skin disease and flood crisis


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  • มีรายงานหลายที่ในโลก มีการแพร่เชืื้อต่างๆมากมาบ
  • เช่น มีรายงาน lepto ในเมืองไทย
  • skin disease and flood crisis

    1. 1. SKIN DISEASEs and flooding crisis <ul><li>TANONGKIET TIENTHAVORN, MD </li></ul><ul><li>, the articles review </li></ul>
    2. 2. Flooding <ul><li>Floods are the most common natural disasters that affect developed and developing countries </li></ul><ul><li>people living in developing countries are more vulnerable to floods, and flood size and populations at risk are variable. </li></ul><ul><li>They cause many problems such as shortage of food and clean water, various health problems and general well being </li></ul><ul><li>According to the OFDA/CRED International Disaster Database , the tsunami of December 26 was undoubtedly the most lethal natural disaster that occurred in 2004 </li></ul><ul><li>In 2004, deaths were reported from flash, river, and urban/small-stream floods. The 0- to 9- and 20- to 29-year-old age groups had the most deaths at 14 each, of which 62% were men. In recent years, 50% or more of all flood-related deaths have occurred in automobiles. </li></ul><ul><li>Surg Clin N Am 86 (2006) 557–578 </li></ul>
    3. 3. <ul><li>Surg Clin N Am 86 (2006) 557–578 </li></ul>
    4. 4. <ul><li>Surg Clin N Am 86 (2006) 557–578 </li></ul>
    5. 6. Cause of flooding <ul><li>1. Topical cyclone : depression, typhoon </li></ul><ul><li>2. Intertropical convergence zone ( ร่องมรสุม ) </li></ul><ul><li>3. Strong monsoon </li></ul><ul><li>4. Prolonged rain storm ( พายุฟ้าคะนอง ) </li></ul><ul><li>5. Hide tide ( น้ำทะเลหนุนสูง ): 2o % higher than regular sea level with sun, moon and earth in line </li></ul><ul><li>6. earthquake, volcano </li></ul>
    6. 7. types of natural flood <ul><li>1. flash flood ( น้ำป่าไหลหลาก ) </li></ul><ul><li>2. drainage flood ( นำ้ท่วมขัง ) </li></ul><ul><li>3. River flood ( น้ำล้นตลิ่ง ) </li></ul><ul><li>4. Storm surges ( คลื่นพายุซัดฝั่ง ) </li></ul><ul><li>5. Tsunami </li></ul>
    7. 8. สถานการณ์น้ําท่วมในประเทศไทย พ . ศ . 2548 - 2552 <ul><li>ประเทศไทยอยู่เขตอิทธิพลของมรสุม 2 ฤดู ประมาณฤดูกาลละ 6 เดือน </li></ul><ul><li>1. มรสุมตะวันตกเฉียงใต้ (Southwest monsoon) ก่อให้เกิดอุทกภัยได้ เนื่องจากเมื่อพัดจาก มหาสมุทรอินเดียปะทะขอบฝั่งตะวันตกของภาคใต้ และเมื่อผ่านอ่าวไทยแล้วจะปะทะขอบฝั่งตะวันออกของ พฤษภาคม - ตลุาคม </li></ul><ul><li>2. มรสุมตะวันออกเฉียงเหนือ (Northeast monsoon) เริ่มตั้งแต่ปลายเดือนตุลาคมถึงสิ้นเดือน กุมภาพันธ์ ตั้งต้นพัดจากประเทศจีนและไซบีเรียผ่านทะเลจีนใต้ปะทะขอบฝั่งเวียดนาม ส่วนท่ีหลุดจากปลาย แหลมอินโดจีนจะพัดผ่านอ่าวไทยตอนใต้ปะทะขอบฝั่งตะวันออกของภาคใต้ หรือฝ่ังตะวันตกของอ่าวไทย </li></ul>
    8. 9. ข้อมูลย้อนหลัง 48 ปี ( พ . ศ .2493-2540) สรุปฤดูกาลเกิดอุทกภัยตามภาคต่างๆดังนี้
    10. 13. Risk assessment <ul><li>Floods can increase the transmission of the following commnicable diseases </li></ul><ul><li>1.Water-borne diseases, such as typhoid fever, cholera, leptospirosis and hepatitis A </li></ul><ul><li>2.Vector-borne diseases, such as malaria, dengue and dengue haemorrhagic fever, yellow fever,and West Nile Fever1. </li></ul><ul><li>3.Risk posed by corpse </li></ul>
    11. 14. Water-borne diseases <ul><li>major risk factor for outbreaks : contamination of drinking-water facilities </li></ul><ul><li>In Tajikistan in 1992, the flooding of sewage treatment plants led to the contamination of river water: no significant increase in incidence of diarrhoeal diseases was reported. </li></ul><ul><li>A typhoon in Truk District, Trust Territories of the Pacific in 1971 disrupted catchment water sources and forced people to use many different sources of groundwater that were heavily contaminated with pig faeces. As a result, there was an outbreak of muntidiasis, an intestinal protozoan. A cyclone and flooding in Mauritius in 1980 led to an outbreak of typhoid fever. </li></ul>
    12. 15. <ul><li>direct contact with polluted water : wound infection, dermatitis, conjunctivitis and ENT infection </li></ul><ul><li>epidermic prone: only leptospirosis spreaded by proliferation of rodents which shed large amounts of leptospires in the urine </li></ul><ul><li>out break of leptospirosis occured in Brazil (1983, 1988 and 1996), in Nicaragua (1995), Krasnodar region, Russian Federation (1997), Santa Fe, USA (1998) Orissa, India (1999) and Thailand (2000) </li></ul>
    13. 16. Vector borne disease <ul><li>expansion in the number and range of vector habitats </li></ul><ul><li>Standing water caused by heavy rainfall or overflow of rivers can act as breeding sites for mosquitoes </li></ul><ul><li>enhance the potential for exposure of the disaster-affected population and emergency workers to infections such as dengue, malaria and West Nile fever. </li></ul><ul><li>Flooding may initially flush out mosquito breeding, but it comes back when the waters recede </li></ul><ul><li>lag time is usually around 6-8 weeks before the onset of a malaria epidemic. </li></ul><ul><li>The risk of outbreaks is greatly increased by complicating factors: human behaviour (increased exposure to mosquitoes while sleeping outside, a temporary pause in disease control activities, overcrowding), habitat which promote mosquito breeding (landslide, deforestation, river damming, and rerouting). </li></ul>
    14. 17. <ul><li>Malaria epidemics in the wake of flooding are a well-known phenomenon in malaria-endemic areas world-wide. For instance, an earthquake and subsequent flooding in Costa Rica ’ s Atlantic region in 1991 and flooding on the Dominican Republic in 2004 led to malaria outbreaks. </li></ul><ul><li>Periodic flooding linked to El Nino-Southern Oscillation (ENSO ) is associated with malaria epidemics in the dry coastal region of northern Peru and with the resurgence of dengue in the past 10 years throughout the American continent. </li></ul><ul><li>West Nile Fever has resurged in Europe subsequent to heavy rains and flooding, with outbreaks in Romania in 1996-97, in the Czech Republic in 1997 and Italy in 1998. </li></ul>
    15. 18. risk posed by corpses <ul><li>Most agents do not survive long in the human body after death (exception of HIV - which can be up to 6 days) </li></ul><ul><li>source of acute infections is more likely to be the survivors. </li></ul><ul><li>Human remains only pose health risks in a few special cases requiring specific precautions deaths from cholera or haemorrhagic fevers. </li></ul><ul><li>workers who routinely handle corpses may have a risk of contracting tuberculosis, bloodborne viruses (such as Hepatitis B/C and HIV), and gastrointestinal infections (such as rotavirus diarrhoea, salmonellosis, E. coli, typhoid/paratyphoid fevers, hepatitis A, shigellosis and cholera ). </li></ul>
    16. 19. <ul><li>-Tuberculosis :bacillus is aerosolized (residual air in lungs exhaled, fluid from lungs spurted up through nose/ mouth during handling of the corpse). </li></ul><ul><li>-bloodborne viruses :direct contact with non-intact skin of blood or body fluid, injury from bone fragments and needles, or exposure to the mucous membranes from splashing of blood or body fluid. </li></ul><ul><li>-Gastrointestinal infections are more common as dead bodies commonly leak faeces: occurs via the faeco-oral route through direct contact with the body and soiled clothes or contaminated vehicles or equipment. Dead bodies contaminating the water supply may also cause gastrointestinal infections. </li></ul><ul><li>The public and emergency workers alike should be duly informed to avoid panic and inappropriate disposal of bodies, and to take adequate precautions in handling the dead (see prevention below). </li></ul>
    17. 20. Other health risks posed by flooding <ul><li>These include drowning and injuries or trauma . </li></ul><ul><li>Tetanus is not common after injury from flooding, and mass tetanus vaccination programs are not indicated </li></ul><ul><li>tetanus boosters may be indicated for previously vaccinated people who sustain open wounds or for other injured people depending on their tetanus immunization history </li></ul><ul><li>Passive vaccination with tetanus immune globulin (Hypertet) is useful in treating wounded people who have not been actively vaccinated and those whose wounds are highly contaminated, as well as those with tetanus </li></ul><ul><li>Hypothermia is a problem in children trapped in floodwaters for lengthy periods. There may also be an increased risk of respiratory tract infections due to exposure (loss of shelter, exposure to flood waters and rain) </li></ul><ul><li>Power cuts related to floods may disrupt water treatment and supply plants thereby increasing the risk of water-borne diseases as described above but may also affect proper functioning of health facilities, including cold chain. </li></ul>
    18. 28. associated skin diseases during the flood
    19. 29. Leptospirosis <ul><li>a worldwide zoonotic disease caused by spirochetes of the genus Leptospira. </li></ul><ul><li>In Thailand, leptospirosis corresponds with the rainy season, with an increase in cases beginning in August and decreasing in November; the peak number of cases occurs in October * </li></ul><ul><li>most infections occur in agricultural workers: rice producers </li></ul><ul><li>Infection in humans occurs through contact of skin or mucous membranes with water or moist soil contaminated with urine of infected animals </li></ul><ul><li>Breaks in skin in facilitate infection, but no previous study has quantified the correlation between skin wounds and leptospirosis </li></ul><ul><li>Heavy rainfall and flooding ; going without shoes; washing in streams; and occupations such as farming, working in sewers, mining, working with animals, and participating in military activities have all been implicated in human infection </li></ul><ul><li>Reported cases and morbidity rate (per 100,000 population of leptospiro- sis by year in Thailand, 1995–2000). Vol. 2002: Disease Notification Report, Leptosipirosis Control Office; 2000 . </li></ul>
    20. 30. Text Darkfield microscopy of leptospiral microscopic agglutination test.
    21. 31. Silver stain, liver, fatal human leptospirosis
    22. 32. <ul><li>Skin manifestation : in anicteric form  transient ( < 24 hrs ) , petechiae </li></ul><ul><li>Ecchynoctic, purpuric skin lesion may occur </li></ul><ul><li>Reported erythema nodosum </li></ul><ul><li>Also reported rare complication : Kawasaki syndrome </li></ul><ul><li>( ‪Emergency Dermatology ‬ By Ronni Wolf, Batya B. Davidovici, Jennifer L. Parish) </li></ul><ul><li>Clinical manifestion: </li></ul><ul><li>vary from asymptomatic to severe. </li></ul><ul><li>Some serovars tend to be associated more often with some syndromes (e.g., severe disease is often associated with serovar icterohaem- orrhagiae ) </li></ul>
    23. 33. <ul><li>a biphasic illness. </li></ul><ul><li>first phase , called the acute or septicemic phase </li></ul><ul><li>-begins abruptly and lasts approximately : nonspecific signs including fever, chills, headache and conjunctival suffusion. Myalgia, which typically affects the back, thighs or calves, is often severe. Occasionally, a transient skin rash occurs . </li></ul><ul><li>-Other symptoms may include weakness, photophobia, lymphadenopathy, abdominal pain, nausea, vomiting, a sore throat, cough </li></ul><ul><li>- symptoms last for approximately 4 to 9 days, then are typically followed by a 1 to 3 day period during which the temperature drops and the symptoms abate or disappear. </li></ul>
    24. 34. <ul><li>Second phase </li></ul><ul><li>second phase of leptospirosis, called the immune phase, is </li></ul><ul><li>characterized by the development of anti- Lepto- spira antibodies, and the excretion of the organisms in the urine </li></ul><ul><li>last up to 30 days or more, but does not develop in all patients. </li></ul><ul><li>Nonspecific symptoms seen in the first stage, such as fever and myalgia, recur but may be less severe than in the first stage of disease </li></ul><ul><li>Two forms of disease, icteric and anicteric, are seen. </li></ul>
    25. 35. <ul><li>The icteric form is more severe. It occurs in 5-10% of all patients, is often rapidly progressive, and may be associ ated with multiorgan failure. The most commonly involved organ systems are the liver, kidneys and central nervous system (CNS). </li></ul><ul><li>Acute renal failure occurs in 16-40% of cases. </li></ul><ul><li>pulmonary symptoms, with clinical signs ranging from cough, dyspnea, chest pain, and mild to severe hemoptysis, to adult respiratory distress syndrome. </li></ul><ul><li>Cardiac involvement can result in congestive heart failure, myo- carditis and pericarditis. </li></ul><ul><li>Hemorrhages may also be seen; epistaxis, petechiae, purpura and ecchymoses are the most common signs, but severe gastrointestinal bleeding, adrenal or subarachnoid hemorrhage, and pulmonary hemorrhages can occur. </li></ul><ul><li>Rare complications include stroke, rhabdomyolysis, thrombotic thrombocytopenic purpura, acute acalculous cholecystitis , erythema nodosum , aortic stenosis, Kawa- saki syndrome, reactive arthritis, epididymitis, nerve palsy, male hypogonadism, Guillain-Barre ‘s syndrome and cerebral arteritis. </li></ul>
    26. 36. <ul><li>Deaths can occur from kidney failure, cardiac involvement. pulmonary hemorrhage or other serious organ dysfunction. </li></ul><ul><li>Convalescence from the icteric form may take 1-2 months. </li></ul><ul><li>Although jaundice can persist for weeks, liver function returns to normal after recovery, and hepatic disease is rarely the cause of death. Most patients also recover kidney function. </li></ul><ul><li>Diagnostic method: </li></ul><ul><li>by culture, detection of antigens or nucleic acids, or serology. </li></ul><ul><li>Most human cases of leptospirosis are diagnosed by serology . The most commonly used serologic tests are the microscopic agglutination test (MAT, previously known as the agglutinationlysis test) or ELISAs. </li></ul><ul><li>MAT test is serogroup but not serovar specific, and can be complicated by cross-reactions. </li></ul>
    27. 37. <ul><li>Treatment </li></ul><ul><li>Antibiotics used in humans include doxycycline, ampicillin, amoxicillin, penicillin and erythromycin. Supportive treatment and management of complications such as renal failure, hepatic complications, hemorrhages and CNS disease may also be necessary. </li></ul>
    28. 40. Dengue Hemorrhagic Fever <ul><li>The first reported outbreaks of dengue hemorrhagic fever were observed in the Philippines in 1953 and 1956. </li></ul><ul><li>strongly associated with urban environments and breeding of A. aegypti vectors in domestic water containers </li></ul><ul><li>Humans are considered to be the main reservoir for the virus </li></ul><ul><li>Classic dengue begins abruptly after an incubation period of 5 to 6 days. </li></ul><ul><li>Fever may be of the “ saddleback ” type, in which remission of all symptoms occurs after 2 to 3 days, followed by a second phase of mild fever and less severe symptoms last ing 1 to 2 days. </li></ul><ul><li>Flushing of the face and conjunctival injection are common features. </li></ul>
    29. 41. <ul><li>An exanthem : tiny glistening vesicles on the soft palate may be seen within 12 hours of onset </li></ul><ul><li>More often, a morbilliform eruption begins on the third to fifth day on the inner surfaces of the upper arms, the lateral surface of the thorax, and in the lumbar area . The macular or scarlatiniform rash spreads to the face, neck, shoulders, and thorax ). Pruritus can occur if the hands and feet are involved. Cervical lymphadenopathy is frequently observed. Bradycardia may occur late in the illness and persist through convalescence. Recovery often requires 1 to 2 weeks and almost invariably is dominated by neurasthenia, mental depression, insomnia, and anorexia . </li></ul>
    30. 42. <ul><li>Hemorrhagic manifestations of dengue are seen predominantly in children. The symptoms are variable and include petechiae, purpura, oozing from venipuncture and injection sites, gingival bleeding, epistaxis, hemoptysis, hematemesis, melena, hematochezia, hematuria, uterine bleeding, and intracranial hemorrhage. </li></ul><ul><li>Shock can occur after several days of symptoms and is characterized by clinical and laboratory signs of hypovolemia. Hemorrhagic manifestations have been reported with all four serotypes. </li></ul><ul><li>Laboratory Findings: leukocytosis, atypical lymphocytes, and thrombocytopenia. Dengue virus inhibits marrow proliferation early in the course of disease but not in later stages. Although laboratory evidence of disseminated intravascular coagulation can be detected in severe cases of dengue hemorrhagic fever, morphologic evidence is usually found only in adolescents and adults. </li></ul><ul><li>Coagulation defects include prolongations of the partial thromboplastin time, prothrombin time, and thrombin time, as well as decreased factors II, V, VII, VIII, IX, and X. Disseminated intravascular coagulation is not central to the pathogenesis of dengue hemorrhagic fever, because treatment with heparin has not proved successful. </li></ul>
    31. 43. <ul><li>Treatment of dengue hemorrhagic fever is supportive. Live attenuated vaccines are currently being developed. The need for vaccination against all four known serotypes of dengue virus is depen- dent on the relative risk of developing hemorrhagic disease during subsequent infections with a different serotype. </li></ul><ul><li>study post flood in HADYAI in 2000, among 180 patients : DHF 29%, Leptospirosis 21%, scrub 1.1% * </li></ul>
    32. 45. MALARIA <ul><li>Plasmodium vivax and P. falciparum occur in about a 20/80 ratio in the north and a 50/50 ratio on the peninsula </li></ul><ul><li>Humans are the only important reservoir of human malaria. </li></ul><ul><li>Transmission: From the bite of an infective female Anopheles mosquito, or from an infectious blood transfusion. </li></ul><ul><li>Incubation Period – Usually 12 to 14 days; in some cases P. vivax may have a protracted incubation period of up to 10 month. </li></ul>
    33. 46. <ul><li>Symptoms : </li></ul><ul><li>Acute febrile illness characterized by chills, fever, headache, sweating, muscular ache and general malaise. </li></ul><ul><li>P. falciparum symptoms may include severe anemia jaundice, renal failure, shock, loss of orientation, convulsions and coma. Symptoms are most severe in P. falciparum malaria. </li></ul><ul><li>Thailand probably has the worst multiple-drug resistance problem in the world </li></ul><ul><li>Some surveys have found nearly 100% of the falciparum isolates are resistant to chloroquine </li></ul><ul><li>Resistance to Fansidar (sulfadoxine-pyrimethamine) is also widespread and resistance to quinine, proguanil, halofantrine, and mefloquine is common along the eastern and western borders. Primaquine-tolerant P. vivax has been reported from southern Thailand. </li></ul><ul><li>Case fatality rates among non-immune adults and children may approach 10%. Relapses are common with improperly treated P. vivax and may occur irregularly for years. </li></ul>
    34. 48. <ul><li>DIAGNOSIS: thick and thin film </li></ul><ul><li>Thin film: fixed with methanol 10 min </li></ul><ul><li>Thicnk film : not fixed </li></ul><ul><li>Then stain with Giemsa for 5 mins  light microscope </li></ul>
    35. 49. Fever with rash Emergency physicians in tsunami relief: a discussion of tsunami-related health conditions and necessary preparations Hong Kong 2005;12:252-260) <ul><li>As outbreaks of meningococcal meningitis occur from time to time, the possibility of meningococcaemia should be carefully considered for patients presenting with fever and rash. T </li></ul><ul><li>he likelihood of meningococcaemia increases if the patient has recently travelled from the&quot;meningitis belt&quot; in Africa (a region of savannah that extends from Ethiopia in East Africa to Senegal in West Africa).In the case of meningococcaemia, the rash is characteristically petechial, small and irregular with &quot;smudged&quot; appearance, and is often raised with pale greyish vesicular centres. It is commonly located on the extremities and the trunk. </li></ul>
    36. 50. <ul><li>meningococcaemia </li></ul>
    37. 51. <ul><li>In the case of typhoid fever , the rose spots will appear as slightly raised, non-tender, pink papules that blanch on pressure. They usually appear in crops of 10 to 20 lesions and are often located between the nipple area and the umbilicus on the anterior trunk. </li></ul><ul><li>In the case of leptospirosis , skin lesions usually appear on the trunk and take the form of macules, papules, urticaria and petechiae. </li></ul><ul><li>In the case of dengue , skin eruptions appear in 80% of patients during the remission of fever. They may appear as centrifugal macular, maculopapular, scarlatiniform or petechial eruptions. The eruptions may become confluent with small round islands of sparing, the so-called white islands in a sea of red. The rash characteristically starts on the dorsum of hands and feet and spreads to the arms, legs, and torso, while the face is relatively spared . The eruption seen in dengue lasts two hours to several days. </li></ul>
    38. 52. <ul><li>leptospirosis rash:Early in the disease, the skin is warm and flushed. Additional skin findings include a transient petechial eruption that can involve the palate. Later in severe disease, jaundice and purpura can develop. </li></ul>
    40. 54. <ul><li>Viral haemorrhagic fever is an acute illness due to infection by four viral families: Arenaviridae, Bunyaviridae, Filoviridae and Flaviviridae . They fall in the same group because of the common underlying pathophysiology. They all attack the vascular bed with resultant microvascular damage and changes in vascular permeability. They are usually transmitted by contact with the natural reservoirs, e.g. mosquitoes, ticks, or rodents. Flaviviridae can be found in the entire tropical zone, including India and Southeast Asia </li></ul><ul><li>For patients with septicaemic plague, they may present with purpuric skin lesions, together with gangrene of acral regions leading to &quot;Black Death&quot; </li></ul>
    41. 56. Immersion Foot syndrome (JOHN ADNOT, M.D.* AND CHARLES W. LEWIS, M.D., IMMERSION FOOT SYNDROMES, Military dermatology) <ul><li>Injuries to the feet from prolonged immersion in water or contact with dampness, in a range of envi- ronmental temperatures, may be collectively re- ferred to as “immersion foot syndromes.” </li></ul><ul><li>Cold weather (< 15 C): trench foot, immersion foot </li></ul><ul><li>Warmer weather (22-32 C) : Tropical immersion foot, Warm water immersion foot </li></ul>
    42. 57. Tropical Immersion Foot <ul><li>warmer environment in troops fight- ing in the Philippines during World War II </li></ul><ul><li>known as “paddy foot” </li></ul><ul><li>continuous or near-continuous immersion of the foot in water or mud of temperatures above 22°C for periods ranging from 2 to 10 days </li></ul><ul><li>Site : Dorsum of foot, ankles </li></ul><ul><li>When footgear is removed feet may initially appear pale, but they rapidly become intensely erythematous in a distribution sharply demarcated at shoe- or boot- top level </li></ul><ul><li>This erythema affects the dorsum of the foot but not the plantar surfaces — an important differentiating point from warmwaterimmersionfoot </li></ul>
    43. 58. <ul><li>Papules,vesicles, or both may appear, sometimes with a hemorrhagic component </li></ul><ul><li>Severely affected soldiers have tender unilateral or bilateral femoral adenopathy and a fever of 38°C to 39°C. </li></ul><ul><li>Histology: epidermal parakeratosis and acanthosis, dermal edema and telangiectasia, and a lymphocytic perivascular infiltrate with associated extravasation of RBC </li></ul>
    44. 59. <ul><li>changes are caused by loss of barrier function of the swollen stratum corneum, with secondary irritation or damage to the underlying tissues </li></ul><ul><li>Management : </li></ul><ul><li>bed rest, elevating and drying the feet, analgesics if necessary ,and antibiotics if indicated </li></ul><ul><li>fever and adenopathy resolve within 72 hours </li></ul><ul><li>erythema and edema subside in 5 to 7 days  fine branny desquamation resulting in normal-appearing feet </li></ul><ul><li>most severe cases usually resolve within 2 weeks without sequelae such as gangrene, persistent sensory changes, ororthopedic disability </li></ul>
    45. 60. <ul><li>Prevention </li></ul><ul><li>24-hour drying-out period alternated with each 48 hours of water exposure. </li></ul><ul><li>rapid-drying boots and socks may delay the onset of tropical immersion </li></ul><ul><li>silicone greases used as a barrier ointment have not proved effective. </li></ul>
    46. 62. Warm Water Immersion Foot <ul><li>“ moon-boot syndrome. ” </li></ul><ul><li>intermittent exposure to wet, warm conditions </li></ul><ul><li>1 to 3 days of exposure: note pain on weight bearing, tingling described as “walking on rope .” </li></ul><ul><li>When footwear is removed, the soles of the feet are thickened, severely wrinkled, and macerated </li></ul><ul><li>changes may extend to the sides of the foot, they do not affect the dorsum </li></ul>
    47. 63. <ul><li>Warm water immersion foot appears to develop faster at higher water temperatures </li></ul><ul><li>Histology: hyperhydration of the stratum corneum is the only finding (thickening of stratum corneum) </li></ul><ul><li>Treatment </li></ul><ul><li>bed rest anddrying the feet </li></ul><ul><li>Wrinkles and maceration resolve within 24 hours, but tenderness may last 2 to 3 days. </li></ul><ul><li>The patient is asymptomatic by the third day. Shortly thereafter, however , thick portions of the sole begin to fissure and peel, shedding completely within 1 to 2 weeks . During this peeling, the stratum corneum may be more susceptible to infection via the fissures </li></ul>
    48. 64. <ul><li>Prevention </li></ul><ul><li>drying the feet for 6 to 8 hours (overnight) of every 24 hours. </li></ul><ul><li>Silicone grease applied to the entire foot or to the soles aloneretards the development of warm water immersion foot. </li></ul><ul><li>Footgear with adequate drainage and composed of rapidly drying materials may also slow the development of this condition </li></ul>
    49. 68. Trench foot
    50. 69. Skin Diseases during Floods in Thailand J Med Assoc Thai Vol. 91 No. 4 2008 <ul><li>In September 2006, a major flood occurred in northern, northeastern and central parts of Thailand and included 47 provinces. Approximately 3.1 million Thai people were affected badly from this catastrophe </li></ul><ul><li>most common skin diseases during floods and identify the organism that causes skin maceration at web space(s) of toes : Hong kong foot </li></ul><ul><li>Infectious dermatoses were the second most common skin problems. Superficial fungal infection and bacterial skin infection were accounted for in most cases. </li></ul>
    51. 70. Ninety-six patients were evaluated by two dermatologists in the present study (58 females and 38 males) with 102 skin conditions. The ages of the patients ranged from 2 to 81 years, with a median age of 46 years. The study was done in both Singhaburi and Utaithani provinces during October 2006.
    52. 72. -Gram negative bacilli, Coryne- bacterium and Staphylococcus species were found in 14, 4 and 4 specimens respectively. - fungal culture showed two (out of 16) positive specimens. They were Trichosporon mucoides and non-spore forming hyaline fungi
    53. 73. <ul><li>In Summary, the authors concluded that eczema was the most common skin problem during the period of the flood. </li></ul><ul><li>Skin maceration at web space(s) of toes which were thought to be fungal infection were chronic irritant dermatitis with secondary bacterial colonization. </li></ul><ul><li>Excessive exposure to contaminated water, friction, high humidity and unhygienic environment might have increased the prevalence of bacterial colonization on eczematous macerated skin. </li></ul><ul><li>Microbiologic investiga- tion should be done in patients who complain of skin maceration at web space(s) of toe </li></ul><ul><li>medications which have the combination of anti- inflammatory, antibacterial and antifungal properties are the most suitable medications. </li></ul>
    54. 74. Occlusion, carbon dioxide, and fungal skin infections <ul><li>( Allen AM, King RD . Occlusion, carbon dioxide, and fungal skin infections. Lancet. 1978 Feb 18;1(8060):360-2. ) </li></ul><ul><li>Occlusion of the skin has the profound effect in producing, aggravating or treating various skin diseases </li></ul><ul><li>the prevalence and severity of inflammatory Trichphyton mentagrophytes (ringworm) infection among US troop in Vietnam were directly related to occlusion of the skin by wet clothing </li></ul><ul><li>CO2 tension on skin surface are usually well below those required to induce arthrospore formation in vitro </li></ul><ul><li>When skin is occluded with wet clothing, thin Teflonn sheet, plastic tape Or in intertriginous area  raise surface Co2 tension : same distribution of dermatophyte and candidal infection </li></ul><ul><li>Trichphyton mentagrophytes infection provide the best support for hypothesis because of their diversity </li></ul>
    55. 77. <ul><li>T. rubrum, T. concentrigum, E. floccosum and C. albican </li></ul><ul><li>Produce experimental human skin infection in rge preence of occlusion </li></ul><ul><li>T. rubrum, and T. mentagrophytes has grunular, sporulating morphological phase which is associated with more virulence </li></ul><ul><li>These postulated relations ( occlusion+ Co2 tension+ infectivity of dermatophyte) lead to prevention and control strategies </li></ul><ul><li>-removal occlusive merterial from the skin </li></ul><ul><li>Application of substances those interfere with action of CO2 </li></ul><ul><li>-development of clothing which would be non-occlusive when wet </li></ul>
    56. 78. Cercarial Dermatitis <ul><li>First describe in 1928 by Cort </li></ul><ul><li>Associated with all types of water such as rice fields, ponds, streams, canals, river and sea </li></ul><ul><li>Commonly found in bodies of water with many water plants, snails and domestic animals such as cows, ducks, and water buffalos </li></ul><ul><li>Caused by schistosome cercaria, a blood fluke </li></ul>
    57. 81. <ul><li>Types those be able to penetrate human skin and cause the rash : Trichobilharzia and Schistosoma spindale </li></ul><ul><li>Types of snail as intermediate hosts are Lymneaea and Indoplanorbis </li></ul><ul><li>Symptoms occur when cercariae penetrate and release histolytic enzyme  immediate lesion </li></ul><ul><li>Delayed type hypersensitivity to protiens from cercariae in epidermis  10-15 hrs </li></ul><ul><li>Erythematous papules  2 weeks faded with PIH </li></ul>
    58. 83. <ul><li>Cercariae could live only 1 day after emerging from snails </li></ul><ul><li>Eosinophilia 30 % ( normal in hoorworm) </li></ul><ul><li>Kullavanijaya P, Wongwaisayawan H. Outbreak of cercarial dermatitis in Thailand. Int J Dermatol. 1993 Feb;32(2):113-5 … was published due to a heavy and prolong flooding in Thailand in 1993 </li></ul>
    59. 84. Leech Class Hirudinea
    60. 86. <ul><li>Most leeches are active predators; however, some are the parasitic, bloodsucking forms. </li></ul><ul><li>Blood suckers have blade like jaws that they use to penetrate the skin of a host. </li></ul><ul><li>Blood is prevented from clotting because they secrete a powerful anticoagulant; anesthetics are also released: hirudin , antihistamine </li></ul><ul><li>A muscular pharynx subsequently pumps blood into the gut </li></ul>
    61. 87. <ul><li>Leeches are classified in the phylum Annelida (segmented worms). </li></ul><ul><li>Fresh-water leeches were used in bloodletting in Europe in the 18th and 19th centuries </li></ul><ul><li>several species of leeches were used, the medicinal leech, Hirudo medicinalis , was the most popular. </li></ul><ul><li>H. medicinalis may measure about 12cm when fully extended. The body tapers towards each extremity, where it is provided with a muscular disc or sucker. Within the anterior sucker is the mouth, bordered by three jaws </li></ul><ul><li>Leeches attach themselves to the skin using these powerful jaws, and feed until engorged, when they release their grip and drop to the ground </li></ul><ul><li>Their saliva possesses anticoagulant, fibrinolytic, vasodilator and probably also anaesthetic properties </li></ul>
    62. 88. (Rook’s Textbook of Dermatology , 8th edition ch. 38.55) <ul><li>Some of the substances introduced by leeches during feeding are antigenic, and if sensitization to these substances develops the reaction to the bite may be urticarial or bullous </li></ul><ul><li>Multiple pseudolymphomas have occurred following application of leeches to the legs </li></ul><ul><li>Unfortunately, the use of leeches carries the risk of introducing wound infection, most frequently with Aeromonas hydrophila , a Gram-negative rod, but occasionally other organisms are involved </li></ul><ul><li>Aeromonas is part of the normal gut flora of the leech, where it is thought to be essential to aid digestion of a blood meal, as proteolytic enzymes are virtually absent from the leech gut. Many plastic surgeons who use leeches employ antibiotic prophylaxis to protect against wound infection. </li></ul>
    63. 91. <ul><li>International reported articles </li></ul>
    64. 92. Leishmaniasis Maryam Baqir et al./Asian Pacific Journal of Tropical Biomedicine (2012)76-79 <ul><li>caused by Leishmania spp transmitted by the sand fly </li></ul><ul><li>lead to deep, disfiguring sores at the site of the bite, which are more likely on the exposed parts of the body. </li></ul><ul><li>Systemic or visceral leishmaniasis which is rarer in Pakistan affects the internal body organs, particularly the spleen and liver </li></ul><ul><li>endemic in Pakistan and Afghanistan, and its incidence has been rising </li></ul><ul><li>Outbreaks have been seen in refugee settlements along the north-western border of Pakistan during the Afghani crisis </li></ul><ul><li>Poor sanitation and malnutrition also help spread the disease by providing a habitat for the sand fly and lowering the general health of the population, making them more susceptible. </li></ul><ul><li>Leishmaniasis is hence common in overcrowded, poverty stricken </li></ul>
    65. 93. <ul><li>Floods can potentially increase the transmission of leishmaniasis. Bihar, a region in India endemic to floods, has seen a surge in the disease since 1977. </li></ul><ul><li>As the relief efforts in flood-hit Pakistan intensify, officials should brace themselves for an outbreak of leishmaniasis </li></ul><ul><li>Residual insecticide spray and impregnated bed nets are effective. Even more important, however, is improving environmental and sanitation living conditions. </li></ul>
    66. 95. Wound infections and sources of infection <ul><li>Whenever skin integrity is breached, the normal flora colonizing the skin can become source of infection. These include staphylococcal and streptococcal species, with aggressive infections typically caused by Staphylococcus aureus and Streptococcus pyogenes (Group A streptococcus) . But in one study, gram-positive cocci were uncommon causes of wound infections in tsunami survivors. </li></ul>
    67. 96. Fresh and seawater pathogens <ul><li>Bacteria classically associated with freshwater exposure are gram-negative bacilli such as Aeromonas , Plesiomonas and Pseudomonas . Atypical mycobacteria may also be seen in wounds with freshwater exposure. Mycobacterium marinum or occasionally, other rapid growers , may form granulomatous infections with a sporotrichoid pattern. </li></ul><ul><li>In Thailand , the most common organisms isolated from wound infection were Aeromonas species </li></ul>
    68. 97. <ul><li>Most isolates were susceptible to aminoglycoside, third- and fourth-generation cephalosporin, quinolone, and imipe nem but were resistant to amoxicillin- clavulanate and first-generation cephalosporin </li></ul><ul><li>85% of isolates of gram-negative bacilli were sensitive to aminoglycosides, third- and fourth-generation cephalosporins, quinolones, and imipenem. </li></ul><ul><li>Most isolates of Aeromonas species, P. aeruginosa , and Proteus species were resistant to first- generation cephalosporins and amoxicillin-clavulanate.3 </li></ul>
    69. 98. <ul><li>Vibrio vulnificus can cause wound infections in patients whose wound are exposed to seawater </li></ul><ul><li>Other Vibrio species seen infrequently in connection with marine exposure are V. alginolyticus and V. parahaemolyticus . </li></ul><ul><li>Vibrio infections should respond to quinolone, or ceftazidime plus doxycycline. It has been reported that Vibrio sp had 1.6% of total wound infections cultured </li></ul>
    70. 99. Soil pathogens <ul><li>Anaerobes bacteria are commonly encountered in wound infection contaminated by soil. Metronidazole and clindamycin possess the added virtue of excellence oral bio-availability with activity against anaerobic bacteria. </li></ul><ul><li>Skin abrasions even superficial cuts, can provide potential portal of entry for Clostridium tetani , the gram-positive rod. TIG 500 to 3000 IU, initiating active immunization with tetanus vaccine, and supportive care. Oral metronidazole therapy may be superior to intramuscular penicillin; other antibiotics with activity against C. tetani include cephalosporins, macrolides and imipenem </li></ul>
    71. 100. <ul><li>Burkholderia pseudomallei : soil-associated organism endemic in southeast Asia. </li></ul><ul><li>Cutaneous injuries resulting from inoculation of the pathogen can lead to cutaneous meliodosis as well as septicemic meliodosis. Other co- isolated organisms included Pseudomonas aeruginosa and Klebsiella sp. </li></ul><ul><li>Mucormycosis has previously been reported in wound infection from trauma and natural disasters. The report of posttraumatic cutaneous mucormycosis in Australian traveler who was injured in Sri Lanka during the tsunami is consistent with likely soil contamination of his wounds. Diagnosis was made on histopathology showing tissue invasion, and fungal culture subsequently grew Aphophysomyces elegans . Treatment in his case consisted of surgical debridement, amphoterincin B (liposomal) and adjunctive hyperbaric oxygen therapy. </li></ul>
    72. 101. Sewage and faecal pathogens <ul><li>gram-negative coliforms, such as Escherichia col i and Proteus and Klebsiella species. Third-generation cephalosporin or quinolone may be used empirically until susceptibility testing is available. In one report, Escherichia coli was 18.1% of all wound infection cultured </li></ul><ul><li>Rat bite , although uncommon, may pose a problem in some area. These injuries are a risk for rare organisms such as Spirillum minus and Streptobacillus moniliformis , which has been described to cause fulminant illness even in healthy persons. Antibiotic treatment includes amoxycilin/clavulanate or doxycycline. </li></ul>
    73. 102. <ul><li>For patients whose traumatic wounds are deep, heavily contaminated, located on the lower body, and/or have a foul-smelling discharge, the possibility of mixed infection with aerobic gram-positive cocci, aerobic gram negative bacilli from fecal bacteria, and anaerobes should be considered. </li></ul>
    74. 103. <ul><li>Noe R, Cohen AL, Lederman E, Gould LH, Alsdurf H, Vranken P, Ratard R, Morgan J, Norton SA, Mott J . </li></ul><ul><li>Skin disorders among construction workers following Hurricane Katrina and Hurricane Rita: an outbreak investigation in New Orleans, Louisiana. </li></ul><ul><li>Arch Dermatol. 2007 Nov;143(11):1393-8. </li></ul>
    77. 107. Fiberglass Dermatitis <ul><li>diagnosis was made among those workers who manifested poorly demarcated diffuse erythema with urticarial, sandpa- pery, or morbilliform texture, predominantly on the volar aspects of the forearms, with intense pruritus that began within 4 hours of exposure of handling fiberglass </li></ul>
    78. 109. Brachioradial Photodermatitis ( Walcyk PJ, Elpern DJ. Brachioradial pruritus: a tropical dermopathy. Br J Dermatol. 1986;115(2):177-180 ) <ul><li>Brachioradial pruritus was first reporteded by Waisman 1968 </li></ul><ul><li>who termed it solar pruritus of the elbows, describing its occurrence in patients in Florida who showed a localized itch of the skin on the dorso-lateral aspect of the arm </li></ul><ul><li>brachioradial pruritus is a photo- neurological disorder caused by sun-induced damage to nerve endings that results in pruritus and altered sensation in susceptible individuals </li></ul>
    79. 110. <ul><li>On the other hand, Hail in South Africa, suggested that brachioradial pruritus may be caused by nerve injury to the cervical spine or by nerve compression at other locations because 5 out of his 14 patients had a history of neck trauma or arthritis </li></ul>
    80. 112. West Nile virus <ul><li>West Nile virus causes sporadic cases and outbreaks of human and equine disease in Europe (western Mediterranean and southern Russia in 1962-64, Belarus and Ukraine in the 1970s and 1980s, Romania in 1996-97, Czechland in 1997, and Italy in 1998) </li></ul><ul><li>Environmental factors, including human activities, that enhance population densities of vector mosquitoes (heavy rains followed by floods , irrigation, higher than usual temperature, or formation of ecologic niches that enable mass breeding of mosquitoes) could increase the incidence of West Nile fever. </li></ul>
    81. 113. <ul><li>West Nile virus is a member of the Japanese encephalitis antigenic complex of the genus Flavivirus, family Flaviviridae </li></ul><ul><li>transmissible by mosquitoes and many of them can cause febrile, sometimes fatal, illnesses in humans </li></ul><ul><li>first isolated from the blood of a febrile woman in the West Nile district of Uganda in 1937 (5) and was subsequently isolated from patients, birds, and mosquitoes in Egypt in the early 1950s (6-7). The virus was soon recognized as the most widespread of the flaviviruses, with geographic distribution in- cluding Africa and Eurasia </li></ul>
    82. 114. Ann Intern Med. 2002;137:173-179.
    83. 116. Reported : MP rash
    84. 118. Ann Intern Med. 2002;137:173-179.
    85. 119. Buruli ulcer Mycobacterium ulcerans Disease <ul><li>M. ulcerans infection has occurred only after significant environmental disturbance </li></ul><ul><li>In the original paper describing the disease, published in 1948, the first patients from the Bairnsdale district in Australia presented in 1939 </li></ul><ul><li>In December 1935, there had been the worst floods on record in the district, when all road and rail links had been cut and much property destroyed </li></ul><ul><li>In Uganda, Barker examined cases of M. ulcerans in the Busoga district on the east side of the Victoria Nile, north of Lake Victoria </li></ul><ul><li>Barker postulated that the outbreak was related to unprecedented flooding of the lakes of Uganda between 1962 and 1964 as a result of heavy rainfall </li></ul>
    86. 120. <ul><li>it has been hypothesized63 that M ulcerans resides in soil as a contaminant or on foliage as a commensal and is transmitted via injury from the environment, transmission from animals to humans has not been demonstrated </li></ul><ul><li>lesions occur on extrem ties. They probably begin as injuries or insect bites that do not heal but instead become indurated, with eventual necrosis and spreading ulceration </li></ul><ul><li>single, firm, sometimes itchy, papule that becomes more indurated and fluctuant over several weeks and then breaks down into a spreading, punched-out ulceration with classically undermined edges </li></ul>
    87. 123. <ul><li>Diagnosis </li></ul><ul><li>The burulin skin test is not useful as a diagnostic tool because early active cases are generally burulin-negative </li></ul><ul><li>However, the skin is generally positive in the healing stages and following recovery from the active disease </li></ul><ul><li>Histo : coagulation necrosis, septate panniculitis, without caseation necrosis, but with granulation tissue and giant cells towards the periphery. Smears and bi-opsy material from the necrotic areas almost always reveal acid-fast bacilli </li></ul>
    88. 125. <ul><li>Laboratory Features . Cultures on Lowenstein- Jensen medium produce nonpigmented colonies at 32°C to 33°C after 6 to 12 weeks, a relatively long incubation time </li></ul><ul><li>Prognossis: untreated, ulcerations tend to progress over months to years to involve large areas (Figure 16- 10), sometimes involving an entire extremity, be- fore healing with residual scarring, deformity, and lymphedema </li></ul>
    89. 126. <ul><li>Treatment </li></ul><ul><li>Small lesions respond to simple surgical curettage and heal by granulation </li></ul><ul><li>heat application to 40°C to the involved area has been helpful in some cases </li></ul><ul><li>mainstay of therapy is surgical excision of the entire area with primary closure or skin grafting </li></ul><ul><li>Drug therapy consisting of dapsone and streptomycin with or without ethambutol </li></ul><ul><li>some response has been seen with trimethoprim-sulfamethoxazole fol- lowed by rifampin and minocycline. </li></ul>
    90. 127. BALAMUTHIA MANDRILLARIS <ul><li>Balamuthia mandrillaris was first isolated from the brain of a mandrill baboon at the San Diego Wild Animal Park </li></ul><ul><li>free-living amebae, at least 3 genera, Naegleria, Acanthamoeba, and Balamuthia, are known to cause disease in humans and animals </li></ul><ul><li>Only 1 species of Naegleria, N fowleri, causes an acute, fulminant, rapidly fatal infection of the central nervous system (CNS) </li></ul>
    91. 128. <ul><li>primary amebic meningoencephalitis, that predominantly affects healthy young persons exposed to freshwater lakes, ponds, and heated swimming pools </li></ul><ul><li>Amebas splashed or inhaled onto the olfactory epithelium migrate up the olfactory nerve to the brain and spread via the subarachnoid space. </li></ul><ul><li>Diagnosis relies on identifying trophozoites by microscopic examination of fresh cerebrospinal fluid specimens or histologic sections of CNS tissue, and on culturing, if necessary. </li></ul>
    92. 129. <ul><li>Clinical manifestations </li></ul><ul><li>Neurologic signs : hemiparesis, seizures, and aphasia; altered mental status; head- ache; stiff neck; and cranial nerve palsies, mainly affecting the third and sixth cranial nerves. Symptoms closely mimic a bacterial or viral encephalitis, leptomeningitis, or tuberculous meningitis. </li></ul><ul><li>Neuroimaging studies usually reveal multifocal, typically hypodense, contrast-enhancing lesions, often in a serpiginous pattern Cerebrospinal findings are generally those of mono- nuclear pleocytosis with an elevated protein and normal to low glucose.4,11 Gastrointestinal complaints, such as vomiting, ab- dominal pain, and diarrhea, have also been reported </li></ul>
    93. 130. <ul><li>many of these patients initially had persistent amebic granulomatous lesions in the nasal region. Other reported sites include the oral cavity, gluteal area, and extremities </li></ul><ul><li>Trophozoites measure 15 to 50 m and are characterized by a round nucleus with a large spherical, densely staining nucleolus and abundant cytoplasm containing empty vacuole </li></ul><ul><li>nucleus might have more than 1 nucleolus, a feature that distinguishes from Acanthamoeba in tissue sections </li></ul><ul><li>Speciation by indirect immunofluorescence is available for definitive diagnosis </li></ul><ul><li>B mandrillaris grows well at 35 to 37°C on monkey kidney cells or human lung fibroblasts, as well as in a complex chemical medium containing fetal bovine serum </li></ul>
    94. 131. <ul><li>Treatment </li></ul><ul><li>no known effective therapy for B mandrillaris infection </li></ul><ul><li>The most effective antimicrobial agents tested in vitro are pentamidine and propamidine isethionates, polymyxin B, and gramicidin </li></ul><ul><li>pentamidine is the best choice among anti- microbials tested thus far for amebic meningoencephalitis and cutaneous infection caused by B mandrillaris </li></ul><ul><li>More recently, phenothiazines were discovered to be effective against B mandrillaris; however, this agent is toxic to mammalian cells at high concentrations </li></ul>
    95. 132. <ul><li>B mandrillaris, a newly recognized pathogenic ameba, should be included in the differ- ential diagnosis of a granulomatous skin lesion, particularly in the nasal region, in both immunocompetent and immunocom promised patients. </li></ul><ul><li>Earlier diagnosis in our patient might not have altered the outcome, but it would have provided an op portunity to attempt earlier treatment with pentamidine </li></ul>
    96. 139. Pentamidine <ul><li>Pentamidine isethionate was approved by the FDA on June 15, 1989, for use in the treatment of Pneumocystis jiroveci (formerly Pneumocystis carinii) pneumonia (PCP), an opportunistic infection in people with HIV/AIDS. Pentamidine is generally used only when patients with PCP cannot tolerate the first-line treatment, sulfamethoxazole-trimethoprim </li></ul>
    97. 140. Schistosomiasis <ul><li>Schistosomiasis has been endemic in Egypt at least since the time of the ancient Pharaohs, as indicated by the presence of calcified ova in the Egyptian mummies </li></ul><ul><li>So called bilharzia, is now a widespread endemic dis- ease currently found in 75 countries </li></ul><ul><li>schistosomiasis is a disease affecting agricultural communities, particularly those dependent upon irrigation to support their agriculture </li></ul><ul><li>especially in areas where the water contains numerous freshwater snails , which may carry the parasite </li></ul>
    98. 141. <ul><li>Schistosoma mansoni and Schistosoma intercalatum cause intestinal schistosomiasis </li></ul><ul><li>Schistosoma haematobium causes urinary schistosomiasis </li></ul><ul><li>Schistosoma japonicum and Schistosoma mekongi cause Asian intestinal schistosomiasis </li></ul><ul><li>Avian schistosomiasis species cause swimmer's itch and clam digger itch </li></ul>
    99. 142. <ul><li>schistosomiasis is a chronic disease. Many infections are subclinically symptomatic, with mild anemia and malnutrition being common in endemic areas. Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum . Manifestations include: </li></ul><ul><li>Abdominal pain,Cough,Diarrhea , Eosinophilia — extremely high eosinophil granulocyte (white blood cell) count., Fever, Fatigue, Hepatosplenomegaly </li></ul><ul><li>Genital sores — lesions that increase vulnerability to HIV infection. Lesions caused by schistosomiasis may continue to be a problem after control of the schistosomiasis infection itself. Early treatment, especially of children, which is relatively inexpensive, prevents formation of the sores. </li></ul><ul><li>Skin symptoms: At the start of infection, mild itching and a papular dermatitis of the feet and other parts after swimming in polluted streams containing cercariae </li></ul><ul><li>Occasionally central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid paraplegia. </li></ul>
    100. 143. <ul><li>Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include: </li></ul><ul><li>Colonic polyposis with bloody diarrhea ( Schistosoma mansoni mostly); </li></ul><ul><li>Portal hypertension with hematemesis and splenomegaly ( S. mansoni , S. japonicum ); </li></ul><ul><li>Cystitis and ureteritis ( S. haematobium ) with hematuria, which can progress to bladder cancer; </li></ul><ul><li>Pulmonary hypertension ( S. mansoni , S. japonicum , more rarely S. haematobium ); </li></ul><ul><li>Glomerulonephritis; and central nervous system lesions. </li></ul><ul><li>Bladder cancer diagnosis and mortality are generally elevated in affected areas. </li></ul>
    101. 145. <ul><li>Microscopic identification of eggs in stool or urine is the most practical method for diagnosis </li></ul><ul><li>Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected. Eggs can be present in the stool in infections with all Schistosoma species </li></ul><ul><li>repeated examinations and/or concentration procedures (such as the formalin-ethyl acetate technique) </li></ul><ul><li>for field surveys and investigational purposes, the egg output can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or the Ritchie technique. </li></ul><ul><li>Eggs can be found in the urine in infections with S. japonicum and with S. intercalatum (recommended time for collection: between noon and 3 PM). Detection will be enhanced by centrifugation and examination of the sediment. Quantification is possible by using filtration through a nucleopore membrane of a standard volume of urine followed by egg counts on the membrane. </li></ul><ul><li>Investigation of S. haematobium should also include a pelvic x-ray as bladder wall calcificaition is highly characteristic of chronic infection </li></ul>
    102. 146. <ul><li>Tissue biopsy ( rectal biopsy for all species and biopsy of the bladder for S. haematobium ) may demonstrate eggs when stool or urine examinations are negative </li></ul><ul><li>The eggs of S. haematobium are ellipsoidal with a terminal spine, S. mansoni eggs are also ellipsoidal but with a lateral spine, S. japonicum eggs are spheroidal with a small knob </li></ul>
    103. 148. Eggs of S. haematobium in wet mounts of urine concentrates, showing the characteristic terminal spine
    104. 152. <ul><li>Treatment </li></ul><ul><li>All individuals with schistosomiasis should receive treatment even if they are symptom-free. </li></ul><ul><li>Praziquantel 40mg/kg/d for 3 days gives 95% cure rate with no relapses Treatment before significant damage or severe complications usually produces good results </li></ul><ul><li>Severe Katayama fever* may require treatment with systemic corticosteroids to manage the acute hypersensitivity reaction. Praziquantel is less effective for Katayama fever and can worsen symptoms due to antigen release. It may be useful to either delay treatment with praziquantel therapy or co-administer with corticosteroids and give a second course of praziquantel after 3-6 months </li></ul><ul><li>*(Katayama fever   fever associated with severe schistosomal infections, accompanied by hepatosplenomegaly and by eosinophilia) </li></ul>
    105. 153. <ul><li>Prevention of schistosomiasis </li></ul><ul><li>There is no vaccine currently available for schistosomiasis. </li></ul><ul><li>Travellers should avoid exposure to freshwater in endemic areas – avoid bathing in ponds and lakes. </li></ul><ul><li>Bath water should be heated for 5 minutes at 65°C. Water held in a storage tank for at least 48 hours should be safe for showering. </li></ul><ul><li>Drink bottled water, or water that has been boiled for at least one minute. </li></ul>
    106. 158. RELATIONSHIP BETWEEN SCHISTOSOMIASIS AND BLADDER CANCER <ul><li>association of bladder cancer with schistosomiasis seems to be related to the endemicity of the parasite </li></ul><ul><li>The consensus of available information strongly implicates an association between S. haematobium infection and the induction of bladder cancer </li></ul><ul><li>It was estimated that of 11,626 cancer cases of all types recorded at the Cairo Cancer Institute from 1970 to 1974, 27.6% were bladder cancer cases associated with schistosomiasis, and that of 2,500 new cancer patients at the Cairo Cancer Institute every year, 27% had cancer of the bladder associated with schistosomiasis </li></ul>
    107. 159. <ul><li>initiation, activated macrophages induced at the sites of inflammation are implicated in the generation of carcinogenic NNA and reactive oxygen radicals that lead to DNA damage and subsequently to events such as mutations </li></ul><ul><li>increased levels of the enzymes responsible for the activation of carcinogenic N-nitroso compounds, aromatic amines, and polycyclic aro- matic hydrocarbons have been found </li></ul><ul><li>Physical damage to the urothelium and mucosa caused by the activities of the worms leads to restorative hyperplasia  promoting stimulus to propagate cells in which the sequence of genotoxic (DNA- damaging) events leading to the initiation of the premalignant change is complete </li></ul>
    108. 160. <ul><li>recognizing this sequence of events, it is fairly clear how prevention could be achieved </li></ul><ul><li>Elimination of the parasite through education, improved hygiene, and improved conditions for living and working are the obvious solutions, but the level of investment required for this is well beyond the resources of most of the countries where infection is endemic. A possible interim solution that requires less extensive financial resources is chemotherapy with effective agents such as prazi- quantel </li></ul>
    109. 161. <ul><li>Prevention and control </li></ul>
    110. 162. Short term measure Chlorination of water <ul><li>safe drinking water is the most important preventive measure to be implemented following flooding, in order to reduce the risk of outbreaks of water-borne diseases. </li></ul><ul><li>Free chlorine is the most widely and easily used, and the most affordable of the drinking </li></ul><ul><li>water disinfectants. : effective against nearly all waterborne pathogens ( except Cryptosporidium parvum oocysts and Mycobacteria species ). </li></ul><ul><li>doses of a few mg/litre and contact times of about 30 minutes, free chlorine generally inactivates >99.99% of enteric bacteria and viruses. </li></ul><ul><li>household water treatment, the most practical forms of free chlorine are liquid sodium hypochlorite, solid calcium hypochlorite and bleaching powder (chloride of lime; a mixture of calcium hydroxide, calcium chloride and calcium hypochlorite). </li></ul><ul><li>. After 30 minutes, the residual concentration of active chlorine in the water should be between 0.2–0.5 mg/l, which can be determined using a special test kit. </li></ul>
    111. 163. Vaccination against hepatitis A: <ul><li>The use of hepatitis A vaccines for mass immunization is not recommended. </li></ul><ul><li>Vaccination of high-risk groups, such as persons involved in the management of drinking water, waste water or sewage might be considered. </li></ul><ul><li>In case of an outbreak of hepatitis A consider immunization of contacts. The use ofimmunoglobulins is not recommended. </li></ul><ul><li>Diagnosis of acute hepatitis A is confirmed by anti-HAV IgM antibodies. </li></ul>
    112. 164. Malaria prevention: <ul><li>flooding does not necessarily lead to an immediate major increase in mosquito numbers , and there may still be time to implement preventive measures such as indoor residual spraying, or the retreatment/distribution of ITNs in areas where their use is well-known. This will also have an effect on other mosquito-borne diseases. </li></ul><ul><li>Early detection: it is important to track weekly case numbers and provide laboratory-based diagnosis (perhaps only for a % of fever cases to track the slide/test positivity rate), to pick up the early stages of a malaria epidemic </li></ul><ul><li>Free medical care: with artemisinin-based combination therapy should be provided when a falciparum malaria epidemic is confirmed , and an active search for fever cases may be necessary to reduce mortality in remote areas with reduced access to health care services. </li></ul>
    113. 165. Health Education <ul><li>Promote good hygienic practice.. </li></ul><ul><li>• Ensure safe food preparation techniques. </li></ul><ul><li>• Ensure boiling or chlorination of water. </li></ul><ul><li>• Vital importance of early diagnosis and treatment for malaria (within 24 hours of onset of fever) </li></ul>
    114. 166. Handling corpses <ul><li>Burial is preferable to cremation in mass causalities and where identification of victims is not possible. </li></ul><ul><li>false belief that they represent an epidemic hazard if not buried or burned immediately. </li></ul><ul><li>Bodies should not be disposed of unceremoniously in mass graves and this does not constitute a public health a public health measure, violates important social norms and can waste scarce resources. </li></ul><ul><li>Families should have the opportunity to conduct culturally appropriate funerals and burials according to social custom. </li></ul><ul><li>Where customs vary, separate areas should be available for each social group to exercise their own traditions with dignity. </li></ul><ul><li>Where existing facilities such as graveyards or crematoria are inadequate, alternative locations or facilities should be provided. </li></ul><ul><li>The affected community should also have access to materials to meet the needs for culturally acceptable funeral pyres and other funeral rites. </li></ul>
    115. 167. For workers that routinely handle corpses <ul><li>Graveyards should be at least 30m from groundwater sources used for drinking water </li></ul><ul><li>The bottom of any grave must be at least 1.5m above the water table with a 0.7m unsaturated zone </li></ul><ul><li>Surface water from graveyards must not enter inhabited areas </li></ul><ul><li>Ensure universal precautions for blood and body fluids </li></ul><ul><li>Ensure use and correct disposal of gloves (no re-use) </li></ul><ul><li>Ensure use of body bags </li></ul><ul><li>Ensure hand-washing with soap after handling bodies and before eating </li></ul><ul><li>Ensure disinfection of vehicles and equipment </li></ul><ul><li>Bodies do not need to be disinfected before disposal (except in case of cholera) • </li></ul><ul><li>Vaccinate workers against hepatitis B </li></ul>
    116. 168. Long term measures <ul><li>Legislative/administrative issues: </li></ul><ul><li>Create Disaster-Preparedness Programmes and Early Warning Systems . </li></ul><ul><li>Improve surveillance on a local, national, international and global level. </li></ul><ul><li>Promote tap-water quality regulation and monitoring. </li></ul><ul><li>Enforce high standards of hygiene. </li></ul>
    117. 169. <ul><li>Technical issues: </li></ul><ul><li>Improve water treatment and sanitation. </li></ul><ul><li>Keep infectious disease control programmes active and efficient </li></ul>