the female genital tract.
  • The worm is ovoviviparous and discharge embryos in successive batches for a period of about 3 weeks until the gravid female completely implies its uterine contents.
  • The body fluid is toxic and causes a bluster if female escapes into the tissue.The life span of female is about 1 year and that of the male is not more than 6 months.

larva:

• First stage Larva
  • It is unsheathed and coiled with a round anterior end and a long slender filariform tail.
  • It is large, measuring 650-750 mm in length and 17-20 mm in breadth.
  • The cuticle is conspicuously striated.
  • It moves about with a shift motion, briskly coiling and uncoiling body.
  • It shows a tad-pole like movement in water.
  • These larva are set free only at the time of partition when the affected part is submerged in water.
  • Further development proceeds in the body of a minute fresh water crustacean of the genus Cylops.
• Third stage of larva:
  • It is the infective stage of the parasite.
  • It is found in the body cavity of Cyclops.

Life cycle of Dracunuculus medinensis :

• Lifecycle is completed in two hosts:
  • Definitive host: Human
  • Intermediate host: Cyclops and other twelve species.

• Entrance into man and development into adult worms:
  • Man acquires infections by drinking unfiltered water containing infected Cyclops.
  • On reaching the stomach, the cyclopses are digested by the gastric juices and L3 larva are liberated.
  •  The larva penetrated the gut wall and enter the retroperitoneal connective tissue where they grow and becomes sexually mature.
  • The males die after fertilizing the females and disappear within 6 months of infection.
  • The gravid female migrates and selects those parts of the skin labile to come in contact with water such as the backs of water carriers, anus and legs of washer men and legs of those who fill water in containers in ‘step wells’ and ponds.
  •  On reaching the skin surface, it secretes a toxin, producing a blister which later ruptures and forms an ulcer, contact with water stimulates the worm to protrude its head through the center of the ulcer and causes a reflex discharge of a milky fluid containing large number of first stage rhabditiform larva.
• Development of larva in Cyclops:
  • The larva discharged in water swims vigorously in water with tad-pole like movement.
  • These larvae further develop when ingested by suitable Cyclops species.
  • In the body cavity of Cyclops, the first stage larva moults twice to develop into third stage larva, the infection from the parasite.
  • These infected Cyclops have short life span than normal non infected ones.
  • The infected Cyclops harboring third stage larva are infective to man and the cycle is repeated.

Mode of transmission:

• Water containing infected Cyclops is the main source of infection.
• Man acquires infections by drinking water contaminated with Cyclops harboring third stage larva.

Pathogenesis:

• The third stage larva are not pathogenesis and do not produce any pathological lesions.
• Only female adult worm is pathogenic.
•  It produces a toxin, forming blister which is formed at the site at which the female worm comes out of the surface of the skin on coming contact with water.
•  The blister is filled with the fluid which is bacteriologically sterile and contains numerous larvae and leucocytes.
• Diffusible toxins produced by the parasite are believed to cause urticaria, dyspnea, vomiting, mild fever and occasional fainting.

Clinical manifestation:

• The pre-patent period is 10-14 months.
•  The symptoms are manifested during parturition of the female and are due to the liberation of a toxic substance causing allergic manifestation and blister formation.
• Septic infection can occur as a result of contamination by secondary organisms drawn in by the worm at the time of retraction.
• Blister formation appears wherever the female worms make an attempt to come to the surface of the body where it can readily discharge its larva.
•  The blister is usually found on the lower extremities of the body especially between the metatarsal bones, sole of the feet or on the ankle and less frequently in arms, buttock, scrotum, head, neck and female breast.
• Blister formation is accompanied by intense burning pain, ‘fiery serpent’.
• This may be accompanied by generalized reactions such as urticaria, nausea, vomiting, diarrhea and giddiness and marked burning sensation over the next few days the lesions vesiculates and blister ruptures producing a painful ulcer.
• The worm is often visible in the opening of ulcer.
• If the female worms break during the attempts of extractions the larva remain trapped in the subcutaneous tissue and may give rise to cellulitis and abscesses.
• In uncomplicated cases, lesions may only last for several weeks until the worm is completely expelled.
• However, many cases infection of the worm track with persistence of the lesions, chronic ulceration and possible sequelae, involving disseminated infection, phlegma of limbs, contractures of tendons, fibrous ankylosis or arthritis in the joints, die prematurely and calcify. The calcified worms can be trigger arthritis, locked joints or permanent clipping and deformations.

Laboratory diagnosis:

• Detection of adult worms:
  • This is possible when the female worm appears at the surface of the skin.
• Detection of first stage larva:
  • Specific diagnosis is made by the microscopic demonstration of the first stage larva in the discharge fluid.
• Intradermal test:
  • Infection of Dracunculus antigens intradermally causes a wheal to appear in the course of 24 hours in positive cases.
• X-ray examination:
  • Worms in deeper tissue after the death either become calcified or absorbed.
  • The position of calcified worm may be located by skiagraphy.
• Blood examination
• Serodiagnosis:
  • IFA, IHA, ELISA and western blot are the frequently used test for demonstration of circulating antibodies in the serum for diagnosis of dracunculiasis.

Treatment:

• There is no specific drugs or medicines to treat or prevent the disease.
• The mainstay of treatment is the extractions of the adult worm from the patient using a stick at the surface and wrapping the worm or few cm per day.
• Full extraction can take several days or weeks.
• Topical antibodies are applied to prevent secondary bacterial infections and the affected body part is bandaged with fresh gauze to protect the site.
• Surgical removal of worm using local anesthesia is another method of treatment
• Albendazole, Mebendazole, Niridazole, thiabendazole and metronidazole are used as anti-inflammatory agents.
• Analgesics such as aspirin or ibuprofen are given to help reduce the pain and inflammation.

Prevention and control:

• The disease can be transmitted only by drinking contaminated water and can be completely prevented through to relatively simple measures.
• Preventing people from drinking Cyclops contaminated water:
• Avoid drinking contaminated water
• Filtering water
• Boiling
• Treatment of water with larvicides to kill Cyclops
• Preventing people infected with the worm from entering water sources used for drinking.

Epidemiology

• D. medinensis infection is reported from 18 century of the world.
• The infection is particularly wide spread in Africa and middle east.
• About 140 million people are estimated to suffer from dracunculiasis.

Dracunculus medinensis: life cycle, pathogenesis, clinical symptoms,diagnosis and treatment

The post Dracunculus medinensis: life cycle, pathogenesis, clinical symptoms,diagnosis and treatment appeared first on Online Biology Notes.

• Infected person with circulating microfilariae is the chief source and reservoirs of infection.
• Person to Person transmission occurs by the bite of infected mosquitos.

Pathogenesis:

• Though L3 larva are infective larva they do not have any pathogenic effect.
• Similarly, circulating microfilariae are also not pathogenic.
• The pathogenic effects are due to the fourth stage larva, moulting stage from L3 and adult worms whether living or dead present in the lymphatic vessels.
• The following stage occur sequentially during the pathogenesis or lymphatic filariasis.
• i. Dilation of lymph vessels:
  • The developing larva and metabolic products released during the moulting of the larva, unsheathing of microfilariae during moulting and the presence of the adult worms induces inflammatory reactions.
  • The intense inflammation of lymph vessels leads to dilation of lymph vessels during the early stage of infection.
  • Besides inflammation, immune reaction of host against the worms and toxic effects of the worms also results in dilation of lymphatic vessels.
  • Dilation of lymphatic causes an increased secretion of proteinaceous material from lymphatics into the surrounding tissue leading to the information of conspicuous lymphedema and thickening of the endothelium.
• ii. Infection of lymphatic vessels (lymphangitis):
  • Progression of infection develops with lymphangitis.
  •  It is characterized by presence of dilated, inflamed and thickened lymphatic vessels associated with erythema, edema and tender painful areas.
  • The main causes of lymphangitis are:
    • Irritation caused by the movement of the adult worm inside the lymphatic system.
    • Release of metabolic wastes by larva
    • Absorption of toxic wastes liberated from dead worms by host cells.
    • Secondary bacterial infection streptococci.
• iii. Obstructions of the lymph node:
  • The lymphangitis is followed by necrosis, sclerosis and obstruction of lymphatic vessels proximal to the lymph nodes.
  • Flow of lymph is obstructed due to-
    • Presence of worm in the lymph vessels
    • Thickening to lymphatic vessels as well as focal necrosis.
    • Giant cell formation, fibrosis as well as cellular changes result in obstruction of lymphatic vessels
    • The obstruction of the lymph flow results in elephantiasis which is the classical feature.
• The course of the events in the pathogenesis of the lymphatic filariasis are variable and depend upon interaction of a variety of host and parasitic factors.

Clinical manifestation: Lymphatic filariasis

• It is caused by the juvenile and adult worms of W. bancrofti.
• The clinical manifestation of the condition depend on stages of the disease as follows:

i. Endemic normal: No overt clinical symptoms

ii. Asymptomatic stage:

• Person in this stage have microfilariae in their blood but do not show any clinical manifestation of filariasis.
• They may remain asymptomatic for years or even after life.

iii. Acute filariasis:

• Acute filariasis or inflammatory phase is caused by antigens released from female adult worms.
• The condition is characterized by Filarial fever (usually low grade but occasionally severe), accompanied by chills, general malaise, headache and pain are other symptoms.
• Lymphedema
• Lymphadenitis
• Adeno-lymphangitis (ADL)

iv. Chronic filariasis:

• It is the obstructive phase usually takes 10-15 years to develop.
• Typical manifestation includes:
• Lymph varices: Caused by the obstruction of lymph flow and accumulation of lymph in the ducts leading to dilation of the ducts.
• Hydrocele: Caused by obstruction of the lymph vessels of the spermatic cord and exudation from the inflamed test and epididymis.
• Elephantiasis: It is the result of wuchererial infection and usually follows years of continual infections.
• It is caused by fibrotic construction of all the afferent lymphatics draining the past.
• Hypertrophy and hyperplasia seen are the result of excessive protein, in the lymph exudates stimulating the connective tissue to excessive growth.
• Elephantiasis in the scrotum, legs and arms of male and legs and arms of female is the feature of chronic elephantiasis.
• The affected part becomes enormously enlarged producing a tumor like solidity.
• The surface of the skin becomes rough, and even papillomatous.
• The hairs become rough and sparse.
• On section the skin cuts like an unripe pear, it is thickened, dense and fibrous.
• The subcutaneous tissue shows a blubbery appearance in which the dilated and thickened lymphatics and veins can be seen.
• The underlying muscles and bones do not usually show any alteration.
• Granuloma of breast: Characterized by the presence of film solitary mass in the breast.
• Chyluria: Urine shows chyle mixed with blood and occasionally microfilariae.
• Caused by escape of chyle through the urine due to the rupture of varicose chyle vessels through the mucous membrane of the urinary tract.

v. Occult filariasis:

• It denotes a condition of hypersensitivity reaction of the host to micro-filarial antigens characteristically microfilariae are not found in the peripheral blood and the classic features of lymphatic filariasis are absent.
• Tropical pulmonary eosinophilia (TPE) is the most important manifestation.
• Arthritis, tenosynovitis, dermatoses etc. in the endemic areas are the less frequent manifestation of occult filariasis.
• TPE is distinct clinical syndrome characterized by chronic pulmonary infiltration in chest X-ray, hypereosinophilia of the peripheral blood and respiratory symptoms like low grade fever, cough, chest pain and asthmatic attacks especially at night.

vi. Less frequent lesions:

• These includes granuloma of the spleen and other organs and the presence of adult W. bancrofti in the anterior chamber of the eye.

Complications:

• Secondary bacterial infections of the overlying skin of elephantiasis of the leg or arm.

Laboratory diagnosis:

Parasitic diagnosis:

• Specimen: Peripheral blood is the specimen of choice.

Methods of examination includes:

i. Microscopy:

• The standard method for diagnosing active infection is the identification of microfilariae in blood smear by microscopic examination.
• Blood collection should be done at night to coincide with the appearance of the microfilariae.
• It can be determined by following method:
• Direct wet mount:
  • 2-3 drops of blood are collected on a clean glass slide and examined microscopically after placing cover slip on it.
  • -ive microfilariae are identified by their characteristic serpentine movement in the blood plasma.
• Stained thick blood film smears:
  • Thick and smear stained with Giemsa or Leishman is the most commonly used method.
  • The presence of sheath but the absence of nuclei in the tail end of microfilaria is diagnostic of W. bancrofti microfilaria.
• Concentration of blood:
  • Increase of low number of microfilariae in blood, their recovery can be increased by various concentration methods like knot’s method of concentration by sedimentation, membrane filtration concentration methods using Nucleopore or Millipore membrane filters.
• DEC provocation test:
  • In this test (Diethylcarbamazine) is given orally at a dose of 2-8 mg/kg. after 30 min the capillary blood is collected by finger prick for demonstration of microfilariae by direct wet amount or staining the smear.
  • DEC stimulates nocturnal periodic microfilariae to circulate in the peripheral blood during the day time.
• QBC:
  • This method can frequently demonstrate the circulating microfilariae in the blood.
• Urine microscopy:
  • Microfilariae can be demonstrated in the chylous urine.
  • 10 ml-20 ml of the first early morning urine is collected for examination and demonstration of microfilariae by microscopy.
  • Microscopy of hydrocele fluid and lymph node aspirations.
  • Microfilariae can also be demonstrated in hydrocele fluid and also in lymph node aspiration. Either is used hydrocele fluid to dissolve fat globules.

II. Immune diagnosis:

 Serological tests:

i. Demonstration of circulating antibodies:

• IHA, IFA, ELISA, RLA, luminescence immune analyses are used to demonstrate the circulating antibodies in the serum
• Disadvantage of these test are that they show cross reactivity with sera from other filarial and helminthic infections and they are unable discriminate between past and current infections.

ii. Demonstration of circulating antigens:

• The circulating antigens are present in serum only during recent or current infections.
• ELISA employing monoclonal antibody AD12 detects a 200 Kda of adult W. bancrofti in the serum.
• The other ELISA using monoclonal antibiotic Og4c3 detects adult worm as well as microfilariae antigen in the serum.

Molecular methods:

• PCR methods have been developed however they are not much sensitivity PCR is positive only when circulating microfilariae are found in the peripheral blood.

Imaging methods:

• X-ray: Chest x-ray shows diffuse pulmonary infiltrates in patients with TPE.
• Ultrasound: Only non-invasive method for detection of adult worms in the affected lymph nodes.
• The live adult worms are identified by a distinctive pattern of their movement known as filarial dance sign.

Other tests:

• Biopsy of lymph node that has been enlarged show cross sections of adult worms
• Eosinophilia can be seen in complete blood cell count

Treatment:

• Diethylcarbamazine (DEC), drug of choice.
• Dose: oral, 3mg to 6 mg/kg daily in divided doses for 3 weeks
• Others: Ivermectin, Levamisole, Mebendazole and Centprazine.

Prevention and control:

• Clinical control of mosquito by spraying DDT, malathion etc.
• Biological control by using of B. sphaericus, B. thuringienesis, Poecilid reticulate molliensis.
• Effective drainage and sewage system to eliminate breeding of mosquito
• Treatment of cases
• Use of bed nets, house screens
• Interrupting transmission of infection.

Lymphatic filariasis (W. bancrofti): transmission, Pathogenesis, clinical manifestation and treatment

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Habitat

• Adult worms are found in the lymphatic vessel, especially the lymph nodes.
• The microfilariae are found in the peripheral blood, occasionally they are also found in chylous urine or in hydrocele fluid.

Morphology of W. bancrofti

1. Adult worms

• W. bancrofti exhibits considerable sexual dimorphism.
• These are minute, long hair like transparent (often creamy in color) nematodes.
• They are filiform in shape with both ends tapering.
• The head end terminating in a slightly round swelling, and surrounded by two rows of 10 sessile papillae. The posterior end contains anus at its terminal end.
• The male measures 2.5-4 cm in length with 0.1 mm in thickness. The tail end is curved ventrally and contains two spicules of unequal length.
• The females are longer than males measure 8-10 cm in length with 0.2-0.3 mm in thickness. Its tail end is narrow and abruptly pointed. The females are oviparous.
• The adults obtain their nourishment from the lymph of the lymphatic system.
• The life span of the adult worms is long, probably several years (5-10 year or even more).

2. Microfilariae (Embryos):

• The first stage of larva is called microfilariae.
• They are very active in their habits and can move both with and against the blood stream, when sustained, they appear as colorless and transparent bodies with blunt heads and pointed tails.
• The embryo measures about 290 mm in length by 6-7 mm in breadth.
• When dead and stained with Romanowsky’s stains, they show the following morphological features:
• Hyaline sheath:
  • It is a sac like envelope which is much longer (359 mm) than the larval body represents the chorionic envelop of the eggs.
  • It remains as investing membrane around the larva.
• Cuticle:
  • It is lined by subcuticular cells and is seen only with vital stains.
• Somatic cells or nuclei:
  • Nucleiappear as granules in the central axis of the body and extend from the head to the tail end, except the terminal 5% of the tip of the tail. This is the distinguishing feature of the parasite.
  • The space at the anterior end devoid of granules is seen called as cephalic space.
  • The granules are broken at definite places serving as the landmarks for identification of the species.
  • They include:
    (a) Nerve ring; an oblique space
    (b) anterior V-spot represents the rudimentary excretory system
    (c) the posterior V spot or tail spot represents the terminal part of the alimentary canal/anus or cloaca.

3. Third stage of larva (infective form):

• The L3 larva the infective form of the parasite is found only in mosquito.
• They are elongated, filariform, measures 1.4-2 cm in length and 18-23 cm in breadth.

Life cycle:

• W. bancrofti completes its life cycle in two hosts:
  • Definite host: Human
  • Intermediate host: mosquito, belonging to genus Culex, Aedes and Anopheles.
• Life cycle in Human: Entrance in the human and development into adult worms
  • Infection is acquired by the bite of infected mosquito during which L3 larva are deposited on the skin.
  • The L3 larva are not directly injected into the blood stream.
  • The L3 larva are deposited on the skin near the site of the puncture.
  • Later attracted by the warmth of the skin, the larva enters through the puncture wound or penetrates through the skin on their own.
  • The L3 larva after penetrating the skin, reaches the lymphatic channels, settles down at some spot (inguinal, scrotal or abdominal lymphatics), metamorphose and becomes sexually mature.
  • The male fertilizes the female and the gravid females discharge microfilariae which usually appear in the peripheral blood in 8-12 month of infection.
  • These micro filariae circulate in the blood for 6 months to 2 years and then die if not taken by mosquito.
• Life cycle in Mosquito: Stages in the development of micro filaria
  • Microfilaria ingested by the mosquito lose their sheath within 2 to 6 hours of their arrival in the stomach.
  • Then they penetrate the gut wall and migrate to the thoracic muscle, where they rest and begin to grow.
  • In the next 2 days, microfilaria become thick, short sausage shaped with a short spiky tail, measuring 124-200 mm in length 10-17 mm in breadth. This is the first stage larva L1.
  • The larvae possesses a rudimentary digestive tract.
  • During 3-7 days of time, the larva grows rapidly, moults once or twice and measures 225-330 mm in length by 15-30 mm in breadth. This is the second stage larva L2.
  • Metamorphosis completes by 10-11days with distinct features such as the tail atrophies to a mere stump and the digestive system, body cavity and genital organs are now fully developed. This is the third stage larva L3.
  • These L3 larva are the infective form which enters the proboscis sheath of the mosquito on or about the 14^th day.
  • When the mosquito bites a man during the blood meal, the L3 larva are released from the tip of proboscis of mosquito and the cycle is repeated.
  • Development in mosquito takes place within 10-20 days.

Epidemiology of Wuchereria bancrofti

• W. bancrofti is largely confined to tropics and subtropics. They are found in India, West-Indies, Puerto Rico, Southern China, Japan, Pacific Island, West and central Africa, South America.
• The disease is endemic in 83 countries with more than 1.2 billion at risk.
• It is estimated that more than 120 million people are infected.
• More than 25 million men suffer from genital symptoms and more than 15 million people suffer from lymphedema or elephantiasis of leg.

Periodicity:

• The microfilariae of oriental countries (India and China) show nocturnal periodicity.
• They are found periodically in peripheral blood at night especially between 10pm to 4 am.

Wuchereria bancrofti: Morphology, life cycle and Epidemiology

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• Trichuris trichiura commonly called the whipworm because of its characteristic whip-like shape.
• It causes trichosis in human which is an intestinal infection caused by invasion of the colon by the adult worm.

Habitat:

• The adult worm lives in the large intestine (caecum) of human
•  It can also be present in the vermiform appendix and rectum.

Morphology

• The adult worms resemble the whip. The anterior 3/5^th of the end is very thin hair like and the posterior 2/5^th is thick and stout resembling the handle of a whip.
• The anterior ends penetrate the mucosa layer and remain deeply embedded.
• Adult worms are pinkish in color.
• The anterior end consists of a long oesophagus which is a minute channel while the posterior end contains the intestine and sex organs.

Male worm:

• The adult males are 3-4 cm in length and are recognized by their characteristic coiled posterior end.

Female worm:

• Female worms are longer than males measuring 4-5 cm in length.
• The caudal extremity is either comma shaped or an arc shaped

Eggs

• Egg of Trichuris trichiura has diagnostic value. Egg is barrel shaped with a mucous plug at each end.
• It is brown colored (bile-stained) and has a double shell.
• The egg measures 50-54 µm in length and 22-23 µm in breadth.
• Eggs contain an un-segmented ovum when it leaves the human hosts.
• The freshly passed eggs are non-infective to human.
• Eggs float in saturated NaCl solution.

Life cycle of Trichuris trichiura:

• The life cycle of T. trichiura is simple and is completed in single host, the man. However, change of host is needed for the continuation of species.
• No intermediate host is required.
• Human acquires infection by ingestion of food or water contaminated with embryonated eggs.
• The digestive enzymes dissolve the eggs shell and the larva emerges out through one of the poles of the eggs.
• The liberated larva then pass down into the caecum which is their site of the localization.
• In caecum the larvae develops into adult worm and become sexually mature within a month from the time of ingestion of eggs.
• The female worm after being fertilized by the male begins to lay the eggs, which is about 3 month after infection.
• The freshly laid eggs are un-embryonated and excreted out with the faeces.
• Each adult female can produce about 5000-7000 eggs per day for upto 5 years.
• Embryogenesis within eggs occur in outside environment in the water or damp soil.
• In tropical climates larva develops within the egg in the course of 3-4 weeks. In temperate climates, the larva takes a long time (6-12 month) to complete its development.
• Once the egg is embryonated, it is infective to human.

Mode of transmission:

1. The food, water and soil contaminated with embryonated eggs are the chief sources of infection.
2. Ingestion of embroynated eggs in the contaminated food and water
3. Contaminated fingers during soil works

Pathogenesis

• The adult worm invades the intestinal mucosa by its thin, thread like anterior end and feeds on tissue secretions but not on blood.
• It causes petechial hemorrhage, inflammation, oedema and mucosal bleeding in the intestinal mucosa at their site of attachment.
• The lumen of appendix can be blocked in case of severe worm load.
• Presence of worms in the mucus membrane irritates the nervous plexus of mucosa causing diarrhea and cramps.
• Occasional eosinophilia can be present
• Approximately 0.005 ml of blood per worm per day is lost in the infected man.

Clinical manifestation

• The clinical manifestation of Trichuris trichiura depends upon the intestinal worm load of the person.
• Infection is asymptomatic in case of light infection with 100-200 worms.
• For moderate infection the number of worm should be more than 200 worms and this can manifest as vague abdominal discomfort and diarrhea (rarely bloody), vomiting, headache etc.
• Trichuriasis: In case of heavy infection with more than 800 worms, serious complications especially in children are observed.
• It causes bloody diarrhea with profuse mucus, abdominal pain and tenesmus weight loss leading to the cachexia, severe anaemia.
• Distribution of a large number of worms throughout the colon and rectum may cause prolapse of the rectum.
• Migrating worms can occasionally cause appendicitis.

Epidemiology

• About 800 million people are affected worldwide
• Trichuris trichiura infection is commonly found in Tropical and subtropical countries with moist and warm soil. Such as tropical Africa, South America and South East Asia.

Diagnosis

• Specimen:  stool, blood
• Microscopy:
  • Finding of characteristic barrel-shaped eggs in the faeces on light microscopy.
  • Stool concentration methods may be required to detect light infection
  • Adult worms may occasionally be present in the stool.
  • The degree of infection can be determined by egg count.
  • In heavy infection stool is frequently mucoid and contains charcot-Leyden crystals.
• Proctoscopy: adult worm can be obtained from rectal mucosa sample.
• Blood test: shows eosinophilia

Treatment

• Mebendazole- drug of choice

Dose: 100 mg twice daily for 3 days

• Albendazole – 400 mg daily for 3 days

Prevention and control

1. Sanitary disposal of faeces.
2. Personal hygiene
3. Food hygiene
4. Treatment of infected cases.

Trichuris trichiura: Morphology, life cycle, pathogeneisis, mode of transmission, diseases, diagnosis and treatment

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• Enterobius vermicularis is commonly called the thread worm, pin or seat worm. It causes an intestinal parasitic infection called enterobiasis (anal itching) that occurs commonly in children.

Habitat:

• Adult worm (gravid females) live in the caecum and vermiform appendix of human, where they remain until the eggs are developed. They generally remain on the surface of the mucosa and may occasionally encyst in the submucosa layer.

Morphology:

• The adult worm is small, white in color, more or less spindle shaped and resembles a short piece of thread.
• They are visible to the naked eye.
• True buccal capsule is absent.
• A pair of cervical alae (wing like expansions) is present as the anterior extremity.
• The posterior end of the oesophagus is dilated into a conspicuous globular bulb/ a double- bulb oesophagus which is a characteristic feature of this nematode.
• The oral end has three lips with a dorso-ventral bladder like expansion of the cuticle.

Male worm:

• An adult male measures 2-4mm in length and 0.1-0.2mm breadth.
•  The posterior third of the body is curved, sharply shortened and possess a exposed terminal copulatory spicule.
• The male worm dies immediately after fertilizing the females, therefore are rarely seen.

Female worm:

• Adult female is longer, 8-12mm in length and 0.3-0.5 mm in breadth.
• The posterior end is extremely straight and drawn out into a long, tapering and finely pointed tail, which is 1/3^rd the length of the worm.
• The female reproductive organs are paired and T-shaped.
• A large number of eggs with an average of 11,105 eggs are present in the uterus of the gravid female that fill up the entire body of the female worm.
• The gravid female dies within 2-3 weeks after laying eggs.

Eggs:

• The embryonated eggs are infective to human.
• The eggs are colorless, measuring 50-60 µm in length and 20-32µ m in breadth.
• They are typically plane convex, with one flattened side and one convex side.
• The eggs are surrounded by a thin, hyaline, transparent shell composed of 2 layers of chitin.
• Egg contains a coiled tadpole like larva.
• Egg can floats in saturated salt solution.
• The egg become infective after exposure to atmospheric oxygen for 6 hours and is  more resistant to antiseptics.

Life cycle of Enterobius vermicularis:

• The life cycle of E. vermicularis is simple and is completed in single host (Human host).
• No intermediate host is required.
• Human acquires infection by ingestion of the embryonated eggs attached to their nails during scratching of the perianal area.
• The egg shells are dissolved by digestive juices and the larva escape in the small intestine than they migrate to the caecum and vermiform appendix, where they develop to adult worms within 15-30 days of infection.
• Female worms may produce a pheromone to attract males.
• The male worm coils around a female worm with its curved area over the female genital pore.
• Male use spicules to hold female during copulation. The male dies immediately after fertilizing the female.
• The gravid female then migrates to the perianal skins at night, stimulated by a drop in body temperature of the host.
• It will only lays eggs on the perineum, because air acts as stimulant for laying eggs.
• The ejection of eggs is so forceful that the eggs can be spread out over the perianal area.
• After oviposition the female often dies.
• Eggs trapped in perianal folds may hatch out the larva and may enter intestine directly via the anus. This process is known as retro-infection.
• Occasionally larva may enter the vulva and infect the vagina of women.
• Whole life-cycle completes within in 2-13 weeks.

Mode of transmission:

• Infected human beings are the only source of infection. No extra human reservoir is known.
• It is primarily a disease of children and intra-family transmission is very common.
• The different modes of transmission are-
• Ingestion of eggs due to contaminated fingers, commonly seen in children.
• Handling contaminated night clothes of the children.
• Inhalation of air-borne eggs present in the dust.
• Retro infection, occasionally seen mainly in adults.

Pathogenesis:

Pathogenicity of eggs:

• Significant pathological lesion are caused by the eggs.
• The eggs adhere well on surface of the skin and by thin natural perianal or perianal itching.

Pathogenicity of adult worms:

• Adult worms attach to the mucosa and feed on intestinal content, bacteria and possibly epithelial cells, causing minute ulceration which may lead to mild catarrhal inflammation with diarrhea, eosinophilia and bacterial infection.
• Infection are characterized by intense perianal itching.
• Patients vigorously scratch themselves attempting to relieve the itching and doing so often cause skin damage, bleeding, bacterial infection and intensified itching
• Allergic reaction in the sensitized hosts is observed due to absorption of metabolites secreted by the worm.

Clinical manifestation: Diseases

• Most patients are asymptomatic.
• In symptomatic patients, the most common complaint is perianal and perianal pruritus, usually nocturnal or in the early morning.
• Other complaints include abdominal pain, irritability and restlessness.
• Heavy infection in children may cause anorexia, behavioral changes such as sleep disturbance, nausea, nail bite, grinding teeth at night.

Complications: Urethritis, Endomeritis, Appendicitis

Epidemiology and geographical distribution:

• The nematode is cosmopolitan, found all over the world.
• Unlike many other parasite disease, the incidence is higher in developed countries and in temperate climate than in tropical countries.
• Rate of infection is highest in children.
• Infection found more in whites than in blacks, which may be due to racial immunity.

Laboratory diagnosis:

• Eggs are rarely found in faeces, so conventional stool sample examination techniques are not useful.
• Infection are best diagnosed by microscope detection of adult worms or microscopic detection of eggs on the perineum.
• Detection of adult worms
  • Motile worms may be seen perianal skin shining under bright light when close visual examination are conducted during night or early in the morning.
  • Adult worms may sometimes be observed on the surface of fresh stool samples, during garments, perianal folds.
• Detection of eggs
  • Microscopic demonstration of characteristic eggs in the perianal scrapings is the method of choice for the diagnosis of enterobiasis
  • Anal or perianal specimens can be collected by NIH swab, cellophane swab or scotch tape swab method.
  • Scotch tape swab method is a simple and effective procedure. In this procedure transparent adhesive tape is pressed firmly against perianal skin and then spread on to a microscope and observed for pinworm eggs.
  • The perianal specimens are best collected in the morning before the child goes to the toilet and takes bath.
  • At least 3 scotch tape swab should be collected for 3 consecutive days to rule out E. vermicularis infection.
  • Since anal itching is a common symptom of pinworm, the third option for diagnosis is analyzing samples from under fingernails under microscope.

Treatment

• Pyrantel pamoate is the drug of choice
  • Single dose
  • Oral administration
  • 5 mg/kg single dose
• Mebendazole is also effective
• Others drug are-  albendazole, piperazine, pyminium pamote

Prevention and control

1. Keeping finger nails short
2. Frequent hand washing before meals and after defecation
3. Good personal hygiene.
4. Treatment of infected case and all other members in the family or institution.
5. Fingers should not be put in mouth as habit.
6. Washing the bed liners and night dress daily.

Enterobius vermicularis- Morphology, Life cycle, transmission, pathogenesis, disease and treatment

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• Brugia malayi is a filarial worm belongs to phylum nematoda which is one of three causative agents of elephantiasis (lymphatic filariasis) in humans. ( other are- Wuchereria bancrofti, Brugia timori)
• Brug in 1927 describe for the first time about new type of microfilaria in blood of natives in Sumatra. From where the genus acquired its name, Brugia.
• The adult B.malayi worm of was described by Rao and Maplestone in India (1940).
• B. malayi has a more restricted distributions than other filarial worms and is commonly found in open swamps and the rice growing areas of coastal regions.
• It is endemic in India, Srilanka, Philippines, Southern Thailand, North Veitnam, China, South Korea and Japan.
• Besides B. malayi, the genus also includes B. timori, which is human parasite causing lymphatic filariasis.
• Other animal species such as B. pahangi and B. patei infecting dogs and cats.
• Human are the primary host.
• Leaf monkeys are also definitive hosts and reservoir of sub periodic B. malayi. Hence, zoonotic infection can occur from infected monkeys to humans.
• Mosquitoes are the intermediate host.

Habitat

• The adult worm B. malayi is found in the lymphatic system of man and other mammals.
• Microfilaria are mainly found in the peripheral blood circulation.

Morphology of Brugia malayi:

Adult worm:

• The adult worm is similar to Wuchereria bancrofti but are smaller in size.
• The worm resembles a delicate white thread.
• The mature females vary in length from 4.3 – 5.5 cm and in breadth from 0.13-0.17 mm.
• Mature males measure 1.2-2.3 cm in length and 0.07- 0.08 mm in breadth.

Microfilaria

• Microfilaria are colorless and transparent with blunt heads and pointed tails in unstained preparations.
• They lie folded with head close to tail.
• Each microfilaria measures 177-230 µm in length and 5-6 µm in diameter. They possess secondary kinks, instead of smooth curves. The presence of two distinct nuclei at the tip of the tail is the distinguishing feature of microfilaria.
• The nuclei is present at the extreme tip of the tail and other midway between the tip and the posterior column nuclei.

Third stage larvae: an Infective form

• L3 larva is the infective form of parasite are found in the mosquito vector.
• They are elongated, filariform and measure 1500 µm to 1800 µm in length and 18-23 µm in breadth.

Periodicity of Brugia malayi:

• B. malayi generally shows nocturnal periodicity. However, two variants of Brugia malayi are recognized.

1. Nocturnal periodic Brugia malayi

• It is the most prevalent form of parasite
• Microfilaria show nocturnal periodicity
• Transmission occurs mainly by Anopheles and Mansonia mosquito

2. Sub periodic Brugia malayi

• It is less common form
• Microfilaria are found in the day time
• Transmission occurs by Mansonia and Coquillettidia mosquitoes

Pathogenesis of Brugia malayi

• Humans are the definitive host and mosquitoes are the intermediate hosts of Brugia spp. Infected human are the main sources and reservoir of infection. Man to Man transmission occurs by the bite of Anapheles and Mansonia.
• The life cycle of filarial parasites involves four larval stages and an adult stage.
• Infection begins with the bite of infected mosquito on the skin and deposition of infective stage larvae (L3).
• The larvae then pass through the puncture wound and reach the lymphatic system.
• Within the lymphatics and lymph nodes, the L3 larvae undergo molting and development to form L4 larvae.
• This takes about 7-10 days for both B. malayi and W. bancrofti
• The L4 larvae undergo a subsequent molting/developmental step to form adult worms. This occurs about 4-6 weeks after L3 entry in the case of B. malayi.
• The adult worms take permanent residence in afferent lymphatics or the cortical sinuses of lymph nodes and generate microscopic live progeny called “microfilariae”.
• The female worms can give birth to as many as 50,000 microfilariae per day, which find their way into the blood circulation from the lymphatics.
• The adult worms are estimated to survive for a period of 5-10 years although longer durations have been recorded.
• The microfilariae of B. malayi, for the large part, exhibit a phenomenon called nocturnal periodicity, i.e., they appear in larger numbers in the peripheral circulation at night and retreat during the day.
• Subperiodic or nonperiodic of B. malayi are also found in certain parts of the world.

I. Pathology of acute filariasis

Lymphadenitis:

• It is the typical feature. The more classical is acute filarial adenolymphangitis, which is felt to reflect an immune-mediated inflammatory response to dead or dying adult worms.
• The attacks of lymphadenitis occur at regular intervals and often are precipitated by hard muscular exercise.
• The episodes of attacks vary from 1-2 attacks per year.
• Lymphadenitis typically occurs in the inguinal region.
• Occasionally the auxillary lymph nodes are also involved.
• It occurs infrequently at atypical sites such as the popliteal lymph nodes or breasts.

Lymphangitis

• Lymphadenitis is followed by Retrograde lymphangitis

Lymphatic abscess

• The infected lymph nodes may suppurate and form abscess.
• These are usually superficial.
• They rupture leaving behind ulcers.

II. Pathology of chronic filariasis

• The common sites of elephantiasis include, the leg below the knee and less frequently the arm below the elbow.
• Genital involvement and chyluria characteristically are absent.

Clinical manifestation of lymphatic filariasis:

• Incubation period is short and varies from 6-16 month.
• B. malayi shows following clinical stages.

i. Endemic normal and asymptomatic stage:

• Most infection are asymptomatic and common among infected persons in endemic areas with no symptoms of filarial infection and yet, on routine blood examinations, demonstrate the presence of significant numbers of parasites.

ii. Acute filariasis:

• It is characterized by recurrent attacks of lymphadenitis (inflammation of lymph nodes) and lymphangitis associated with fever, chill and other constitutional symptoms.
• The attacks are followed by a characteristics retrograde lymphangitis. The affected lymph vessels become cord-like and tender. The frequency of attacks per year to several attacks per month.
• The infected lymph nodes may suppurate and form abscesses.
• The lymph node abscess is the characteristics of Malayan filariasis.
• Incomplete resolution of the oedema after each attacks leads to the characteristics chronic stage.

Chronic filariasis:

• It is characterized by elephantiasis that develops after 10-15 years in a small number infected population.
• The legs below the knee, less frequently the arms below the elbow are characteristically affected.
• Genital involvement and chyluna are not reported in Malayan filariasis, this occurs only along with bancroftian filariasis.

Lab Diagnosis

• Same as lab diagnosis of W. bancrofti

Treatment of Brugia malayi

• Diethylcarbamagine (DEC): is relatively effective in smaller dose.
• Dose regimen consists of 50 mg on first day; 50 mg three times daily on 2^nd day; 100 mg three times daily on 3^rd day and finally 2 mg/kg/day in three divided doses from 4^th day till 21^st day.

Brugia malayi: Introduction, Morphology, Pathogenesis, Clinical manifestation and Treatment

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• Nematodes are ubiquitous, found in almost all habitats. Mostly nematodes are parasitic in nature infecting humans, animals, insects and other invertebrates.
• Some other nematodes are plant parasites which can cause economic damage to cultivated plants.
• Nematodes are abundantly present in marine, freshwater, and in soil.
• Soil is an excellent primary habitat for nematodes. Due to microscopic nature of most nematodes, 100 grams of soil contains several thousands of nematodes.
• In soil most of the nematodes exhibit role with agriculture significance and those nematodes are plant parasite nematodes as well as free soil nematodes.
• Free soil nematodes plays significant role in decomposition of organic matters in soil and are beneficial to plants.
• Soil also contains human, animals and insects parasites as in juvenile larval form and mostly parasitic eggs.
• Most of the soil nematodes are present in plant root region in rhizosphere. The soil surrounding the plant root where root exudate migrate and microbiological activity is exceptionally high is called rhizosphere and the surface of root is called rhizoplane.
• Examples: Globodera pallida, Caenorhabditis elegans

Types of nematodes found in soil:

Most nematodes studied on the soil parasitic and they are classified on the basis of their feeding habits. The most common groups of nematodes present in agricultural soil are the bacterial-feeders, fungal-feeders, plant parasites, predators, and omnivores.

• Predatory nematodes feed on protozoa and other soil nematodes whereas Omnivores feed on different foods depending on environmental conditions and food availability
• Omnivorous nematodes primarily feeds on protozoans and other small nematodes as predators. But in the absence of their primary food source, they can feed on fungi or bacteria.

Important role of nematodes in Agriculture and health:

1. Nematodes as biological Pest control:

• Some predator nematodes attack and kill a range of pests such as borers, grubs, thrips and beetles with negligible effects on other organisms.
• These nematodes are known as ‘entomopathogenic’ nematodes.
• Nematodes generally feed on smaller organisms like protozoa, bacteria, fungi and other nematodes.
• Some nematodes live in association with specific bacteria that can infects wide ranges of insect pests. When such nematodes infects insects, it releases bacteria that multiplies in host insect and kill them

2. Improve soil fertility; Nitrogen cycle

• Nematodes directly helps in nutrient mineralization through their feeding interactions.
•  For example, bacterial-feeding nematodes consume Nitrogen in the form of proteins and other N-containing compounds in bacterial tissues and release excess Nitrogen in the form of ammonium (NH4+), which is readily available for plant use.

3. Decomposition of organic matters:

• Free-living nematodes in soil are very important and beneficial in the decomposition of organic material and the recycling of nutrients in soil.
• Bacteria and fungi feeding Nematode do not feed directly on soil organic matter, but feed on the bacteria and fungi which decompose organic matter.
• The presence of theses nematodes and their feeding activity accelerate the decomposition process.
• Nematodes feeding recycles minerals and other nutrients from bacteria, fungi, and other substrates and returns them to the soil where they are accessible to plant roots.

4. Plant parasitic nematodes:

• Some plant parasitic nematodes infects roots of plants and damage crops. Eg. Globodera
• The mouthpart of plant parasitic nematodes is a needlelike stylet which is used to puncture cells during feeding.
• There are two types of plant parasitic nematodes; Ectoparasitic nematodes which remain in the soil and feed at the root surface and Endoparasitic nematodes which enter roots and can live and feed within the root.

5. Nematodes as bioindicators of soil health or condition:

• Population of nematodes depends on condition of soil, climate, seasons, crops etc. Therefore indicates the condition of soil health.
• Analysis of the diversity and complexity of nematode communities in the soil is a valuable tool, which indicates soil biological fertility, or soil health.

6. Nematodes dispense microbes for infection:

• Nematodes carrying live and dormant microbes on their surfaces and in their digestive systems and help in distribution of bacteria and fungi throughout soil and also in rhizosphere region.  
• Sometimes nematodes acts as a vector for plant viruses. Eg.  Nepo viruses, Tobraviruses.

7. Human and animal pathogenic nematodes;

• Nematodes are pathogenic to animals and human.
• Eg. Ascaris,

Role of nematodes in Agriculture: Importance of nematodes in soil

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