1. Definition of STHSoil-transmitted helminths (STHs) form one of the most important groups of

infectious agents and are the cause of serious global health problems; more than a billion people have been infected by at least one species of this group of pathogens. Soil-transmitted helminthiasis (STH) is a sub-group within the group of helminth infections (helminthiasis). It is caused specifically by those helminths which are transmitted through soil contaminated with faecal matter and are therefore called soil-transmitted helminths. At a global level, the most important STHs are roundworms (Ascaris lumbricoides), whipworms (Trichuris trichiura) and hookworms (Necator americanus or Ancylostoma duodenale) and are estimated to have infected 807 million, 604 million and 576 million people, respectively. The greatest numbers of STH infections occur in Sub-Saharan Africa (SSA), East Asia, China, India and South America.

Mascarini-Serra L. Prevention of Soil-transmitted Helminth Infection. Journal of Global Infectious Diseases. 2011;3(2):175-182.

a. Clinical Manifestaion Ascaris Lumbri

CLINICAL MANIFESTATIONSThe clinical presentation depends on the intensity of infection and the organs

involved. Most individuals have low to moderate worm burdens and have no symptoms or signs. The most common clinical problems are from pulmonary disease and obstruction of the intestinal or biliary tract. Larvae migrating through these tissues may cause allergic symptoms, fever, urticaria, and granulomatous disease. The pulmonary manifestations resemble Loeffler syndrome and include transientrespiratory symptoms such as cough and dyspnea, pulmonary infiltrates, and blood eosinophilia. Larvae may be observed in the sputum. Vague abdominal complaints have been attributed to the presence of adult worms in the small intestine, although the precise contribution of the parasite to these symptoms is difficult to ascertain.

A more serious complication occurs when a large mass of worms leads to acute bowel obstruction. Children with heavy infections may present with vomiting, abdominal distention, and cramps. In some cases, worms may be passed in the vomitus or stools. Ascaris worms occasionally migrate into the biliary and pancreatic ducts, where they cause cholecystitis or pancreatitis. Worm migration through the intestinal wall can lead to peritonitis. Dead worms can serve as a nidus for stone formation. Studies show that chronic infection with A. lumbricoides (often coincident with other helminth infections) impairs growth, physical fitness, and cognitive development.

Nelson, Woldo, E. 2015. Textbook of Pediatric. Edisi 20. Volume 1. Philadelphia: Elsevier

b. Pathogenesis Ancylodestoma duodenale

PATHOGENESISThe major morbidity of human hookworm infection is a direct result of intestinal

blood loss. Adult hookworms adhere tenaciously to the mucosa and submucosa of the proximal small intestine by using their cutting plates or teeth and a muscular esophagus that creates negative pressure in their buccal capsules. At the attachment site, host inflammation is downregulated by the release of antiinflammatory polypeptides by the hookworm. Rupture of capillaries in the lamina propria is followed by blood extravasation, with some of the blood ingested directly by the hookworm. After ingestion, the blood is anticoagulated, the red blood cells are lysed, and the hemoglobin released and digested.

Each adult A. duodenale hookworm causes loss of an estimated 0.2 mL of blood/day; blood loss is less for N. americanus. Individuals with light infections suffer from very little blood loss and, consequently, may have hookworm infection but not hookworm disease. There is a direct correlation between the number of adult hookworms in the gut and the volume of fecal blood loss. Hookworm disease results only when individuals with moderate and heavy infections experience sufficient blood loss to develop iron deficiency and anemia. Hypoalbuminemia and consequent edema and anasarca from the loss of intravascular oncotic pressure can also occur. These features depend heavily on the dietary reserves of the host.

Nelson, Woldo, E. 2015. Textbook of Pediatric. Edisi 20. Volume 1. Philadelphia: Elsevier

c. Immunology respond Ancylostomad. Immunology respond necator americanus

AKU GABUNG JAWABANNYA

IMMUNE RESPONSE TO ADULT HOOKWORMS

Humoral Response

Like most intestinal helminthiases, hookworm infection is characterized by antibody responses dominated by IgG1, IgG4, and IgE, which in turn are under the control of Th2 cytokines, typically mediated by the effects of IL-4. Various methods have been used to identify these antibody responses, ranging from observation of immunoprecipitates around oral openings to more detailed analyses of Ig subclasses against somatic and excretory/secretory (ES) products by enzyme-linked immunosorbent assay and Western blot analysis .

Studies of Papua New Guineans infected with Necator americanus showed that antibody isotypes responded differently before and 2 years after anthelmintic treatment . Egg counts and worm burdens rose to about 50% of pretreatment levels 1 year after the initial chemotherapy. IgG and IgM levels against adult ES antigens had fallen significantly 1 year after treatment, and IgG levels continued to decline over the following year, while IgM levels increased again but did not reach pretreatment levels, consistent with ongoing reinfection. IgE levels fell only slightly,

and, in contrast, IgA and IgD levels increased over the 2-year period. The levels of all isotypes raised to larval antigens except for IgD dropped after the first year, but each isotype had recovered to its original level by the following year except for IgG, whose level continued to decline. Interpreting these data proved difficult, given that the patients were reinfected by 12 months post treatment. The authors suggested that sufficient reinfection might have provided the smaller quantities of antigen required to maintain the local IgA and IgE responses compared with the larger quantities needed to maintain systemic IgG and IgM responses, accounting for the isotype profiles observed. It was concluded that levels of IgG and IgM against adult ES antigens provided the best indicator of both current infection with adult parasites and efficacy of chemotherapy, since these isotypes were the most strongly affected by treatment. However, despite this vigorous response, there is little evidence that antibody levels correlate with protection against hookworms.

Like acute allergy, tissue invasion by helminths is associated with elevated levels of IgE in serum. Much of this IgE induced by helminth parasites seems to be directed against heterologous antigens and is tightly regulated by opposing cytokines. Th2 cytokines (typically IL-4, IL-5, and IL-13) predominate, with IL-4 promoting the synthesis of IgE, while Th1 cytokines such as gamma interferon inhibit its production . This observation led to speculation that helminth parasites secrete proallergic mediators that induce polyvalent, non-parasite-specific IgE, thus saturating IgE receptors on effector cells . A recent study has shown that IgE antibodies were more specifically directed against N. americanusepitopes than were other Ig isotype responses. Preadsorption of human N. americanus infection sera with antigens from closely related hookworm species had little effect on anti-Necator IgE levels (1.0 to 2.4% decrease in mean optical density values), while the IgG levels dropped by 19 to 23%. In human intestinal infection with A. caninum, IgE responses proved to be more specific than IgG responses to ES antigens, with selected patients generating detectable levels of IgE but not IgG to a diagnostic antigen. Patients infected withA. duodenale produce both systemic and jejunal IgE that specifically binds to larval antigens, suggesting that some hookworm allergens are shared by migrating larvae and adults residing in the gut.

Circulating IgG1 and IgG4 levels are frequently elevated in helminthiases, including hookworm infections, and specific IgG4 has been suggested to be a marker of active infection with N. americanus. The role of IgG4 is poorly understood, although, like IgE, it is upregulated in atopic conditions and helminthic infections. It is thought to downregulate immune responses by competitively inhibiting IgE-mediated mechanisms, e.g., by blocking mast cell activation. In addition, IgG4 does not fix complement and only weakly binds to Fcγ receptors. Therefore, antigen binding by IgG4 is likely to be less harmful to the host than binding by IgE. The potentially harmful effects to the host of an exuberant IgE response are further restricted by the production of IgG autoantibodies to IgE . This complex area needs further exploration, especially if vaccines are to be developed against hookworm infections.

Adult hookworms induce the production of secretory IgE , IgG, and IgM but not IgA , and the levels of these Igs return to normal after anthelmintic treatment. The absence of secretory IgA in these patients was intriguing and might be accounted for by the secretion of hookworm proteases that specifically cleave IgA.

Cellular Response

Information on the cellular immune response in human hookworm infections is sparse: essentially, a Th2 response predominates, generating IgE and eosinophilia.

Eosinophils

Eosinophils feature prominently in the leukocytic response to adult hookworms, and their circulating numbers reflect the worm burden. Infections of volunteers with N. americanus and A. duodenale were characterized by blood eosinophilia, although the dynamics of the response varied with the species. Larval hypobiosis and reactivation in A. duodenaleinfection was thought to underlie the small initial increase followed by the sudden rise in eosinophil levels at week 33 of infection, shortly preceding the appearance of hookworm eggs in feces. With Necator, volunteers exposed to L3 rapidly developed blood eosinophilia, which peaked between days 38 and 64. Systemic eosinophilia is also pronounced in human enteric infections with A. caninum.

Obviously, eosinophils in the blood are in transit from the bone marrow to their effector sites, the small intestine in this case. In human infections with both anthropophilic and zoonotic hookworms, infiltration of the worm feeding site with eosinophils is an almost universal feature, but it varies according to the stage and intensity of infection as well as to individual host factors. In extreme cases, exemplified by human eosinophilic enteritis associated with A. caninum, all layers of the gut from the mucosa to the serosa can be severely affected by intense eosinophilic inflammation.

T Cells and Cytokines

Very little is known about T-cell reactivity in hookworm infections; only two studies have examined human blood lymphocyte responses, both in Necator infections. Peripheral T cells reacted strongly to mitogens and weakly to hookworm antigens . Clinical manifestations did not correlate with lymphocyte responses, either in these studies or in animal models.

In general, nematode infections drive a strong Th2 response, promoting IgE synthesis and eosinophil production and migration, as well as production and proliferation of suppressor cell populations. This response is mediated by parasite secretions and can be induced by immunizing naive animals with ES products alone. While cytokine profiles have not yet been reported from either animal or human hookworm infections, many detailed reports have been published from other helminthiases, including those in cytokine transgenic and gene knockout mice. It is very likely that many of the findings will apply directly to hookworm infection, although this remains speculative in the absence of data.

Mast Cells

Mast cell degranulation in response to IgE-allergen interaction plays a critical role in the local mobilization and activation of eosinophils. Mast cell proteases degrade cuticular collagens of adult N. americanus and no doubt are important in the host response to hookworms, but they have attracted sparse research attention. Hamsters infected with host-adapted A. ceylanicum

quickly developed resistance to infection with this species, characterized by increased antibody production and mucosal mastocytosis.

Mast cells are instrumental in resistance to some other intestinal helminthiases. While the mechanisms are unclear, neutralizing antibodies to IL-9 inhibit the production of mast cell protease I and prevent normally resistant mice from clearing infections withTrichinella spiralis. In contrast, abrogation of IL-3 and IL-4 cytokines required for mast cell hyperplasia led to an 85 to 90% decrease in mucosal mast cell numbers in mice infected with Nippostrongylus but had no effect on worm expulsion.

Hookworms appear to be more resistant to intestinal inflammation than are most other intestinal nematodes, perhaps reflecting their attachment and feeding strategies. Hamsters coinfected with T. spiralis and A. ceylanicum or N. americanus produced an intense mucosal response that clearedT. spiralis (albeit more slowly than in hamsters with justT. spiralis), while the hookworms remained relatively unaffected. Indeed, depressed anti-T. spiralis antibody levels indicate that hookworms might protect other parasites by generally suppressing immune responses.

Loukas, Alex. 2001. Immune Response in Hookworm Infections. Australia: Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane, QLD 4006 and Australian Center for International Tropical Health and Nutrition.

e. Clinical manifestation tricuhira trichuira

CLINICAL MANIFESTATIONSMost persons harbor low worm burdens and do not have symptoms. Some

individuals may have a history of right-lower-quadrant or vague periumbilical pain. Adult Trichuris suck approximately 0.005 mL of blood per worm per day. Children, who are most likely to be heavily infected, frequently suffer from disease. Clinical manifestations include chronic dysentery, rectal prolapse, anemia, poor growth, as well as developmental and cognitive deficits. There is no significant eosinophilia, even though a portion of the worm is embedded in the mucosa of the large bowel.

Nelson, Woldo, E. 2015. Textbook of Pediatric. Edisi 20. Volume 1. Philadelphia: Elsevier

f. Diagnosis strongly stercoralis

DIAGNOSISIntestinal strongyloidiasis is diagnosed by examining feces or duodenal fluid for

the characteristic larvae. Several stool samples should be examined either by direct smear, the Koga agar plate method, or the Baermann test. Alternatively, duodenal fluid can be sampled by the enteric string test (Entero-Test) or aspiration via endoscopy. In children with the hyperinfection syndrome, larvae may be found in sputum, gastric aspirates, and, rarely, in small intestinal biopsy specimens. An enzyme-linked immunosorbent assay for immunoglobulin G antibody to Strongyloides may be more sensitive than parasitologic methods for diagnosing intestinal infection in the

immunocompetent host. The utility of the assay in diagnosing infection in immunocompromised subjects with the hyperinfection syndrome has not been determined. Eosinophilia is common.

Nelson, Woldo, E. 2015. Textbook of Pediatric. Edisi 20. Volume 1. Philadelphia: Elsevier

g. Clinical manifestation Stongly

CLINICAL MANIFESTATIONSApproximately 30% of infected individuals are asymptomatic. The remaining

patients have symptoms that correlate with the 3 stages of infection: invasion of the skin, migration of larvae through the lungs, and parasitism of the small intestine by adult worms. Larva currens is the manifestation of an allergic reaction to filariform larvae that migrate through the skin, where they leave pruritic, tortuous, urticarial tracks. The lesions may recur and are typically found over the lower abdominal wall, buttocks, or thighs, resulting from larval migration from defecated stool. Pulmonary disease secondary to larval migration through the lung rarely occurs and may resemble Loeffler syndrome (cough, wheezing, shortness of breath, transient pulmonary infiltrates accompanied by eosinophilia). Gastrointestinal strongyloidiasis is characterized by indigestion, crampy abdominal pain, vomiting, diarrhea, steatorrhea, protein-losing enteropathy, proteincaloric malnutrition, and weight loss. Edema of the duodenum with irregular mucosal folds, ulcerations, and strictures can be seen radiographically. Infection may be chronic in nature and is associated with eosinophilia.

Strongyloidiasis is potentially lethal because of the ability of the parasite to replicate within the host and cause overwhelming hyperinfection in immunocompromised persons. The hyperinfection syndrome is characterized by an exaggeration of the clinical features that develop in symptomatic immunocompetent individuals. The onset is usually sudden, with generalized abdominal pain, distention, and fever. Multiple organs can be affected as massive numbers of larvae disseminate throughout the body and introduce bowel flora. The latter may result in bacteremia and septicemia. Cutaneous manifestations may include petechiae and purpura. Cough, wheezing, and hemoptysis are indicative of pulmonary involvement. Whereas eosinophilia is a prominent feature ofstrongyloidiasis in immunocompetent persons, this sign may be absent in immunocompromised persons. Because of the low incidence of strongyloidiasis in industrialized countries, it is often misdiagnosed, resulting in a significant delay in treatment.

Nelson, Woldo, E. 2015. Textbook of Pediatric. Edisi 20. Volume 1. Philadelphia: Elsevier

2. What is growth and development screening and how to screen?

KONSEP KUESIONER PRA SKRINING PERKEMBANGAN (KPSP)

Definition                    KPSP   Is   a   short   questionnaire   addressed   to   parents   and   used   as   a   preliminary screening tool for development of children aged 3 months to 6 years.

Uses KPSP

KPSP can be used to determine the presence or absence of obstacles, interference or problems in child development.

How to Use KPSP

Health officials read KPSP first. Then provide an opportunity for parents to answer the question group in accordance with the child's age. Results are recorded in the Card Data Growth.

How to Calculate Age Children

The   child's   age   determined  by   year   and  month.   Excess   16  days   rounded  up   to   1  month.Example: Children aged 3 months to 16 days, rounded to 4 months, Children aged 5 months and 15 days, rounded to 5 months.

How to Select Question KPSP

Questions  posed to  the parents  and the  chosen group of  questions   in  accordance with  the child's age.

How to Assess KPSP

a) Re-examine whether all the questions have been answered.

b) Calculating the number of answers Yes.

c) If the number of answers Yes = 9 or 10 means children who examined normal (N).

d) If the number of Yes = less than 9, then it needs to be examined again on:

How to calculate the age of the child.

How to choose KPSP question, whether in accordance with the child's age.

Whether the answer to the parents / caregivers of children in accordance with which one.

If the number of answers Yes = 7 or 8, specify a schedule for re-examination one week later (U).

If the re-examination of the number of answers Yes fixed 7 or 8, then the child requires further examination / referenced (TN).

Note: Questions KPSP used in the re-examination tailored to the child's age on the date of the re-examination.

e) If the number of answers Yes = 6 or less, then the child requires further examination / referenced (TN).

How to Conduct Inspection Repeat with KPSP

Reexamination using 3 held on the following circumstances:

a) KPSP negative results or the number of answers Yes = 9 or 10, re-examination can be done.

b) every 3 months to under 12 months of age.

c) every 6 months to age 12 s / d 72 months nevertheless more frequent examinations will be better.

d) Results KPSP the number Yes = 7 or 8, reexamination conducted 1 week later next to the first examination.

e) Results KPSP to answer Yes = less or reexamination remains 7-8, the child needs to be referred to health care facilities more complete.

How to Record Results KPSP

KPSP results are recorded in the Data Card Growth (page 4). Write the answer age Yes or No in the box provided for each question according to age groups of children.  Then compute the answer Yes.

If the assessment KPSP = 9 or 10 answers Yes, it means a good child development (code N).If the assessment KPSP = 7 or 8, means dubious and children need to be re-examined 1 week later.If the assessment KPSP = less than 7 means positive children should be referred (code TN)

I. Definition of DDST (Denver Development Screening Test)

DDST is one method of screening for developmental disorders of children. This test is not a diagnostic test or IQ test

II. Function DDST

DDST used to estimate the personal development of social, fine motor, language and gross motor skills in children aged 1 month to 6 years.

III. Aspects of development Assessed

In DDST there are 125 tasks of development where all the developmental tasks are arranged in   the   order   of   development,   and   arranged   in   four   large   groups   called   sectors   of development, which include:

A. Personal Social (Social Behavior)

B. Aspects related to the ability of independent, socialize and interact with their environment, such as:

1. Staring face2. Replying to smile checker3. spontaneous smiling4. Observing hand5. Trying to reach toys6. Eat yourself7. Applause8. Declare wishes9.-Daag Daag by hand10. Main ball with examiner11. Imitate activities12. Drinking cup13. Help at home14. Using a spoon and fork15. Opens clothing16. Feeding dolls17. Wearing18. Brush your teeth with help19. Wash and dry hands20. The name of a friend21. Wearing a T-shirt22. Dressing unaided23. Playing snakes and ladders / card24. Brush teeth without help25. Taking eat

B. Adaptive Fine Motor (Motor Movement Fine)Aspects related to the child's ability to observe something, do movements that involve certain body parts and performed in:1. Adhering to the midline2. Following through midline3. Holding icik-icik4. Following 18005. Observing beads6. Hand touch7. Achieved8. Looking thread9. Scratching beads10. Move the cube11. Take two cubes12. Hold with thumb and finger13. banging two cubes14. Put the cubes in the cup

15. Doodling16. Take the beads indicated17. Tower of two cubes18. The tower of four cubes19. The tower of six cubes20. Imitating vertical line21. The tower of cubes22. Wiggle of thumb23. Modeled O24. Drawing with 3 parts25. Modelling (point)26. Choosing a longer line27. Modeled ð shown28. Drawing the 6 parts29. Modeled ð

C. Language (English)Ability to respond to the voice, and spoke spontaneously follow orders that include:1. React2. Voice3. Oooo? Aaaah4. Laugh5. Yelling6. Turning to the sound icik-icik7. Turning toward the sound8. One syllable9. Mimic the sounds of the words10. Papa / Mama unspecific11. The combination of syllables12. Babbling13. Papa / Mama specific14. 1 word15. 2 words16. 3 words17. 6 words18. Pointing 2 images19. The combination of the word20. calls 1 image21. Calls body parts22. Referring 4 pictures23. Talk with understandable24. Calling 4 image25. Knowing 2 activities26. Understand 2 adjectives27. Mention one color28. Uses 2 objects29. Knowing30. Talk all understandable

31. Understand 4 preposition32. Mention 4 colors33. Deciphering 6 words34. Knowing the 3 adjectives35. Counting 6 cubes36. Contrary 237. Deciphering 7 words

D. Gross Motor (Motion Motor Coarse)Aspects relating to the movement and posture, including the ability to:1. Movement of balance2. Raising the head3. The head lifted upward4. Sit upright head5. The body rested on foot6. Chest lifted one arm rested7. Flipping8. Rise heads held9. Sit without handles10. Standing without handles11. Rise time standing12. Risen keeps sitting13. Stand 2 seconds14. Stand-alone15. Bowing then stood16. Walk with good17. Walk to resign18. Lari19. Walk up stairs20. Kick the ball forward21. Jumping22. Throwing the ball, arms up23. Skip24. Stand one foot 1 sec25. Stand one foot 2 seconds26. Jump on one foot27. Stand one foot 3 seconds28. Stand a foot 4 seconds29. Walk heel to toe30. Stand a foot 6 seconds

IV. How to Measure Child Development with DDSTAt the time of the test, a task that needs to be checked every time a screening usually ranges between 20-30 duties, so it does not take long, only about 15-20 minutesA. Tool Used1.Alat props: a red wool yarn, raisins / beads, cubes of red-yellow-green-blue, kids games, small bottles, tennis balls, small bells, paper, and pencils.2. The DDST form

3. User guide as a reference that explains the ways to test and how to vote.

B. DDST procedure consists of two stages, namely:1. The first stage: periodically performed on all children aged 3-6 months, 9-12 months, 18-24 months, 3 years, 4 years, 5 years.2. The second stage: done on those suspected developmental delays in the first stage and then reconstituted with a complete diagnostic evaluation.

C. AssessmentAssessment of whether the pass (Passed: P), failed (Fail: F), or if the child does not get a chance to do a task (No Opportunity: NO). Then the line is drawn based on chronological age, which cut a horizontal line on the form DDST development tasks. After it is calculated in each sector, how the P and how the F, then based on the guidelines, the test results were classified into normal, abnormal, dubious (Questionable) and can not be tested (Untestable).1. Abnormal- When you got two or more delay, the 2 sectors or more- When in one or more sectors gained 2 or more delay plus one sector or more with one delay and in the same sector is no pass in the box that intersects the vertical lines of age.2. Doubtful- When the first sector gained 2 delay or more.- When the first sector obtained one or more delay and in the same sector nobody pass in the box that intersects the vertical lines of age.3. Do not be tested- In the event of rejection that caused the results of tests become abnormal or doubtful.4. NormalAll that is not listed in the above criteria.

In order to more quickly in implementing screening, it can be used pre-screening phase by using:1. DDST Short Form, which each sector are taken only 3 tasks (making a total of 12 tasks) asked his mother. When obtained one fails or is rejected, it is considered "suspect" and should be continued with full DDST.2. PDQ (Pre-Screening Questionnaire Development)The questionnaire form used for parents who had high school education can be filled up parents at home or while waiting in the clinic. Selected 10 questions on the questionnaire that corresponds to the child's age. Then assessed based on the criteria that have been set and in the case of suspected testing DDST complete. (Soetjiningsih, 1998)

Soetjiningsih. 2012. Tumbuh Kembang Anak. Jakarta: EGC.

3. Malnutrition

Malnutrition is the condition that develops when the body does not get the right amount of the vitamins, minerals, and other nutrients it needs to maintain healthy tissues and organ function. The term malnutrition generally refers both to undernutrition and overnutrition, but in this guide we use the term to refer solely to a deficiency of nutrition. Many factors can cause malnutrition, most of which relate to poor diet or severe and repeated infections, particularly in underprivileged populations.

Blössner, Monika, de Onis, Mercedes. Malnutrition: quantifying the health impact atnational and local levels. Geneva, World Health Organization, 2005. (WHO Environmental Burden of Disease Series, No. 12).

4. How to manage malnutrion