Preventive measures are pruning which allows light and air to enter the tree, to achieve fast drying. Strong growth within the root area dams up moisture and facilitates infection.

A prognostic model called Sooty Blotch RIMpro has been developed, which still awaits validation. Similar to the apple scab model it numerically grades risk and degree of infection and can serve as a warning system. It allows conventional growers to spray more targeted. The parameters for calculation are wetness of leaves, amount of rain fall and temperature.

Conventional orchards that spray fungicides against apple scab, treat soot blotch and flyspeck at the same time. Therefore, the problem is not seen in conventional non-resistant varieties. However, scab-resistant varieties, which are not sprayed frequently show the infection. In organic orchards, spraying 4–5 with lime sulphur or coco soap during the main infectious periods is recommended.

The blotches are cosmetic damage "unacceptable to consumers" and downgrade fruit from premium fresh-market grade to processing use, i.e. reduce its market value, but leaf and fruit development are not affected.

Yellow-band disease (similar to Yellow Blotch disease) is a coral disease that attacks colonies of coral at a time when coral is already under stress from pollution, overfishing, and climate change. It is characterized by large blotches or patches of bleached, yellowed tissue on Caribbean scleractinian corals.

Yellow-band disease is a bacterial infection that spreads over coral, causing the discolored bands of pale-yellow or white lesions along the surface of an infected coral colony. The lesions are the locations where the bacteria have killed the coral’s symbiotic photosynthetic algae, called zooxanthellae which are a major energy source for the coral. This cellular damage and the loss of its major energy source cause the coral to starve, and usually cause coral death. There is evidence that climate change could be worsening the disease.

Yellow-band disease has severely affected reef building corals in the Caribbean. This disease have been associated with lower coral fecundity, altered tissue composition and a lower activites of antixenobiotic and antioxidant enzymes. Compared to the late 1990s, current data suggests that the disease remains a severe epidemic. In one study, 10 meter belt transects were taken at various depths, sampling coral colonies in the Lesser Antilles. At a depth of 5 m, yellow band rings and lesions were found on 79% of the colonies per transect, and only 21% of the colonies in this depth range appeared healthy.

Recent research indicates that yellow-band disease continues to be in an infectious phases in the Caribbean. It has been

found to cause infection in Pacific coral as well.

For simple cases of cystic echinococcosis, the most common form of treatment is open surgical removal of the cysts combined with chemotherapy using albendazole and/or mebendazole before and after surgery. However, if there are cysts in multiple organs or tissues, or the cysts are in risky locations, surgery becomes impractical. For inoperable cases such as these, chemotherapy and/or PAIR (puncture-aspiration-injection-reaspiration) become alternative options of treatment. In the case of alternative treatment using just chemotherapy, albendazole is preferred twice a day for 1–5 months. An alternative to albendazole is mebendazole for at least 3 to 6 months. The other alternative to surgery is PAIR with chemotherapy. PAIR is a minimally invasive procedure that involves three steps: puncture and needle aspiration of the cyst, injection of a scolicidal solution for 20–30 min, and cyst-re-aspiration and final irrigation. Patients who undergo PAIR typically take albendazole or mebendazole from 7 days before the procedure until 28 days after the procedure. While open surgery still remains as the standard for cystic echinococcosis treatment, there have been a number of studies that suggest that PAIR with chemotherapy is more effective than surgery in terms of disease recurrence, and morbidity and mortality. In addition to the three above mentioned treatments, there is currently research and studies looking at new treatment involving percutaneous thermal ablation (PTA) of the germinal layer in the cyst by means of a radiofrequency ablation device. This form of treatment is still relatively new and requires much more testing before being widely used. An alternative to open surgery is laparoscopic surgery, which provides excellent cure rates with minimal morbidity and mortality.

Recovery from an anaerobic infection depends on adequate and rapid management. The main principles of managing anaerobic infections are neutralizing the toxins produced by anaerobic bacteria, preventing the local proliferation of these organisms by altering the environment and preventing their dissemination and spread to healthy tissues.

Toxin can be neutralized by specific antitoxins, mainly in infections caused by Clostridia (tetanus and botulism). Controlling the environment can be attained by draining the pus, surgical debriding of necrotic tissue, improving blood circulation, alleviating any obstruction and by improving tissue oxygenation. Therapy with hyperbaric oxygen (HBO) may also be useful. The main goal of antimicrobials is in restricting the local and systemic spread of the microorganisms.

The available parenteral antimicrobials for most infections are metronidazole, clindamycin, chloramphenicol, cefoxitin, a penicillin (i.e. ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (i.e. clavulanic acid, sulbactam, tazobactam), and a carbapenem (imipenem, meropenem, doripenem, ertapenem). An antimicrobial effective against Gram-negative enteric bacilli (i.e. aminoglycoside) or an anti-pseudomonal cephalosporin (i.e. cefepime ) are generally added to metronidazole, and occasionally cefoxitin when treating intra-abdominal infections to provide coverage for these organisms. Clindamycin should not be used as a single agent as empiric therapy for abdominal infections. Penicillin can be added to metronidazole in treating of intracranial, pulmonary and dental infections to provide coverage against microaerophilic streptococci, and Actinomyces.

Oral agents adequate for polymicrobial oral infections include the combinations of amoxicillin plus clavulanate, clindamycin and metronidazole plus a macrolide. Penicillin can be added to metronidazole in the treating dental and intracranial infections to cover "Actinomyces" spp., microaerophilic streptococci, and "Arachnia" spp. A macrolide can be added to metronidazole in treating upper respiratory infections to cover "S. aureus" and aerobic streptococci. Penicillin can be added to clindamycin to supplement its coverage against "Peptostreptococcus" spp. and other Gram-positive anaerobic organisms.

Doxycycline is added to most regimens in the treatment of pelvic infections to cover chlamydia and mycoplasma. Penicillin is effective for bacteremia caused by non-beta lactamase producing bacteria. However, other agents should be used for the therapy of bacteremia caused by beta-lactamase producing bacteria.

Because the length of therapy for anaerobic infections is generally longer than for infections due to aerobic and facultative anaerobic bacteria, oral therapy is often substituted for parenteral treatment. The agents available for oral therapy are limited and include amoxacillin plus clavulanate, clindamycin, chloramphenicol and metronidazole.

In 2010 the American Surgical Society and American Society of Infectious Diseases have updated their guidelines for the treatment of abdominal infections.

The recommendations suggest the following:

For mild-to-moderate community-acquired infections in adults, the agents recommended for empiric regimens are: ticarcillin- clavulanate, cefoxitin, ertapenem, moxifloxacin, or tigecycline as single-agent therapy or combinations of metronidazole with cefazolin, cefuroxime, ceftriaxone, cefotaxime, levofloxacin, or ciprofloxacin. Agents no longer recommended are: cefotetan and clindamycin ( Bacteroides fragilis group resistance) and ampicillin-sulbactam (E. coli resistance) and ainoglycosides (toxicity).

For high risk community-acquired infections in adults, the agents recommended for empiric regimens are: meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, ciprofloxacin or levofloxacin in combination with metronidazole, or ceftazidime or cefepime in combination with metronidazole. Quinolones should not be used unless hospital surveys indicate >90% susceptibility of "E. coli" to quinolones.

Aztreonam plus metronidazole is an alternative, but addition of an agent effective against gram-positive cocci is recommended. The routine use of an aminoglycoside or another second agent effective against gram-negative facultative and aerobic bacilli is not recommended in the absence of evidence that the infection is caused by resistant organisms that require such therapy.

Empiric use of agents effective against enterococci is recommended and agents effective against methicillin-resistant "S. aureus" (MRSA) or yeast is not recommended in the absence of evidence of infection due to such organisms.

Empiric antibiotic therapy for health care-associated intra-abdominal should be driven by local microbiologic results. Empiric coverage of likely pathogens may require multidrug regimens that include agents with expanded spectra of activity against gram-negative aerobic and facultative bacilli. These include meropenem, imipenem-cilastatin, doripenem, piperacillin-tazobactam, or ceftazidime or cefepime in combination with metronidazole. Aminoglycosides or colistin may be required.

Antimicrobial regimens for children include an aminoglycoside-based regimen, a carbapenem (imipenem, meropenem, or ertapenem), a beta-lactam/beta-lactamase-inhibitor combination (piperacillin-tazobactam or ticarcillin-clavulanate), or an advanced-generation cephalosporin (cefotaxime, ceftriaxone, ceftazidime, or cefepime) with metronidazole.

Clinical judgment, personal experience, safety and patient compliance should direct the physician in the choice of the appropriate antimicrobial agents. The length of therapy generally ranges between 2 and 4 weeks, but should be individualized depending on the response. In some instances treatment may be required for as long as 6–8 weeks, but can often be shortened with proper surgical drainage.

For alveolar echinococcosis, surgical removal of cysts combined with chemotherapy (using albendazole and/or mebendazole) for up to two years after surgery is the only sure way to completely cure the disease. However, in inoperable cases, chemotherapy by itself can also be used. In treatment using just chemotherapy, one could use either mebendazole in three doses or albendazole in two doses. Since chemotherapy on its own is not guaranteed to completely rid the patient of disease, patients are often kept on the drugs for extended periods of times (i.e. more than 6 months, years). In addition to surgery and chemotherapy, liver transplants are being looked into as a form of treatment for alveolar echinococcosis although it is seen as incredibly risky since it often leads to echinococcosis re-infection in the patient afterwards.

The cornerstone of prevention and treatment of podoconiosis is avoidance of exposure to irritant soils. Wearing shoes in the presence of irritant soils is the primary method of exposure reduction. In Rwanda, a country of high disease prevalence, the government has banned walking barefoot in public, in order to curtail podoconiosis and other soil-borne diseases.

Once the disease has developed, rigorous foot hygiene including daily washing with soap and water, application of an emollient, and nightly elevation of the affected extremity has been shown to reduce swelling and disability. Compression wrapping and decongestive physiotherapy of the affected extremity has been shown to be effective in other forms of lymphedema, but the benefits of these therapies have not been rigorously studied in podoconiosis. Nodules will not resolve with these conservative measures, although surgical removal of the nodules can be performed.

Treatment for fiddler’s neck is unnecessary if it is painless and shows minimal swelling, particularly since minor cases are taken as a mark of pride. But fiddler’s neck may lead to worse disorders. The primary methods of treatment involve adjustments to playing of the instrument:

- good hygiene for the affected area and for the instrument

- use of a clean cotton cloth that is changed frequently

- use of a shoulder rest to reduce pressure below the jaw

- a suitable chin rest, especially one carved or molded for the individual

- Covering or changing potentially allergenic materials on the instrument.

- shifting the chin rest to the center of the body over the tailpiece

- smoothing coarse surfaces to reduce abrasion

- for males, growing a beard to avoid folliculitis

Surgery is necessary for sialolithiasis, parotid tumors, and cysts. Cervical lymph nodes that are larger than 1 cm must be biopsied. Connective tissue can be removed by excision when a non-inflamed mass is large, and there is generally little recurrence. Infections should be treated conservatively, and causative species should be identified through smear and culture for appropriate antibiotic selection. Reduction of playing time may be helpful for cases without inflammation, but in 30% of cases this did not improve the symptoms.

The main treatment for acral erythema is discontinuation of the offending drug, and symptomatic treatment to provide analgesia, lessen edema, and prevent superinfection. However, the treatment for the underlying cancer of the patient must not be neglected. Often, the discontinued drug can be substituted with another cancer drug or cancer treatment.

Symptomatic treatment can include wound care, elevation, and pain medication. Corticosteroids and pyridoxine have also been used to relieve symptoms. Other studies do not support the conclusion.

A number of additional remedies are listed in recent medical literature. Among them henna and 10% uridine ointment which went through clinical trial.

In eye disease, surgical removal is necessary for cysts within the eye itself as treating intraocular lesions with anthelmintics will elicit an inflammatory reaction causing irreversible damage to structural components. Cysts outside the globe can be treated with anthelmintics and steroids. Treatment recommendations for subcutaneous cysticercosis includes surgery, praziquantel and albendazole.

PPE invariably recurs with the resumption of chemotherapy. Long-term chemotherapy may also result in reversible palmoplantar keratoderma. Symptoms resolve 1–2 weeks after cessation of chemotherapy (Apisarnthanarax and Duvic 2003).

Asymptomatic cysts, such as those discovered incidentally on neuroimaging done for another reason, may never lead to symptomatic disease and in many cases do not require therapy. Calcified cysts have already died and involuted. Further antiparasitic therapy will be of no benefit.

Neurocysticercosis may present as hydrocephalus and acute onset seizures, thus the immediate therapy is emergent reduction of intracranial pressure and anticonvulsant medications. Once the seizures have been brought under control, antihelminthic treatments may be undertaken. The decision to treat with antiparasitic therapy is complex and based on the stage and number of cysts present, their location, and the persons specific symptoms.

Adult "Taenia solium" are easily treated with niclosamide, and is most commonly used in taeniasis. However cysticercosis is a complex disease and requires careful medication. Praziquantel (PZQ) is the drug of choice. In neurocysticercosis praziquantel is widely used. Albendazole appears to be more effective and a safe drug for neurocysticercosis. In complicated situation a combination of praziquantel, albendazole and steroid (such as corticosteroids to reduce the inflammation) is recommended. In the brain the cysts can be usually found on the surface. Most cases of brain cysts are found by accident, during diagnosis for other ailments. Surgical removals are the only option of complete removal even if treated successfully with medications.

Antiparasitic treatment should be given in combination with corticosteroids and anticonvulsants to reduce inflammation surrounding the cysts and lower the risk of seizures. When corticosteroids are given in combination with praziquantel, cimetidine is also given, as corticosteroids decrease action of praziquantel by enhancing its first pass metabolism. Albendazole is generally preferable over praziquantel due to its lower cost and fewer drug interactions.

Surgical intervention is much more likely to be needed in cases of intraventricular, racemose, or spinal neurocysticercosis. Treatments includes direct excision of ventricular cysts, shunting procedures, and removal of cysts via endoscopy.

On post-mortem examination (necropsy), the most obvious gross lesion is subcutaneous oedema in the submandibular and pectoral (brisket) regions. Petechial haemorrhages are found subcutaneously and in the thoracic cavity. In addition, congestion and various degrees of consolidation of the lung may occur. Animals that die within 24–36 hours, have only few petechial haemorrhages on the heart and generalised congestion of the lung, while in animals that die after 72 hours, petechial and ecchymotic haemorrhages were more evident and lung consolidation are more extensive.

Specific pretreatments, drugs to prevent chemically induced lung injuries due to respiratory airway toxins, are not available. Analgesic medications, oxygen, humidification, and ventilator support currently constitute standard therapy. In fact, mechanical ventilation remains the therapeutic mainstay for acute inhalation injury. The cornerstone of treatment is to keep the PaO2 > 60 mmHg (8.0 kPa), without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more versatile than volume control, although breaths should be volume limited, to prevent stretch injury to the alveoli. Positive end-expiratory pressure (PEEP) is used in mechanically ventilated patients with ARDS to improve oxygenation. Hemorrhaging, signifying substantial damage to the lining of the airways and lungs, can occur with exposure to highly corrosive chemicals and may require additional medical interventions. Corticosteroids are sometimes administered, and bronchodilators to treat bronchospasms. Drugs that reduce the inflammatory response, promote healing of tissues, and prevent the onset of pulmonary edema or secondary inflammation may be used following severe injury to prevent chronic scarring and airway narrowing.

Although current treatments can be administered in a controlled hospital setting, many hospitals are ill-suited for a situation involving mass casualties among civilians. Inexpensive positive-pressure devices that can be used easily in a mass casualty situation, and drugs to prevent inflammation and pulmonary edema are needed. Several drugs that have been approved by the FDA for other indications hold promise for treating chemically induced pulmonary edema. These include β2-agonists, dopamine, insulin, allopurinol, and non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Ibuprofen is particularly appealing because it has an established safety record and can be easily administered as an initial intervention. Inhaled and systemic forms of β2-agonists used in the treatment of asthma and other commonly used medications, such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require further study. A recent study documented in the "AANA Journal" discussed the use of volatile anesthetic agents, such as sevoflurane, to be used as a bronchodilator that lowered peak airway pressures and improved oxygenation. Other promising drugs in earlier stages of development act at various steps in the complex molecular pathways underlying pulmonary edema. Some of these potential drugs target the inflammatory response or the specific site(s) of injury. Others modulate the activity of ion channels that control fluid transport across lung membranes or target surfactant, a substance that lines the air sacs in the lungs and prevents them from collapsing. Mechanistic information based on toxicology, biochemistry, and physiology may be instrumental in determining new targets for therapy. Mechanistic studies may also aid in the development of new diagnostic approaches. Some chemicals generate metabolic byproducts that could be used for diagnosis, but detection of these byproducts may not be possible until many hours after initial exposure. Additional research must be directed at developing sensitive and specific tests to identify individuals quickly after they have been exposed to varying levels of chemicals toxic to the respiratory tract.

Currently there are no clinically approved agents that can reduce pulmonary and airway cell dropout and avert the transition to pulmonary and /or airway fibrosis.

A wide variety of clinical signs have been described for HS in cattle and buffaloes. The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varies according to the route of infection. The incubation period is 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.

There is variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals. It has also been recorded from field observations that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.

Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by fever, with a rectal temperature of , loss of appetite and depression. Phase two is typified by increased respiration rate (40–50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia. The three phases overlap when the disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with a shorter duration.

There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting

contaminated premises.

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

One strategy to control the disease in areas where it is common is the treatment of entire groups of people regardless of symptoms via mass drug administration. This is often done among school-age children and is known as deworming. While testing and treating children who are infected looks like it is effective, there is insufficient evidence to conclude that routine deworming, in the absence of a positive test, improves nutrition, haemoglobin, school attendance or school performance.

For this purpose, broad-spectrum benzimidazoles such as mebendazole and albendazole are the drugs of choice recommended by WHO. These anthelminthics are administered in a single dose are safe, relatively inexpensive, and effective for several months. Mebendazole can be given with a single dose twice a day for three consecutive days. Albendazole is given at a single dose. WHO recommends annual treatment in areas where between 20 and 50% of people are infected, and a twice a year treatment if it is over 50%; and in low risk situation (i.e. less than 20% prevalence) case-by-case treatment. In addition to these, pyrantel pamoate is also equally effective on ascaris. However, it has been reported that albendazole, mebendazole, and pyrantel pamoate are not entirely effective against "T. trichiura" with single oral doses in population-based control.

Fiddler’s neck does not usually form unless the musician is practicing or playing for more than a few hours each day, and only seems to develop after a few years of serious playing. Thus, when not infected or otherwise problematic, fiddler’s neck may be known as a benign practice mark and may be worn proudly as an indication of long hours of practice. Blum & Ritter (1990) found that 62% of 523 professional violinists and violists in West Germany experienced fiddler’s neck, with the percentage among violists being higher (67%) than among violinists (59%). Viola players are believed to be more predisposed to developing fiddler’s neck than violinists because the viola is larger and heavier, but this has not been empirically confirmed.

The development of fiddler’s neck does not depend on preexisting skin problems, and Blum & Ritter find that only 23% of men and 14% of women in their study reported cutaneous disorders in other parts of the face (mainly acne and eczema) that were independent of playing the violin or viola. Fiddler’s neck may exacerbate existing acne, but acne may also be limited solely to the lesion and not appear elsewhere. Nonetheless, musicians with underlying dermatologic diseases like acne and eczema are more endangered by fiddler’s neck than others. Males may develop folliculitis or boils due to involvement of beard hair.

Podoconiosis, also known as nonfilarial elephantiasis, is a disease of the lymph vessels of the lower extremities that is caused by chronic exposure to irritant soils. It is the second most common cause of tropical lymphedema after filariasis, and it is characterized by prominent swelling of the lower extremities, which leads to disfigurement and disability.

Ensuring proper nutrition of pregnant and lactating mothers is essential. Achieving so by helping women of reproductive age be in good nutritional status at conception is an excellent preventive measure. A focus on the pre-conception period has recently been introduced as a complement to the key phase of the 1000 days of pregnancy and first two years of life. An example of this is are attempts to control anemia in women of reproductive age. A well-nourished mother is the first step of stunting prevention, decreasing chances of the baby being born of low birth-weight, which is the first risk factor for future malnutrition.

After birth, in terms of interventions for the child, early initiation of breastfeeding, together with exclusive breastfeeding for the first 6 months, are pillars of stunting prevention. Introducing proper complementary feeding after 6 months of age together with breastfeeding until age 2 is the next step.

The World Health Organizations recommended albendazole or mebendazole for treatment.

In summary, key policy interventions for the prevention of stunting are:

- Improvement in nutrition surveillance activities to identify rates and trends of stunting and other forms of malnutrition within countries. This should be done with an equity perspective, as it is likely that stunting rates will vary greatly between different population groups. The most vulnerable should be prioritized. The same should be done for risk factors such as anemia, maternal under-nutrition, food insecurity, low birth-weight, breastfeeding practices etc. By collecting more detailed information, it is easier to ensure that policy interventions really address the root causes of stunting.

- Political will to develop and implement national targets and strategies in line with evidence-based international guidelines as well as contextual factors.

- Designing and implementing policies promoting nutritional and health well-being of mothers and women of reproductive age. The main focus should be on the 1000 days of pregnancy and first two years of life, but the pre-conception period should not be neglected as it can play a significant role in ensuring the fetus and baby's nutrition.

- Designing and implementing policies promoting proper breastfeeding and complementary feeding practice (focusing on diet diversity for both macro and micronutrients). This can ensure optimal infant nutrition as well as protection from infections that can weaken the child's body. Labor policy ensuring mothers have the chance to breastfeed should be considered where necessary.

- Introducing interventions addressing social and other health determinants of stunting, such as poor sanitation and access to drinking water, early marriages, intestinal parasite infections, malaria and other childhood preventable disease (referred to as “nutrition-sensitive interventions”), as well as the country's food security landscape. Interventions to keep adolescent girls in school can be effective at delaying marriage with subsequent nutritional benefits for both women and babies. Regulating milk substitutes is also very important to ensure that as many mothers as possible breastfeed their babies, unless a clear contraindication is present.

- Broadly speaking, effective policies to reduce stunting require multisectoral approaches, strong political commitment, community involvement and integrated service delivery.

There is no standard approach to the treatment of lymphangiomatosis and treatment often is aimed at reducing symptoms. Surgical intervention may be indicated when complications arise and a number of reports of response to surgical interventions, medications, and dietary approaches can be found in the medical literature.

Unfortunately, there is no standardized treatment for lymphangiomatosis and no cure.

Treatment modalities that have been reported in the medical literature, by system, include: