CONFIRM INFOZ

Straight Up Conversation: LEAP Innovations CEO Phyllis Lockett

Phyllis Lockett is CEO of LEAP Innovations, which runs an 18-month program preparing educators in 140 Chicago schools how to execute personalized learning. Before beginning LEAP, Phyllis was establishing president and CEO of New Schools for Chicago, where she helped raise more than $70 million to contribute to open 80 new sanction schools. I as of late conversed with Phyllis about LEAP and how to prepare teachers in actualizing personalized learning.

Rick Hess: So, what does LEAP do?

Phyllis Lockett: We need to make custom-made learning pathways for each and every understudy. Our work gives locale and schools necessary to change the executives backing to make supportable movements to a personalized learning model. Jump's most significant program, the Pilot Network, is an 18-month program that furnishes educators with direct front arranging, proficient improvement and structure, on-the-ground instructing, and association with personalized learning rehearses and a curated tech item—we accumulate a board of inward and outside specialists to assess edtech devices for adequacy against our customized learning framework, and schools are then coordinated to the item that best meets their requirements. The teacher preparing project incorporates a six-month arranging procedure, and afterward, an entire year of nonstop hands-on help from our group of mentors. We are focused on helping schools actualize the best practices and versatile innovation devices, which help educators tailor the learning knowledge for each understudy.

Rick: What's the enormous thought behind it? What's more, how massive is the association?

Phyllis: LEAP Innovations is established on the conviction that all kids, paying little respect to race, social foundation or financial status, have boundless potential and the privilege to a top-notch instruction. At LEAP, our build for the eventual fate of training is grounded in our framework for personalized learning. Integrating discoveries from neuroscience, learning science, instructional improvement, and the universe of work into a strong, noteworthy vision for schools, the LEAP Learning Framework gives educators robust methodologies to tailor a personalized learning plan to the requirements and chances of their learning surroundings. Our association works in tight organization with the distinct neighbourhood and national establishments, over 2400 educators, and 140 schools crosswise over Chicagoland. All the while, we've affected about 40,000 understudies, 90 percent of whom are offspring of shading, and more than 80 percent of whom are qualified for nothing or discounted value lunch. Our framework has additionally authoritatively been received by the territory of Utah and utilized by schools in 23 states as a major aspect of their work to make learning progressively close to home.

Rick: How would you figure out which schools and teachers take part?

Phyllis: We have expected to fabricate a model that meets schools and networks—just as understudies—where they are. While we work with a various cluster of open, contract and archdiocese schools, we by and extensive search for situations with reliable, comprehensive managerial authority and a culture of coordinated effort and drive for development. Generally speaking, it's essential that each school's needs and objectives line up with the estimations of personalized learning, and that school heads are happy to join forces with their teachers, giving them the opportunity and backing to improve starting from the earliest stage.

Rick: You referenced on-the-ground mentors for these teachers. What do the mentors really do?

Phyllis: After a six-month arranging period, during which educators make and sharpen their study hall plan, our mentors work close by teachers for a full school year as they set their structures to work. They are full-time colleagues, every single previous educator themselves. Mentors visit educators in any event once like clockwork to give nearby help and are accessible as needs are for normal get in contact and direction. They mentor educators through three development cycles, through which they help teachers guide out plans that push toward their enormous picture objectives, assemble estimations that benchmark their advancement, and actualize new practices.

Rick: What sorts of work do teachers do throughout their interest?

Phyllis: For the initial half-year of the Pilot Network, school groups work seriously with our expert advancement group. Our mentors help educators manufacture their structure and set clear plans. Taking interest educators work together intimately with their regulatory groups—and one another—and direct a progression of learning visits to watch propelled schools in real life. As a significant aspect of their plan procedure, teachers make a profile of each understudy in their study hall. This pursues large gatherings with every understudy and frequently begins with "sympathy strolls" to continue the way, indeed, that understudies take to and through school. Teachers at that point plan the various modalities of learning they'll bolster. These incorporate little gathering guidance, kids working together on activities or issues, and students working freely. As opposed to doled out seats and mechanical style columns of work areas, the situations are totally reset frequently to incorporate coordinated effort zones, delicate seating, and understudy portfolio "libraries." Teachers redo their timetables to suit expanded understudy decision and mentorship, setting time for understudy drove conferencing, little gathering guidance, and free tasks. En route, we help educators distinguish ways for understudies to show authority. Parent-teacher meetings are reframed to move toward becoming understudy driven gatherings, where students control discussions about their advancement and where they need more help.

Rick: How have another workforce at the schools responded to the teachers who take part and to the pilot ventures?

Phyllis: There is, as you most likely are aware, a ton of "activity exhaustion" out there. Be that as it may, when teachers see their partners making all the more captivating, personalized homerooms, they unavoidably need to participate. Those underlying study halls become models that the entire school can rally around as educators advance with their own interpretation of personalized learning. This has implied that, during LEAP's initial five years inactivity, the request has developed each year. Of the schools that have taken an interest in our Pilot Network program, about 40 percent have drawn in various groups for different years. Teachers become interested when they see their friends re-stimulated with the experience.

Rick: What's been the response from principals and focal workplaces?

Phyllis: They are excited. They see the positive effect both in their schools' exhibition, and all the more significantly, with the improvement of their students. Our principals state that this synergistic methodology, which carries teachers to the table as co-pioneers, has changed their school societies. As educators and principals perceive the capability of this new methodology, Chicago Public Schools has ventured up to fulfill the need. Personalized learning has shown up unmistakably in the locale's 5-year plan, and it's made another office to help the extension of personalized learning.

Rick: How would you know how powerful the program has been? What sorts of assessments have been directed?

Phyllis: Our initial outcomes are demonstrating twofold digit percentile point gains in proficiency. Schools are announcing higher participation rates and lower suspension rates. Above all, understudies are eager to be in school. Take Perkins Bass Elementary in Englewood. After executing school-wide personalized learning, Perkins Bass has totally changed from a battling Level 3 school—on post-trial supervision for a long time—to a Level 1 school throughout the previous two years. In that time, understudies' math and perusing scores have significantly increased. Before personalized learning, teacher maintenance was underneath state and region levels. Presently it surpasses state and region levels, at 89 percent. Even though class size can be as large as 42 understudies, personalized learning makes an engaged, beneficial, and invigorated learning condition. In our subsequent Pilot Network companion, understudies in our ELA pilot picked up a normal of 2.94 test-score focuses over the control bunch on NWEA, a national evaluation that estimates understudy development. As such, a run of the mill understudy in the Pilot Network picked up 13 other percentile focuses over an ordinary correlation understudy beginning with a similar score—i.e., 50th percentile to the 63rd percentile.

Rick: How much does this expense?

Phyllis: Last year, we charged an independent research firm to take a gander at the expenses of executing personalized learning in schools. It revealed that entire school personalized learning models require unobtrusive venture to begin—start-up expenses ran from $338K to $780K over the six schools and $233 to $1,135 on a for every student premise—and demonstrate maintainable without progressing award financing. It is essential to us—and the examination recommends—this is a model that can withstand and continue moving state and neighbourhood spending plans.

Rick: Where does the financing originate from?

Phyllis: We are blessed to have liberal benefactors that permit school groups to get to our administrations at financed rates. Accordingly, the expense per-school group of doing this work is radically lower than the expense of running the program on our end. Our 18-month program costs us $75,000 per school group, however through altruistic endorsing, we can charge schools just $27,500. This incorporates access to our nonstop, personalized proficient learning administrations, just as year-long utilization of one of our thoroughly screened advantageous edtech items for every single partaking understudy. We've raised more than $30 million to help our work. Our contributors have included nearby Chicago pioneers like The Pritzker Foundation and The Crown Family Philanthropies, just as national philanthropies like the Bill and Melinda Gates Foundation, the Michael and Susan Dell Foundation, New Profit, and the Chan Zucker

Trichinella spiralis

Historical aspect

  In 1835, a man died of tuberculosis in St Bartholomew’s Hospital, London. Dr Paget, a first-year student, carried out the autopsy and observed fine hard white inclusions in the muscles. Similar inclusions had been observed by doctors from time to time in the past, but were attributed to commonplace muscle calcification, which quickly blunted the dissecting scalpel. Dr Paget inspected the lesions with a hand lens and quickly recognised their worm-like structure. The name "Trichina
spiralis" was suggested.

   This name Trichina had already been given to a certain fly, however, and the name was later changed to "Trichinella". The discovery of the parasite was published by the famous biologist and palaeontologist Richard Owen, at that time assistant conservator of the museum of the Royal College of Surgeons. In 1859 Rudolph Virchow carried out transmission experiments in
which infected human muscle was fed to a healthy dog. After only 3 to 4 days adult Trichinella worms were found in the dog’s duodenum and jejunum.

   Life cycle

More than 100 species of mammals are susceptible to the infection. Infections with Trichinella spiralis affect chiefly carnivores and omnivores, although infection of horses has also been described. People become infected with this nematode by eating raw or insufficiently cooked infected meat, often pork or wild boar. The larvae of Trichinella spiralis which are in the meat develop in a few
days into adult worms (2-4 mm) in the wall of the small intestine. There they lay larvae (100 m m). These spread via the bloodstream to various muscles, including the heart, where they undergo encapsulation [Trichinella pseudospiralis does not form a capsule]. The larvae cannot continue to survive in the heart. The larvae are localised within the cells of the muscles, which is unique for a worm.

    After penetrating the muscle cell, a larva excretes a number of signal molecules and
proteins, which convert the cell to what is called a nurse cell. In the cell the behaviour of the worm is rather similar to that of a virus. Many of its proteins are glycosylated and often carry an unusual sugar (tyvelose). These proteins are excreted from a special organ in the larva (the stichosome). Various muscle proteins such as actin and myosin change or disappear, nuclear division is  stimulated and mitochondria are damaged. Local angiogenesis is stimulated by excretion of a blood vessel growth factor and new blood vessels, originating from nearby venules, develop and form a network around the infected cell.

  The metabolism of the nurse cell and the parasite is essentially anaerobic. After 1 to 4 months the adult worms die. The larvae in the muscles sometimes survive for years and can remain viable for a long time even in rotting flesh. Trichinella is unique among worms in that all development stages take place in the same host. There is never a free stage outside the mammalian body.

 Symptoms

Infection may be asymptomatic. In typical cases there is diarrhoea, abdominal pain, vomiting and fever a few days after eating infected meat. After 10 days the fever increases, the patient is very ill and debilitated, there are muscle pains and a typical peri-orbital oedema (differential diagnosis acute trypanosomiasis and nephrosis). This oedema is caused by invasion of the small muscles around the
eye. There may be signs of myocarditis, encephalitis, urticaria and asthma. There is often very significant eosinophilia. The myositis causes an increase in the muscle enzymes (creatine phosphokinase, CK). After a few months the symptoms are reduced or disappear. Mild infections are self-limiting.

 Diagnosis

Not many nematodes are found in muscle tissue. Occasionally a migrating third stage larva of Ancylostoma, Toxocara or Gnathostoma may be found (visceral larva migrans). Dracuncula medinensis may also be found in muscle tissue. Another, less common nematode which may be found here is Haycocknema perplexum (Tasmania).

 Prevention

Meat should be well boiled or roasted thoroughly.  Importance of meat inspection. The diaphragm of a slaughtered animal is inspected (the piece of muscle is flattened between two glass slides and examined using transillumination). This technique (trichinoscopy) is not so good for Trichinella pseudospiralis because it is not surrounded by a capsule and is easily missed.

Pig food (which may include infected rats) should be boiled for 30 minutes.

 
To store pork for 10 days at -25° C is generally impractical in developing countries. In the West meat is sometimes irradiated with high doses of gamma rays, which will kill any larvae. Trichinella spiralis nativa is cold-hardy.

BLOOD AND TISSUE NEMATODES

INTRODUCTION

Filariasis is caused by nematodes (roundworms) that inhabit the lymphatics and subcutaneous tissues. Eight main species infect humans. Three of these are responsible for most of the morbidity due to filariasis: Wuchereria bancrofti and Brugia malayi cause lymphatic filariasis, and Onchocerca volvulus causes onchocerciasis (river blindness). The other five species are Loa loa, Mansonella
perstans, M. streptocerca, M. ozzardi, and Brugia timori. (The last species also cause lymphatic filariasis).

   Among the agents of lymphatic filariasis, Wuchereria bancrofti is encountered in
tropical areas worldwide; Brugia malayi is limited to Asia; and Brugia timori is restricted to some islands of Indonesia. The agent of river blindness, Onchocerca volvulus, occurs mainly in Africa, with additional foci in Latin America and the Middle East. Among the other species, Loa loa and Mansonella streptocerca are found in Africa; Mansonella perstans occurs in both Africa and South America; and Mansonella ozzardi occurs only in the American continent. Another tissue invading parasite is Trichinella spiralis whose larval form is found in the muscular tissue of the host animal. Trichinella spiralis is in fact a complex of three closely related worm species.

   They are morphologically identical, but differ in their host specificity and their biochemical characteristics. T. spiralis spiralis occurs in moderate regions and infects mainly pigs. T. spiralis nativa occurs in the polar regions (polar bear, walrus). These parasites are resistant to freezing which is important for meat storage. T. spiralis nelsoni occurs in Africa and southern Europe with a reservoir in wild carnivores and wild pigs. T. britovi and T. pseudospiralis rarely cause infections. T. pseudospiralis can also infect some birds as well as mammals, unlike the other Trichinella species.

Filarial worms

Wuchereria bancrofti

Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical distribution. Among them are:

Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C. pipiens);
Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia).

During a blood

meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound. They develop in adults that commonly reside in the lymphatics. The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by .1 mm. Adults produce microfilariae measuring 244 to 296 µm by 7.5 to 10 µm, which are sheathed and have nocturnal periodicity, except the South Pacific
microfilariae which have the absence of marked periodicity.

  The microfilariae migrate into the lymph and blood channels moving actively through lymph and blood. A mosquito ingests the microfilariae during a blood meal. After ingestion, the microfilariae loose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles. There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae. The third-stage infective larvae migrate through the haemocoel to the mosquito's prosbocis and can infect another human when the mosquito takes a blood meal.

Onchocerca volvulus

    During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound. In subcutaneous tissues the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues Adults can live in  the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33 to 50 cm in length and 270 to 400 µm in diameter, while males measure 19 to 42 mm by 130 to 210 µm. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years.

   The microfilariae, measuring 220 to 360 µm by 5 to 9 µm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues. A blackfly ingests the microfilariae during a blood meal. After ingestion, the microfilariae migrate from the blackfly's midgut through the haemocoel to the thoracic muscles. There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae. The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal.

Loa loa

 

  The vector for Loa loa filariasis are flies from two species of the genus Chrysops, C. silacea and C. dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound. The larvae develop into adults that commonly reside in subcutaneous tissue. The female worms measure
40 to 70 mm in length and 0.5 mm in diameter, while the males measure 30 to 34 mm in length and 0.35 to 0.43 mm in diameter.

  Adults produce microfilariae measuring 250 to 300 µm by 6 to 8 µm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from the spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs. The fly ingests microfilariae during a blood meal. After ingestion, the microfilariae lose their sheaths and migrate from the fly's midgut through the haemocoel to the thoracic muscles of the arthropod. There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae. The third-stage infective larvae migrate to the fly's proboscis and can infect another human when the fly takes a blood meal.

Brugia malayi

 

The typical vector for Brugia malayi filariasis are mosquito species from the genera Mansonia and Aedes. During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound. They develop into adults that commonly reside in the lymphatics.

  The adult worms resemble those of Wuchereria bancrofti but are smaller. Female worms measure 43 to 55 mm in length by 130 to 170 µm in width, and males measure 13 to 23 mm in length by 70 to 80 µm in width. Adult produce microfilariae, measuring 177 to 230 µm in length and 5 to 7 µm in width, which are sheathed and have nocturnal periodicity. The microfilariae migrate into the lymph and enter the blood stream reaching the peripheral blood.

   A mosquito ingests the microfilariae during a blood meal. After ingestion, the microfilariae lose their sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic muscles. There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae. The third-stage larvae migrate through the haemocoel to the mosquito's prosbocis and can infect another human when the mosquito takes a blood meal.

Clinical Features and Pathology

   Lymphatic filariasis most often consists of asymptomatic microfilaremia. Some patients develop lymphatic dysfunction causing lymphedema and elephantiasis (frequently in the lower extremities) and, with Wuchereria bancrofti, hydrocele and scrotal elephantiasis. Episodes of febrile lymphangitis and lymphadenitis may occur. Persons who have newly arrived in disease-endemic areas can develop
afebrile episodes of lymphangitis and lymphadenitis. An additional manifestation of filarial infection, mostly in Asia, is pulmonary tropical eosinophilia syndrome, with nocturnal cough and wheezing, fever, and eosinophilia.

    Onchocerciasis can cause pruritus, dermatitis, onchocercomata (subcutaneous nodules), and lymphadenopathies. The most serious manifestation consists of ocular lesions that
can progress to blindness. Loiasis (Loa loa) is often asymptomatic. Episodic angioedema (Calabar swellings) and sub-conjunctival migration of an adult worm can occur. Infections by Mansonella perstans, which is often asymptomatic, can be associated with angioedema, pruritus, fever, headaches, arthralgias, and neurologic manifestations.

   Mansonella streptocerca can cause skin manifestations including pruritus, papular eruptions and pigmentation changes. Eosinophilia is
often prominent in filarial infections. Mansonella ozzardi can cause symptoms that include arthralgias, headaches, fever, pulmonary symptoms, adenopathy, hepatomegaly, and pruritus.

Treatment and control

Ivermectin is effective in killing the larvae, but does not affect the adult worm. Preventive measures include vector control, treatment of infected individuals and avoidance of black fly.

 Laboratory Diagnosis of filarial worms

Identification of microfilariae by microscopic examination is the most practical diagnostic procedure.

Microscopy

   Examination of blood samples will allow identification of microfilariae of Wuchereria bancrofti, Brugia malayi, Brugia timori, Loa loa, Mansonella perstans, and M. ozzardi. It is important to time the blood collection with the known periodicity of the microfilariae. The blood sample can be a thick smear, stained with Giemsa or haematoxylin and eosin. For increased sensitivity, concentration techniques can be used.

   These include centrifugation of the blood sample lyzed in 2% formalin (Knott's technique), or filtration through a Nucleopore® membrane. Examination of skin snips will identify microfilariae of Onchocerca volvulus and Mansonella streptocerca. Skin snips can be obtained using a corneal-scleral punch, or more simply a scalpel and needle. The sample must be allowed to incubate for 30 minutes to 2 hours in saline or culture medium, and then examined for microfilariae that would have migrated from the tissue to the liquid phase of the specimen.

Preparing Blood Smears for Microscopy Examination

If one uses venous blood, blood smears should be prepared as soon as possible after collection (delay can result in changes in parasite morphology and staining characteristics).

  Life cycle of Human Hookworms

Pathology of Infection.

     The Pathology associated with hookworm infections may be divided roughly into two areas. Firstly the pathology associated with the presence of the adult parasite in the intestine, and secondly the pathology associated with the penetration of, and migration of the larval worms within the skin. The adult hookworms attach themselves to the intestinal wall using their buccal capsules. Their preferred site of infestation is in the upper layer of the small intestine, but in very heavy Adults in intestinal mucosa infections (where many thousands of worms may be present) the parasites may
spread down as far as the lower ileum.

   Once attached to the intestinal wall, the hookworm mouthparts penetrate blood vessels, and the parasites obtain nutrition by sucking blood. A single Necator americanus will take approximately 30 µl of blood daily, while the larger Ancylostoma duodenale will take up to 260 µl. The gross pathology of the disease is very dependent on the intensity of infection. Light infections appear asymptomatic, but in heavy infections, the continuous loss of blood leads to a chronic anaemia, with down to 2gm of haemoglobin per 100ml of blood in extreme cases. Experiments carried out in the 1930's showed that in dogs infected with 500 Ancylostoma caninum a similar species to the human parasite, nearly a pint of blood a day was lost.

  This leads to permenant loss of iron and many blood proteins as well as blood cells. This in turn has consequences for further production of erythrocytes, which have been shown to contain less haemoglobin, as well as being reduced in size and smaller in numbers. This form of anaemia may be directly fatal, but more often, it induces more non-specific
symptoms, the most noticeable being the severe retardation in growth and development, both physical and mental, in infected children, and a general weakness and lassitude, often wrongly interpreted as "laziness".

Diagnosis

Identify characteristic eggs in feacal samples. Note the eggs of N. americanus and A. duodenale are morphologically identical

Epidemiology and Control
 
The factors of epidemiological importance include;
- Poor sanitation through contamination of soil through direct defaecation on the ground.
- Skin exposure to infections e.g. by walking about bare-footed
- Favourable environmental conditions that enhance eggs and larval development.
- Loose, humus soil with reasonable drainage and aeration
- Even distribution of rainfall throughout the year.

Control is by improvement in the standard of sanitation, raising the nutritional status of the population especially in relation to iron content, and mass treatment with suitable worm expeller (vermifuge)

Trichuris trichiura (human whipworm)

The first written record of Trichuris trichiura was made by Morgani, an Italian
scientist, who identified the presence of the parasite in a case of worms residing in
the colon in 1740. Exact Morphological description and figures were first recorded
in 1761 by Roedere, a German physicist. Soon after morphology and visual
representation of the worms, Trichuris trichiura was given taxonomy (during the
18th century).
This is the third most common round worm of humans. It is distributed
worldwide, with infections more frequent in areas with tropical weather and poor sanitation practices, and among children. It is estimated that 800 million people
are infected worldwide. The southern United States is endemic for trichuriasis.

Morphology

Adult worms are usually 3–5 cm long, with females being larger than males as is typical of nematodes. The thin, clear majority of the body (the anterior, whip-like end) is the oesophagus, and it is the end that the worm threads into the mucosa of the colon. The widened, pinkish gray region of the body is the posterior, and it is the end that contains the parasite’s intestines and reproductive organs.Trichuris trichiura has characteristic football-shaped eggs, which are about 50-54µm long
and contain polar plugs (also known as refractile prominences) at each end.

Life cycle and transmission

  Humans can become infected with the parasite due to ingestion of infective eggs by mouth contact with hands or food contaminated with egg-carrying soil. However, there have also been rare reported cases of transmission of Trichuris trichiura by sexual contact. Some major outbreaks have been traced to contaminated vegetables (due to presumed soil contamination).

   Unembryonated eggs (unsegmented) are passed in the faeces of a previous host to the soil. In the soil, these eggs develop into a 2-cell stage (segmented egg) and then into an advanced cleavage stage. Once at this stage, the eggs embryonate and then become infective, a process that occurs in about 15 to 30 days).

   Next, theinfective eggs are ingested by way of soil-contaminated hands or food and hatch inside the small intestine, releasing larvae into the gastrointestinal tract. These larvae burrow into a villus and develop into adults (over 2–3 days). They then migrate into the cecum and ascending colon where they thread their anterior portion (whip-like end) into the tissue mucosa and reside permanently for their year-long life span. About 60 to 70 days after infection, female adults begin to release unembryonated eggs (oviposit) into the cecum at a rate of 3,000 to 20,000 eggs per day, linking the life cycle to the start.

Signs and symptoms

  Light infestations are frequently asymptomatic (have no symptoms). Heavier infestations, especially in small children, can present gastrointestinal problems including abdominal pain and distention, bloody or mucous-filled diarrhoea, and tenesmus (feeling of incomplete defecation, generally accompanied by involuntary straining). While damage may be done to the GI tissue and appendicitis may be brought on (by damage and oedema of the adjacent lumen) if there are large numbers of worms or larvae present, it has been suggested that the embedding of the worms into the ileo-cecal region may also make the host susceptible to bacterial infection.

  Severe infection may also present with rectal prolapse, although this is typically seen only in heavy infections of small children. High numbers of embedded worms in the rectum cause oedema, which causes the rectal prolapse. The prolapsed, inflamed and oedematous rectal tissue may even show visible worms. Growth retardation, weight loss, nutritional deficiencies, and anaemia (due to long-standing blood loss) are also characteristic of infection, and these symptoms are more prevalent and severe in children.

Diagnosis

   A stool ova and parasites examination reveals the presence of typical whipworm eggs. Typically, the Kato-Katz thick-smear technique is used for the identification of the Trichuris trichiura eggs in the stool sample. Although colonoscopy is not typically used for diagnosis, but there have been
reported cases in which colonoscopy has revealed adult worms. Colonoscopy can directly diagnose trichuriasis by identification of the threadlike form of worms with an attenuated, whip-like end. Colonoscopy has been shown to be a useful diagnostic tool, especially in patients infected by only a few male worms and with no eggs presenting in the stool sample.

Epidemiology

     Trichuris trichiura is the third most common nematode (roundworm) of humans. Infection of trichuris trichiura is most frequent in areas with tropical weather and poor sanitation practices. Trichuriasis occurs frequently in areas in which human feces is used as fertilizer or where defecation onto soil takes place.

   Trichuriasis infection prevalence is 50 to 80 percent in some regions of Asia (noted especially in China and Korea) and also occurs in rural areas of the southeastern United States. Infection is most prevalent among children, and in North America, infection occurs frequently in immigrants from tropical or sub-tropical regions. It is estimated that 600-800 million people are infected worldwide with 3.2 billion individuals at risk.

Control and Prevention

   Improved facilities for faeces disposal have decreased the incidence of whipworm. Handwashing before food handling, and avoiding ingestion of soil by thorough washing of food that may have been contaminated with egg-containing soil are other preventive measures. Mass Drug Administration (preventative chemotherapy) has had a positive effect on the disease burden of trichuriasis in East and West Africa, especially among children, who are at highest risk for infection.

  Improvement of Sewage and Sanitation systems, as well as improved facilities for faeces disposal have helped to limit defecation onto soil and contain potentially infectious faeces from bodily contact. A study in a Brazil Urban Centre demonstrated a significant reduction in prevalence and incidence of geohelminth infection, including trichuriasis, following implementation of a city-wide sanitation programme.

  A 33% reduction in prevalence of trichuriasis and a 26% reduction in incidence of trichuriasis was found in the study performed on 890 children ages 7–14 years old within 24 different sentinel areas chosen to represent the varied environmental conditions throughout the city of Salvador, Bahia, Brazil. Control of Soil Fertilizers has helped eliminate the potential for contact with human faecal matter in fertilizer in soil.

The human hookworms

 

introduction 

   The hookworms belong to the Order Strongylida, a large order, and of great interest as it contains many important pathogens of man and domesticated animals. This order is further subdivided into three Superfamilies, the Strongyloidea (the hookworms in man), and two related groups, the Superfamily ‘Trichostrongyloidea’, intestinal nematodes which are of veterinary importance in many domesticated animals (e.g. Haemonchus contortus in cattle and Nippostrongylus brasiliensis in rodents) and members of the Superfamily ‘Metastrongyloidea’ (the lungworms, in domesticated animals).


  In man, there are two species capable of causing intestinal infections, Ancylostoma duodenale native to parts of Southern Europe, North Africa and Northern Asia parts of Western South America, and Necator Americans in Central and Southern Africa, Southern Asia, Australia and the Pacific Islands. These are very important human pathogens. It has been estimated that there are 1200 million cases of hookworm infection in man annually, of which about 100 million of which are symptomatic infections with accompanying anaemia. Also, the larvae of several species of hookworms infecting domesticated animals may penetrate human skin, causing pathology even though they do not develop to the adult parasites in man.

Morphology

    The adult parasites are small cylindrical worms, 0.5-1.5mm long (Ancylostoma duodenale being slightly larger than Necator americanus ). The posterior end of the male worm is equipped with a normal copulatory bursa, used to hold the female nematode in place during mating. The females themselves have a vulva situated near the centre of the body, slightly anterior in Necator and slightly posterior in Ancylostoma.

  The anterior end of the parasites are formed into a buccal  Scanning electron micrograph of the mouth capsule of Ancylostoma duodenale (left), note the presence of four "teeth," two on each side and Necator americanus (right) capsule, absent in members of the other Strongylida superfamilies, by which the different genera and species within the group may be differentiated. For example, members of the genus, Necator have capsules equipped with cutting plates on the ventral margins and within the tablet itself small dorsal teeth. In contrast members of the family, Ancylostoma has pairs of teeth on the ventral margin of the capsule. The number of teeth will vary between different species of Ancylostoma but is usually between one and four pairs.

The eggs are bluntly rounded, thin-shelled, and are almost indistinguishable between the different species, measuring approximately 60 by 40 µm, the eggs of Ancylostoma being slightly larger than those of Necator.

Life cycle

   The life cycles of all the hookworms are very similar. The eggs are passed in the faeces, once exposed to air they mature rapidly if conditions are right, with both moisture and warmth essential for development. When developed, they hatch to liberate a rhabditiform (i.e. having an oesophagus where a thick anterior region is connected via a neckline region with a posterior bulb) L1 larvae after a few days. These larval nematodes feed on bacteria and organic material in the soil, where they live and grow for about two days before undergoing the first moult.

  After about five days more growth they moult again, to produce a much more slender L3 larvae. The L3 larvae have a much shorter oesophagus, is a non-feeding form, and is the infective form of the parasite. Infection takes place by penetration of the skin, for example, when walking with bare feet over contaminated damp soil, followed by entry into the circulatory system.

    Here they are carried to the heart, and then lungs. Once in the lungs, they are too large to pass through the capillary bed there. Instead, they become trapped, and the burrow through the capillary epithelium, entering the air spaces. They then migrate up through bronchi and trachea and are then swallowed. Once swallowed, they pass into the intestine and bury themselves between the intestinal villi. Here they moult to form the L4 larvae, equipped with a buccal capsule allowing adherence to the gut wall. After about thirteen days post-infection they moult for the final time, producing immature adult worms.

 These mature over three to four weeks (i.e. five to six weeks after infection), then mate and commence egg-laying to complete the life cycle. These parasites show a very high fecundity, female Necator americanus  producing up to 10,000 eggs daily, while female Ancylostoma duodenale produces up to 20,000 eggs daily

SOIL TRANSMITTED HELMINTHS

 INTRODUCTION

   Soil-transmitted helminth (STH) infection is highly endemic in tropical and subtropical areas of sub-Saharan Africa, Asia and Latin America, where up to 2 billion people have active infections. STH disease has mainly remained neglected by the global health community because the people most affected are among the most impoverished and because the disease causes chronic ill health with insidious clinical presentations, rather than severe acute illness or high mortality.

  However, it is now recognised that STH infection causes significant morbidity worldwide with 39 million disability-adjusted life years (DALYs) lost each year - more than those lost to malaria (36 million yearly) and approaching those lost to tuberculosis (47 million annually). Hookworm infection alone causes
a loss of 22 million DALYs.

   Ascaris lumbricoides (large roundworm of man) Infection with this roundworm is widespread, with estimates of the annual incidence of infection being higher than 1500 million cases, or around one quarter of the world's population. In addition to the species in man, Ascaris lumbricoides, a morphologically indistinguishable species Ascaris suum is found in the pig. Other related genera include Parascaris in equines and Toxascaris in a variety of domesticated animals.

Morphology

   The adult Ascaris lumbricoides are largely white, or pinkish-white, cylindrical roundworms, slightly narrower at the head. The more slender male's measure between 10 to 30cm long and have a curved tail with two spicules, but no copulatory bursa. The females are very similar, being slightly larger at between 20 to 35cm long, a vulva approximately a third of the length of the body down from
the head, and have a blunt tail. They are both characterised by having a smooth, finely striated, cuticle, and a mouth, which is characteristic of all of the Ascarids (e.g. Toxocara), having three lips each equipped with small papillae. Internally they follow the generalised body plan of all nematodes and have a cylindrical oesophagus opening into a flat ribbon-like the intestine. The eggs consist of a thick transparent inner shell which is covered in a thick, warty, albuminous coat.

Life cycle

  These parasites have a direct life cycle, with no intermediate hosts. The adult parasite lives in the lumen of the small intestine of man, usually only feeding on the semi-digested contents of the gut, although there is some evidence that theycan bite the intestinal mucous membrane and feed on blood and tissue fluids. The female parasite is highly prolific, laying an estimated 2 million eggs daily. In the intestine, these only contain an unembryonated mass of cells, differentiation occurring outside the host.

 This requires a temperature less than 30°C, moisture and oxygen, before the development of the young L1 larvae after approximately 14 days. Eggs containing the L2 larvae take another week to develop, before they are infective to man, and may remain viable in the soil for many years if conditions are optimal. Infection occurs on ingestion of raw food, such as fruit or vegetables, that is contaminated with these infective eggs. The eggs then hatch in the small intestine, to release the L2 rhabditiform larvae (measuring approximately 250 by 15µm in size.

  These do not only grow into the adult forms in the intestine, but must then undergo a migration through the body of their host. These L2 larvae penetrate the intestinal wall, entering the portal blood stream, and then migrate to the liver, then heart, then after between 1 to 7 days, the lungs. Here they moult twice on the way to form the L4 larvae, (measuring approximately 1.5mm Long), then burrow out of the blood vessels, entering the bronchioles. From here they migrate up through the air passages of the lungs, to the trachea. They then enter the throat and are swallowed, finally ending up in the small intestine where they mature and mate, to complete their life cycle

Pathology of Infection.

The majority of infections (~85%) appear to be asymptomatic, in that there is no gross pathology seen. However, the presence of these parasites seems to be associated with the same general failure to thrive in their hosts seen with many of these intestinal nematodes. In terms of more easily identified pathology, this may be divided into three areas; Pathology Associated with the Ingestion and Migration of Larvae Severe symptoms of Ascaris infection may be associated with the migrating
larvae, particularly in the lungs.

   If large numbers of these larvae are migrating through the lungs simultaneously, this may give rise to severe haemorrhagic pneumonia. More commonly, as is the case with most infections, the haemorrhages are smaller in scale, but still may lead to breathing difficulties, pneumonia and/or fever.

  A complication here is that many of the parasites proteins are highly allergenic. Due to this, the presence of the migrating larvae in the lungs is often associated with allergic hypersensitivity reactions such as asthmatic attacks, pulmonary infiltration and urticaria and oedema of the lips. Pathology Associated with Adult Parasites in the Intestine The most common symptoms of infection are due to the adult parasite, and consist of rather generalised digestive disorders, such as a vague abdominal discomfort, nausea, colic (e.t.c.).

  These symptoms are dependent to some extent on the parasite’s burden of the host, which in severe cases may consist of many hundreds or even thousands of parasites, although these are extreme cases. In the case of
these heavy infections, the presence of many of these large parasites may contribute to malnutrition in the host, especially if the hosts (often children) are undernourished.

  A more serious, and potentially fatal, the condition may arise in these more heavy infections, where the mass of worms may block the intestine and need to be surgically removed. This may also occur sometimes on treatment for other. intestinal nematodes such as hookworms, where the curative drug dose for these parasites irritate the ascarids. Pathology due to "Wandering" Adults outside of the Intestine Adult parasites often leave the small intestine to enter other organs, (sometimes in
response to anti-helminthic drugs used to treat other intestinal nematode infections), where they may cause various types of pathology, sometimes with severe consequences.

  For example, adult Ascaris worms may migrate to the bile duct, which may then become blocked, causing jaundice and general interference in fat metabolism. Adult parasites may also migrate to the appendix, or through the intestinal wall, both conditions which may cause fatal peritonitis as they may well carry intestinal bacteria to these sites. They may, alarmingly, sometimes migrate forward through the intestinal tract, to be either vomited up or emerging through the nose. More seriously, if they enter the trachea, they may cause suffocation.

Diagnosis

Definitive diagnosis is by the demonstration of the characteristic eggs in faecal samples or by identifying adult worms passed out spontaneously by the host.

 Epidemiology and Control

Infection occurs through ingestion of parasites’ eggs in the food. The eggs are highly resistant to adverse environmental conditions. This with other factors highlighted below are often associated with the transmission of infection;
- Lack of or inadequate waste disposal facilities
- Improper washing of hands before eating
- Incorrect washing of fruits and vegetables before consumptions
- Unkept rooms and dwelling places that harbour mechanical carriers of parasites, etc.
Provision of the good waste disposal system and good personal hygiene will help to control infections.

GENERAL FEATURES AND LIFE CYCLES OF NEMATODES

INTRODUCTION

Nematode infections in humans include ascariasis, trichuriasis, hookworm, enterobiasis, strongyloidiasis, filariasis, and trichinosis, among others. The phylum Nematoda, also known as the roundworms, is the second-largest phylum in the animal kingdom, encompassing up to 500,000 species. Members of Nematoda are elongated, with bilaterally symmetric bodies that contain an intestinal system and a large body cavity.


   Many roundworm species are free-living in nature. Recent data have demonstrated that approximately 60 species of roundworms parasitize humans. Intestinal roundworm infections constitute the largest group of helminthic diseases in humans. According to a
2005 report by the World Health Organization (WHO), approximately 0.807-1.221 billion humans have ascariasis, 604-795 million have trichuriasis, and 576-740 million have hookworm infections worldwide.

General features

  Nematodes are cylindrical rather than flattened; hence the common name roundworm. The body wall is composed of an outer cuticle that has a noncellular, chemically complex structure, a thin hypodermis, and musculature. The cuticle in some species has longitudinal ridges called alae. The bursa, a flap-like extension of the cuticle on the posterior end of some species of male nematodes, is used to grasp the female during copulation.


   The cellular hypodermis bulges into the body cavity or pseudocolour to form four longitudinal cords; a dorsal, a ventral, and two lateral cords which may be seen on the surface as lateral lines. Nuclei of the hypodermis are located in the region of the cords. The somatic musculature lying beneath the hypodermis is a single layer of smooth muscle cells. When viewed in cross-section, this layer can be seen to be separated into four zones by the hypodermal cords. The musculature is innervated by extensions of muscle cells to nerve trunks running anteriorly and posteriorly from ganglion cells that ring the midportion of the oesophagus.


The space between the muscle layer and viscera is the pseudocolour, which lacks a mesothelium lining. This cavity contains fluid and two to six fixed cells (coelomocytes), which are usually associated with the longitudinal cords. The function of these cells is unknown. The alimentary canal of roundworms is complete, with both mouth and anus. The mouth is surrounded by lips bearing sensory papillae (bristles). The oesophagus, a conspicuous feature of nematodes, is a muscular structure that pumps food into the intestine; it differs in shape in different species.
The intestine is a tubular structure composed of a single layer of columnar cells possessing prominent microvilli on their luminal surface.

The excretory system of some nematodes consists of an excretory gland and a pore located ventrally in the mid-oesophagal region. In other nematodes this structure is drawn into extensions that give rise to the more complex tubular excretory system, which is usually H-shaped, with two anterior limbs and two posterior limbs located in the lateral cords. The gland cells and tubes are thought to serve as
absorptive bodies, collecting wastes from the pseudocolour, and to function in osmoregulation.
Nematodes are usually bisexual. Males are usually smaller than females, have a curved posterior end, and possess (in some species) copulatory structures, such as  Structure of nematodes. (A) Female. (B) Male. Transverse sections through the mid-region of the female worm (C) and through the  oesophagal region (D).

Spicules (usually two), a bursa, or both. The males have one or (in a few cases) two testes, which lie at the free end of a convoluted or recurved tube leading into a seminal vesicle and eventually into the cloaca. The female system is tubular also and usually is made up of reflexed ovaries. Each ovary is continuous, with an oviduct and tubular uterus. The uteri join to form the vagina, which in turn opens to the exterior through the vulva.

A copulation between a female and a male nematode is necessary for fertilization except in the genus Strongyloides, in which parthenogenetic development occurs (i.e., the development of an unfertilized egg into a new individual). Some evidence indicates that sex attractants (pheromones) play a role in heterosexual mating. During copulation, sperm is transferred into the vulva of the female. The sperm enters the ovum, and a fertilization membrane is secreted by the zygote. This membrane gradually thickens to form the chitinous shell.

A second membrane, below the shell, makes the egg impervious to essentially all substances except carbon dioxide and oxygen. In some species, a third proteinaceous membrane is secreted as the egg passes down the uterus by the uterine wall and is deposited outside the shell. Most nematodes that are parasitic in humans lay eggs that, when voided, contain either an uncleaved zygote, a group of blastomeres, or a completely formed larva. Some nematodes, such as the filariae and Trichinella spiralis, produce larvae that are deposited in the host.