parasitology

factful

1. AMOEBIASIS Jagadish Prasad Mishra Roll no-16 6 th semester

2. Learning Objectives Definition Epidemiology Epidemiological determinants Clinical presentation Diagnosis and further investigation Prevention and treatment

3. Amoebiasis Amoebiasis is an infection with the intestinal protozoa Entamoeba histolytica . About 90% of infections are asymptomatic Remaining 10% produce a spectrum of clinical syndromes

4. Amoebiasis

5. Epidemiology World Worldwide in distribution 3 rd most common parasitic death India, China, Mexico, Africa, South America 2-60% prevalence(based on ELISA and PCR studies from stool samples) 100,000 deaths/yr 500 million infections 50 million cases/yr Data-2007

6. Epidemiology India 15% prevalence (3.6-47.4%) Variation according to sanitation level and clinical diagnostic criteria

7. Epidemiological determinants Agent Virulence factor Host factor Environmental factor Mode of transmission Incubation period

8. Agents Entamoeba histolytica Trophozoites 18-40 μ m in D Cytoplasm – # outer clear ectoplasm # inner granular endoplasm # food vacuoles with RBCs, leukocytes & tissue debris Motile by pseudopodia extensions Nucleus with central karyosome , surrounded by delicate membrane lined with chromatin granules Non infectious

9. Agents Entamoeba histolytica Precyst Intermediate form Oval with blunt pseudopodia No food vacuoles Cysts Spherical, 10 - 15 μ m in D Uninucleate , later bi- or quadri - nucleate Thick chitinous wall Glycogen mass – not in quadrinucleate Chromidial or Chromatoid bars Infectious

10. Invasive x Noninvasive strains A zymodem comprises those Entamoeba strains that share the same electrophoretic pattern and mobility for certain enzymes like – malic enzyme, phosphoglucomutase , hexokinase , glucose phosphate isomerase , aldolase etc 24 different zymodems – 21 of human strains 7 pathogenic zymodems The invasive and non invasive strains may appear identical may represent two distinct species Invasive strain – E.histolytica (give rise to fecal cysts) Non invasive strains reclassified as E.dispar .

11. Agent factor Source of infection is a case or carrier -1∙5 X 10 7 cysts per day Reservoir is only human – several years Resistant to chlorine in normal conc. Readily killed by freezing or heating(55°C) Period of communicability- very long

12. Host factor People in developing countries that have poor sanitary conditions Immigrants from developing countries Travellers to developing countries People who live in institutions that have poor sanitary conditions HIV-positive patients Men who have sex with men All age groups affected No gender or racial differences Severe if children, old, pregnant, PEM Develops antiamoebic antibodies in tissue invasion

13. Host factor Liver abscesses due to amoebiasis are 10 times more frequent in adults than in children Amoebic liver abscess 7 times more in men than women Predominance among men aged 18-50 years Increased among postmenopausal women Hormonal effect and alcohol can be risk factors

14. Environment factor Low socio-economic status Poor sanitation, sewage contamination Night soil for agriculture Seasonal variation(more in rainy season)

15. Faeco - oral route Contaminated water and food D irect hand to mouth(cysts under finger nails) Vegetables irrigated with sewage polluted water Agency of flies, cockroaches, rats, etc. Sexual contact via oral-rectal route Modes of transmission

16. Incubation period 2- 4 weeks

17. Life cycle of E. histolytica Source:- medical-dictionary.com

18. Life Cycle of E. histolytica

19. Clinical presentation Most common type of amoebic infection is asymptomatic cyst passage Intestinal amoebiasis – abdominal cramps with mild diarrhea to colitis and dysentery Extra-intestinal amoebiasis – Amoebic liver abscess, rarely lungs, skin, genitalia and CNS are affected Amoeboma – inflammatory and edematous reaction around trophozoites

20. Clinical presentation Asymptomatic carriers 90% without symptoms does not damage lumen

21. How the Amoebiasis Manifests Most cases of amoebiasis have very mild symptoms or none. Wide spectrum, from asymptomatic infection to luminal amoebiasis and amoebic colitis Clinical symptoms are usually vague More severe infection may cause fever, profuse diarrhoea, vomiting, abdominal pain, jaundice, anorexia, and weight loss. Invasive intestinal amoebiasis (dysentery, colitis, appendicitis, toxic mega colon, amoebomas )

22. Clinical presentation Amoebic colitis- Abdominal cramp to severe pain Fever, vomiting, anorexia Mucus in stool, dysentery Flask shaped ulcer in intestine

23. <0.5% S everely ill with high fever Intestinal bleeding , perforation P aralytic illus CFR-40% Uncommonly, a chronic form of amoebic colitis can be confused with inflammatory bowel disease Clinical presentation Fulminant colitis-

24. Amoeboma Pseudotumoral lesion Necrosis, edema and inflammatory thickening of mucosa and submucosa of intestinal wall 1% of cases Palpable mass with trophozoites Always coexists with ulceration Single, rarely multiple in different parts of colon, on skin at site of amoebic liver aspiration

25. Difference between amoebic and bacillary dysentery Character Amoebic dysentery Bacillary dysentery Number 6-8 motions per day > 10 motions per day Amount Copious Small Odour Offensive Odourless Colour Dark red Bright red Reaction Acidic Alkaline Consistency Non-adherent Adherent Macroscopy

26. Difference between amoebic and bacillary dysentery Character Amoebic dysentry Bacillary dysentry RBCs In clumps Discrete or in Rouleaux Pus cells Few Numerous Macrophages Few Numerous, many have RBCs and may mimic EH Eosinophils Present Scarce Charcot-Leyden crystals Present Absent Pyknotic bodies Present Absent Ghost cells Absent Present Parasites Trophozoites of EH Absent Bacteria Many motile bacteria Few or Absent Microscopy

27. Metastatic lesions in liver Amoebic liver abscess- Most common extra-intestinal presentation The parasite reaches liver via portal system Occurs within 5 months of dysentery in 95% of cases But concomitant active diarrhea is seen in less than a third of cases Pain and point tenderness over right hypochondrium and fever Jaundice rare, pleural effusion is common

28. Amoebic liver abscess

29. Older pt. from endemic areas usually have chronic disease Right lobe is commonly affected, abscess of left lobe is more dangerous due to its proximity to heart –> rupture –> pericardial effusion Necrotic cavitary lesion filled with cellular debris and parasite trophozoites – Anchovy sauce pus Metastatic lesions in liver

30. Complications of ALA Rupture is the most dreaded complication It may spread to pleura, lungs, peritoneum, pericardium or open outside through the anterior abdominal wall

31. Pulmonary amoebiasis - Rupture from ALA into pleural space Hepato -bronchial fistula with necrotic material in sputum may mimic blood – trophozoites can be present Serous pleural effusion or contiguous spread from ALA Metastatic lesions in other organs

32. Metastatic lesions in other organs

33. Cerebral amoebiasis - Rare, complication of hepatic/ pulmonary abscess Single small lesion in cerebral hemisphere Cutaneous amoebiasis - In areas of drainage of liver abscess/colostomy wound Granulomatous ulcerations Metastatic lesions in other organs

34. Splenic amoebiasis - Amoebiasis of penis- Amoebic pericarditis - Rupture of liver left lobe abscess High fever, epigastric pain dyspnoea , pericardial rub Metastat ic lesions in other organs

35. Samples : Stool ( 3 consecutive samples) Biopsy material from the ulcers (colonoscopy or sigmoidoscopy ) Aspirate from liver abscess Serum Pleural fluid Pericardial fluid Sputum Laboratory diagnosis

36. Microscopy - Both saline and iodine wet mounts are prepared Any motile trophozoite is better seen in saline mount Iodine mount stains the internal structures and is used to identify cysts Charcot- leyden crystals can be seen Permanent stains can also be used to stain smears Laboratory diagnosis

37. Laboratory diagnosis For amoebic liver abscess and other metastatic lesions- Radiological examination Radio isotope tracing of liver Ultrasonogrphy of upper abdomen CT and MRI abdomen

38. Serology- Antibody detection ELISA IHA IFA Copro -antigen detection by ELISA is another recent and very useful method Antigen detection Coagglutination ELISA Laboratory diagnosis

39. Symptomatic case :- (amoebic colitis and amoebic liver abscess) Treatment

40. Luminal infections and -(with above) Treatment

41. Treatment Percutaneous radiography guided aspiration of abscess:- large left lobe liver abscess, bacterial superinfection , pyogenic abscess, pleuropulmonary amoebiasis , empyema , amebic pericrditis Simple aspiration of amoebic liver abscess

42. Asymptomatic cases and cyst passers- Treatment

43. Prevention 1.Primary prevention- a. Sanitation-safe disposal of human excreta, good sanitary practice like washing hands after defecation and before eating b. Water supply-water filtration(sand filters), boiling c. Food hygiene- prevent fecal contamination of food and drink, vegetables washed with aqueous acetic acid(5-10%) d. Health education- food handlers and public 2.Secondary prevention

44. Prevention 2. Secondary prevention- a. Early diagnosis b. Treatment

45. Contd … E. dispar is morphologically indistinguishable from E. histolytica and so is E. moshkovskii Most asymptomatic cases of amoebic infestation are believed to be one of these two species The other species are also non-pathogenic but can be microscopically differentiated

46. Summary Amoebiasis is an infection with the intestinal protozoa Entamoeba histolytica . About 90% of infections are asymptomatic Worldwide in distribution Infectious- cyst form Poor sanitation, sewage contamination Wide spectrum, from asymptomatic infection to luminal amoebiasis and amoebic colitis Invasive intestinal amoebiasis (dysentery, colitis, appendicitis, toxic mega colon, amoebomas ) Amoebic liver abscess- Most common extra-intestinal presentation Diagnosis by stool microscopy and other investigations Treatment tinidazole is prefered Prevention is good sanitary practice

47. Reference PARK’S TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE PARASITOLOGY, K. D. Chatterjee HARRISON’S PRINCIPLE OF INTERNAL MEDICINE Medscape Wikipedia

48. Thank You

49. Q A 4 year old male child presented in pediatric opd with the chief complain of failure to thrive and abdominal distension . The child is having abdominal pain for four days and vomiting for one day . Mother reported that the child had passed a worm in stool 15 days back which was approx.30 cm in length , smooth surface and brownish in colour .

50. Ascariasis

51. Ascariasis Introduction Geographical distribution Epidemiology Mode of transmission Clinical feature Prevention Mass treatment(deworming)

52. Introduction An infection of intestinal tract caused by ascaris lumbricoides . Largest intestinal nematode parasiting human. Most common intestinal helminthic infection. It occurs when man swallows infective eggs of ascaris with contaminated food and water. It is more common in children than adult. Soil transmitted helminthiasis is recognized by WHO as neglected tropical disease.

53. Geographical distribution Cosmopolitan Specially prevalent in tropics and subtropics. 45% prevalence in some areas of Asia and Latin America. It is estimated that 1.3 billion people are infected worldwide. Estimation reveals near 10,00,000 new cases annually and 60,000 fatalities. Intestinal obstruction-2 per 1000 children per year.

54. Geographical distribution Ascariasis is highly prevalent in areas of poor sanitation and poor hygiene.

55. Epidemiology Agent -Worm lives in small intestine (jejunum) of man. -Both sexes are separate ,measuring 20-35 cm in length . -Egg production is heavy –an estimated 2.4 lacs per day by each female. - Female liberates fertilized or unfertilized eggs which are passed out of the host with faeces .

56. Ascaris lumbricoides

57. Epidemiology -Eggs are excreted out and become embryonated . - Rhabditiform larva develops in 2-3 week. -Ingested with contaminated food and water. -Egg are resistant to common chemical disinfectants but can be removed by filtration and boiling. -Liberation of larva and migration through gut wall. -Entry into pulmonary circulation and reentry into intestine. -Sexual maturity and liberation of eggs.

58. Epidemiology Reservoir of infection –man Infective material- feces containing the fertilized egg Host- children are most important disseminators Environment- temperature, moisture , oxygen pressure and ultraviolet radiation are favorable Human habits - seeding of soil by eggs caused by indiscriminate open air defecation Period of communicability – until all fertile females are destroyed and stools are negative for eggs The usual life span is 12 month however it was reported as long as 24 month.

59. Mode Of Transmission Faecal -oral route Other means – Direct spread by fingers Ingestion of soil- in children Dust may play an important role in arid areas

60. Mode Of Transmission Embryonated eggs are transferred with food where untreated human excreta is used as fertilizers.

61. Clinical Features Due to migration of larva a) Ascaris pneumonia( Loeffler syndrome) fever, cough dyspnoea ,blood tinged sputum with ascaris larvae b)Larvae in general circulation- filtered out to various organ and may set up unusual clinical symptoms disturbances have been reported due to their presence in brain, spinal cord, heart and kidney

62. Clinical Features Due to adult worm- Asymptomatic Malnutrition Abdominal discomfort Severe abdominal pain Vomiting Restlessness Disturbed sleep Worm in stool and vomitus Partial or total intestinal blockage

63. Clinical Feature Ectopic ascariasis – Worm may migrates into stomach and may be vomited out or may pass up through esophagus at night , comming out through nose and mouth.

64. Complications Intussusception Intestinal perforation Intestinal obstruction-38 to 88% Allergic manifestation Appendicitis Obstructive jaundice Hemorrhagic pancreatitis Liver abscesses

65. Lab diagnosis Direct evidence- 1. Finding of adult worm in stool or vomit 2.X ray diagnosis 3.Finding of egg in stool or vomit

66. Lab diagnosis Indirect evidence- 1.Blood eosinophilia - 2. Larva in sputum- 3. Scratch test – Serological test are useful for Loeffler syndrome .

67. Prevention P rimary prevention –most effective in interrupting the transmission -Sanitary disposal of human excreta -Discourage open air defecation -Provision of safe drinking water -Better food hygiene habits -Health education of community in the use of sanitary latrines ,personal hygiene and changing behavioral patterns should be undertaken.

68. Prevention Education of community regarding ascariasis and its possible complication can help in prevention .

69. Faeces Fluid Field Flies Finger Food New Host Sanitation Water quality Water quantity Hand washing

70. Prevention The best way to prevent transmission of ascariasis is hand washing before handling the food and peel the fruits and cook well all raw vegetables.

71. Prevention Secondary prevention – Effective drugs are available for the treatment of human reservoir 1) Albendazole – in adults and children over 2 years of age in a single dose of 400 mg 2) Mebendazole - for all ages above 2 years in a dose of 100mg twice daily for 3 days 3)Levamisole- 2.5 mg per kg B w single dose 4) Pyrantel pamoate - single dose of 11mg per kg

72. Mass treatment Who strategy for prevention and control of STH Aim- periodic administration of anti helminthic drugs to control morbidity from STH by reducing the worm load. procedure- periodic deworming is undertaken – once a year if prevalence in community is 20% and twice a year if prevalence exceeds 50%

73. Mass treatment WHO donates medicines to ministries of health in all endemic countries for the treatment of all children of School age. Global target- to eliminated morbidity due to STH by 2020 This will be obtained by regularly treating at least 75% of children in endemic areas

74. Rod of Caduceus RR

75. Rod of Asclepius

76. Dracunculosis By John Fernando G 3 rd Year MBBS AIIMS BBSR

77. Also Known As…. Guinea Worm Serpent worm Dragon worm Medina worm

78. Outline What is this disease? Epidemiology What causes it? How do people get it? Treatment/Prevention

79. What is this disease?

80. Historical Accounts Egyptian mythology pertaining to the Serpent of Isis. Early Greek and Roman physicians associated the disease with certain watering holes and wells. Some say Guinea worm is the "fiery serpent" referred to in the Bible. The symbol of a Physician is the "Caduceus". This is the staff of Hermes and contains coiled serpents on a staff. The serpents are believed to represent Guinea worm.

81. Discovery About guinea worms and treatment in the Ebers papyrus, dating back to 1550 B.C ., A calcified guinea worm was discovered in the abdominal cavity of an adolescent Egyptian mummy Persian physicians removing the Dracunculus medinensis parasite from the leg of a patient

82. History( contd …) D. medinensis complete life cycle was discovered by Alexei Pavlovitch Fedchenko in 1870. Indian bacteriologist, Dyneshvar Atmaran Turkhud , solidified Fedchenkos knowledge in 1913

83. Guinea Guinea coast of West Africa

84. Epidemiology

85. Epidemiology In the 1980s approximately 10 million people per year were infested by this worm

86. Guinea worm- Globally Source: WHO website

87. Africa Map

88. Guinea worm- Globally( contd …) In 1980, 20 countries were endemic In 2012 the disease was confined to 4 countries Chad Ethiopia Mali South Sudan

89. Eradication efforts have reduced cases by 99%!

90. Annual Reported cases 1989-2014 Source: WHO website

91. According to WHO, Cases reported in 2013 -148 Cases reported in 2014 -126 These cases were all reported from among the 4 endemic countries stated before

92. In India

93. Guinea worm morbidity in India in 1984 Endemic States Cases A.P. 4461 Gujarat 426 Karnataka 5239 M.P. 11341 Maharashtra 3115 Rajasthan 15210 Tamil Nadu Nil Total 39792

94. In India( contd …) The last reported case was from Rajasthan in 1996

95. The last Guinea worm case from India 6 July 1996 Mr Bhanwara Ram, 25 years Village: Aau , PHC: Peelwa District: Jodhpur, Rajasthan Father had guineaworm in 1995 Brother and sister had guineaworm in 1996

96. In India( contd …) Adequately contained Rajasthan deleted from list of Endemic states in 1999 Source: NCDC website

97. Strategies adopted by NCDC Guinea worm case detection and continuous surveillance through three active case search operations and regular monthly reporting

98. Strategies adopted by NCDC( contd …) The first was GW case management

99. Strategies adopted by NCDC( contd …) Second was, Vector control by the application of Temephos in unsafe water sources eight times a year Use of fine nylon mesh/double layered cloth strainers by the community to filter cyclops in all the affected villages

100. Temephos / Temfos An Organophosphate larvicide Used to kill disease contained insects Even mosquitoes

101. Strategies adopted by NCDC( contd …) The third and final was, -Provision and maintenance of safe drinking water supply on priority in GW endemic villages

102. Tools used by NCDC Trained manpower development Intensive health education Concurrent evaluation and operational research.

103. Guinea worm Free… ICCDE visited India from 9 th – 25 th November, 1999 Declared India free of Guinea worm in a meeting in 8 th January 2000 In the presence of Hon’ble Health Minister Shri N T Shanmugam and Dr. Gro Harlem Brundtland Director General, WHO, Geneva

104. Recent Activities Surveillance activities still carried out in the 7 states and 89 districts

105. Morphology Male worms: 12-30 mm 0.4 mm in breadth Female worms: 60 cm – 1m 1.5-1.6 mm breadth

106. Life Cycle

107. Inside Cyclops Embryos metamorphose inside the body cavity of Cyclops into larvae Cyclops can ingest upto 20 Guinea Worm embryos Heavily infected Cyclops die in about 15 days

108. Inside Cyclops

109. Inside Man Enter inside the gut of man through contaminated water Cyclops digested but larvae are not Penetrate gut wall and enter retroperitoneal connective tissues

110. Inside Man( contd …) Male and female worms mate inside the body cavity ‘Not inside the Gut’ 6 months to decide for the gravid female to select the site of its parturition

111. Inside Man( contd …)

112. Inside man( contd …) Gravid female selects water contact areas to liberate its embryos It secretes some toxins which produce a blister finally rupturing to form an ulcer

113. Life Cycle of Guinea worm

114. How patient presents?

115. Patient presents with Patient presents with Allergic manifestation Blisters Or even the worm protruding out

116. How to Diagnose?

117. Lab Diagnosis Worm seen through the centre of erosion Embryos seen from secretions of the ulcer Intradermal test X-Ray: Calcified worms Serology

118. What is the treatment?

119. There is no cure.

120. Drugs Nitrothiazole Niridazole Metronidazole and Thiabendazole These drugs may kill the worm but not eliminate it from the body

121. So the Caduceus or Asclepius?

122. So which is ours…?

123. Prevention is Better than Cure

124. Prevention Boreholes or hand dug wells

125. Prevention: Filtering Filters cyclops out

126. Prevention: Clean water source Prevent people with emerging worms from entering ponds/wells used for drinking

127. Educating people

128. Why still bother? Even now four countries are endemic to Guinea worms Possible chance of worm infestation, especially travellers So, surveillance programmes are carried out by India and other previously endemic countries.

129. Sources Belcher, D.W., F.K. Wurapa , W.B. Ward, and I.M. Lourie (1975), “Guinea Worm in Southern Ghana: Its Epidemiology and Impact on Agricultural Productivity,” American Journal of Tropical Medicine and Hygiene 24:243-249. CDC. Renewed transmission of dracunculiasis ---Chad, 2010. MMWR 2011;60:744—8 Donald R. Hopkins, Ernesto Ruiz- Tiben , Philip Downs, P. Craig Withers, Jr., James H. Maguire (2005). " Dracunculiasis Eradication: The Final Inch". American Journal of Tropical Medicine and Hygiene 73 (4): 669–675.

130. Sources( contd …) http://www.stanford.edu/class/humbio103/ParaSites2006/Dracunculiasis/history.html http://www.who.int/en/ http://www.astdhpphe.org/infect/guinea.html http://ucdnema.ucdavis.edu/imagemap/nemmap/Ent156html/nemas/dracunculusmedinensis http://www.who.int/wer/2015/wer9019/en/

131. HOOKWORM Mahesh ku . Sethi Roll no.-19 MBBS AIIMS,BBSR

132. Headings Introduction Epidemiology Indian scenario Life cycle Pathological effects Clinical features Laboratory diagnosis Prevention and control Mass drug administration

133. Introduction Any infection caused by Ancylostoma duodonale or Necator americanus It is known as hookworm because the anterior end of the worm is slightly bent dorsally Ancylostoma duodonale is also known as Old world hookworm Necator americanus is also known as New world hookworm

134. Differences between A.duodonale and N.americanus are:- Features A.duodonale N.americanus 1 .Size Larger and thicker Smaller and slender 2 .Anterior end Bends in the direction of body curvature Bends in opposite direction of body curvature 3 .Copulatory bursa Dorsal ray is single Dorsal ray is split from base 4 .Posterior end of female A spine is present There is n o spine 5 .Vulval opening Behind the middle of the body In front of the middle of the body 6 .Pathogenicity More pathogenic (more blood loss) Less pathogenic

135. Differences between A.duodonale and N.americanus are:-

136. Differences between A.duodonale and N.americanus are:-

137. May occur as single or mixed infection in the same person Mostly asymptomatic Symptomatic in severe infection Factors contributing for developing the disease are:- Heavy worm burden A prolong duration of infection Inadequate iron intake Introduction

138. Epidemiology Prevalence is 700 million people worldwide, including 44 million pregnant women Mainly in tropical and sub-tropical environments in poverty-stricken areas of Africa, Latin America, South-east Asia and China A.duodenale is predominant in tropical Africa and South-east Asia N.americanus is predominant in Europe and America

139. Epidemiology It is world’s leading cause of anaemia and protein malnutrition, particularly in pregnant women and childrens

140. Indian scenario A.duodenale is predominant in North India N.americanus is predominant in South India A.ceylanicum is reported in villages near Kolkata

141. Indian scenario Heavily infected areas – Assam, Bihar, Odisha , Andhra Pradesh, Maharastra , Tamil Nadu, Kerala, West Bengal More than 200 million peoples are infected

142. Endemic index Chandler’s index: -based on the average number of eggs per gram of stool Used in epidemiological studies No. of eggs/gm of stool <200 Not much significant 200-250 May be regarded as potential danger 250-300 Minor public health problem >300 Important public health problem

143. Epidemiological determinants Agent factor: - Agent:- Ancylostoma duodonale and Necator americanus Size:- Female is 12-15mm and males is 8-10 mm in length Habitat:- They resides mainly in the Jejunum where they remains attached to the villi Host:-Man is the only definitive host (no intermediate host is required)

144. Epidemiological determinants A. Agent factor :- IV. Infective material:- Soil contaminated with faeces containing 3 rd larval stage( filariform larva) V. Period of infectivity:- As long as person harbours the parasite

145. Epidemiological determinants Host factors ;- Age:- All the age groups are susceptible But more common in age group from 15 to 25 yr (they works in the field) II. Sex:- Both the sexes are equally susceptible Nutrition:- I. Malnutrition is a predisposing factor II. Inadequate iron intake also favours the infection Occupation:- Farmers are more susceptible (More common in rural areas)

146. Epidemiological determinants Environmental factors: - Soil:- Damp soil and with decaying vegetation are more favourable for growth of the egg Temperature:- Most favorable temp. for growth is 24 to 32 °C If temp. <13 ° c , then the e gg fails to develop If the temp. >45°c,then larva gets killed

147. Epidemiological determinants Epidemiological determinants:- Human habits:- I. Open field defaecation, sharing of same place for defaecation, going barefoot and children wading in the infected mud will lead to infection. IV. Oxygen, moisture and shady areas are other favourable conditions for the growth of egg.

148. Life cycle Incubation period:- A.duodenale - 5weeks to 9months N.americanus- 7weeks Mode of infection:- Mainly by direct penetration into skin And in children, the transmission is mainly by faeco -oral route Site of entry:- Mainly the thin skin between the toes Dorsum of feet Inner side of the soles

149. Life cycle

150. Pathogenic effects 1. By larva :- In the skin:- Ancylostoma dermatitis at the site of entry Creeping eruption, particularly seen with non-human hookworm ( A.braziliense and A.caninum )

151. Pathogenic effects 1. By larva :- In lungs:- I. Bronchitis and Broncho -pneumonia may occur when the larva break through and enters alveoli

152. Pathogenic effects 2. By adult worm :- Microcytic hypochromic anaemia by chronic blood loss from GI tract Effects of anaemia On children:- Decreases growth and development On mother:- Increases morbidity due to PPH Low birth weight babies Abortion, still birth and impaired lactation On adults:-decreases capacity for sustained hard work

153. Effects of disease on community It causes economic loss and decreased quality of life by:- Decreasing the nutrition, growth and development Decreasing the work and productivity Increasing the medical care cost

154. Clinical features 1. Gastrointestinal manifestations :- Dyspepsia Epigastric tenderness Loss of appetite Constipation

155. Clinical features 2. Effects of anaemia :- Pallor, koilonychia , generalised edema Hyperkinetic circulation Decreased growth and development of the children

156. Laboratory diagnosis Direct examination :- Examination of stool under microscope:- Presence of characteristic hookworm egg is diagnostic Study of duodenal content:- May reveals either eggs or adult worms

157. Laboratory diagnosis Indirect examination :- General stool examination:- Occult blood in the stool Charcot-Leyden crystals Blood examination:- Eosinophilia Decreased Hb level

158. Prevention and control Primary prevention: - By sanitary disposal of human excreta through instillation of sewage disposal system in urban areas By promoting the use of sanitary latrines in rural areas By using of sandals By preventing open field defaecation Maintanance of good hygiene

159. Prevention and control Secondary prevention:- Chemotherapy :- If not available, alternate drug is tetrachlorethylene ALBENDAZOLE MEBENDAZOLE LEVAMISOL PYRANTEL Dose 400mg (>2yr) 500mg (>2yr) 50-150mg (3mg/kg body wt.) 10mg/kg body wt. d aily for 3days Species sensitivity A.duodenale N.americanus A.duodenale N.americanus Side effects Rare and mild GI disturbances Transient GI disturbances Headache and dizziness Contraindications Age <2yr, pregnancy Age <1yr, kidney diseases, liver dysfunctions

160. Prevention and control Tertiary prevention:- Treatment of anaemia :- Ferrous sulphate, 200mg, orally, TDS and continue for 3 months after Hb has raised to 12mg/dl Treat folic acid deficiency, if present

161. Mass drug administration:- At Global network, there is integrated treatment approach, called rapid impact approach, which treats 7 most common neglected tropical diseases (NTDs) through combination of four drugs ( Albendazole , Praziquantel , Zithromax and DEC) For soil transmitted helminthes (hookworm, ascaris and whipworm) and four other “ neglected tropical diseases” (river blindness, lymphatic filariasis, schistosomiasis and trachoma)

162. Mass drug administration:- In India, mass drug administration is done for lymphatic helminthes Single dose of diethylecarbamazine and albendazole is given Prevention and control

163. Mass drug administration:- Conducted annually or several times a year until an area is free of the disease It is highly cost effective Prevention and control

164. References WHO (1987) Tech. Resp. Ser. 749 WHO (1981) Tech. Resp. Ser. 666 WHO (1998), World Health Report 1998, Report of the Director General WHO. Patel, J.C (1954).J. Com. Dis., 3 (3-4)146-158 Rao, C.K. et al (1967) .J. Com. Dis., 5 (2) 80-86

165. AVIAN INFLUENZA: H5N1 KULDEEP RATHOR ROLL NO. 18 172

166. Objectives Introduction to i nfluenza virus Genetic drift Vs genetic shift Introduction avian influenza Major events of avian influenza Ecology Pathogenicity Management Prevention of avian flu 173

167. Influenza virus Orthomyxoviridae family 80-120 nm in size Enveloped Containing 2-8 fragments of negative stranded RNA 174

168. Classification Of Influenza SR NO TYPE HOSTS DISEASE SEVIRITY SUBTYPES 1. A Human Birds(avian flu) Pig Most severe (Pandemics) By H(1-16) & N(1-9) 2. B Human Moderate No 3. C Human Pig Least No On the basis of antigenic characteristics & matrix (M) protein H1,H2,H3 & N1,N2 are associated with pandemics in human

169. Genetic Drift Point mutations in the haemagglutinin gene cause minor antigenic changes to HA Immunity to new subtype partially Continuous process 6-8 months to cause seasonal epidemics Viruses still belong to the same subtype Example- A/chicken/Shantou/423/2003 ( H5N1) A/bar-headed goose/Qinghai/5/2005 (H5N1 ) 176

170. Nomenclature Of Influenza Virus A/chicken/Shantou/423/2003 ( H5N1 ) Type of influenza Animal in which it found Place of origin Specific laboratory number- helps in differentiating it from other influenza Year of isolation 177

171. Genetic Shifts Genetic material of two or more strains of virus recombines leading to the emergence of new haemagglutinin subtype new HA subtype +/- NA No immunity in the population- pandemics Examples- H1N1 ( 1918–1919) H2N2 ( 1957–1958) H3N2 (1968–1969 ) 178

172. Genetic Drift Vs Genetic Shift 179

173. Avian Influenza ‘‘ Avian flu’’ or ‘‘bird flu’’ Avian influenza is a contagious disease of animals caused by “H5N1 virus” that normally infect only birds and sometimes pigs Infects both Domestic and Wild Birds Highly species-specific Rarely crosses the species barrier to infect humans 180

174. Human influenza virus: ‘Human influenza virus’ usually refers to those subtypes that spread widely among humans H1N1 H1N2 H3N2 http:// www.nwhc.usgs.gov/csr/en/avian_flu.asp

175. Avian Influenza: Timeline Of Major Events Date Events in Animals Events in Humans 1996 HPAI isolated from goose in China 1997 Reported in poultry in Hong Kong In Hong Kong 18 cases (6 fatal) are reported first known instance of human infection Feb 2003 2 human cases of avian influenza H5N1 infection (1 fatal) are confirmed in a China http://www.who.int/timelines/avian_influenza.asp

176. Avian Influenza: Timeline Of Major Events Date Events in Animals Events in Humans 12 Dec 2003 Republic of Korea Dec 2003 – Jan 2004 2 tigers and 2 leopards die in Thailand due to eating infected poultry meat Viet Nam reported first human case in country 8 Jan 2004 Viet Nam 12 Jan 2004 Japan 23 Jan 2004 Thailand Thailand reports 2 of human infection cases with H5N1 24 Jan 2004 Cambodia 27 Jan 2004 Lao http://www.who.int/timelines/avian_influenza.asp

177. Avian Influenza: Timeline Of Major Events Date Events in Animals Events in Humans 1 Feb 2004 Family cluster of H5N1 cases occurred in Viet Nam 2 Feb 2004 Indonesia 4 Feb 2004 China 20 Feb 2004 A report from Thailand confirms that a domestic cat http://www.who.int/timelines/avian_influenza.asp

178. World W ide Deaths

179. World Wide Deaths

180. Outbreaks in India Occurred only in poultry 2006- outbreak in Maharashtra 2008- outbreak in West Bengal 2014- outbreak in Kerala 2015- Chandigarh Agra, Uttar Pradesh Thorrur, Telengana Imphal , Manipur 187

181. Outbreaks in India 2006 H5N1 outbreak in Maharashtra On 19 February 2006 The first outbreak of bird flu in India In village Nawapur in the Nandurbar district of  Maharashtra 188

182. Outbreaks in India Action taken by Govt . 2.5 lakh birds culled & 6 lakh eggs were destroyed Villagers exhibiting flu-like symptoms kept under observation Blood samples from 150 persons were taken Movement of people into the area was strictly regulated 189

183. Outbreaks in India Action taken by Govt . T rains were instructed not to halt at nawapur Govt. b anned the import & export of poultry The government also started stocking Tamiflu Drug was distributed among people in that area 190

184. Outbreaks in India Impacts of outbreak Prices of chicken products across India increased because of less supply steep rise in the prices of  mutton  and fish The poultry industry is expected to have lost hundreds of millions Many Airlines  took chicken off their in-flight menu. 191

185. Outbreaks in India 2014 H5N1 outbreak in K erala  O ccurred November 2014 ,   Kuttanad ,  Alappuzha, Pathanamthitta &   Kottayam district  V irus killed about 16,000 ducks 192

186. Outbreaks in India Action taken by Govt. 41,000 persons were examined in  A ppuzha 7,000 persons were examined in K ottayam 3,000 persons were examined in  P athanamthitta Persons were also given awareness about the diseases and the precautions Provided about 80,000 tablets Tamiflu Surveillance campaign launched in a 10 km radius around the area 193

187. Outbreaks in India Action taken by Govt. About two lakh ducks were culled Poultry owners, whose birds were culled, got compensation Total ban on the transportation of poultry and poultry products in trains 194

188. Deaths In India 840 laboratory-confirmed human cases of Avian Influenza Virus were reported from 16 countries in the world from 2003 to March 31, 2015 Fortunately , India is not one of these 16 countries Total 447 death in the affected countries http://www.who.int/diseases/avian_influenza/data/india.asp

189. WHO Pandemic Influenza Phases(2009) Phase Description Phase 1 No animal influenza virus circulating among animals causing infection in humans Phase 2 Animal influenza virus circulating in animals causing infection in humans Phase 3 An animal or human-animal influenza reassortant virus has caused disease in people but has not resulted in human-to-human transmission Phase 4 animal or human-animal influenza reassortant virus Human to human transmission Phase 5 Human-to-human spread of the virus in two or more countries in one WHO region Phase 6 human-to-human spread of virus in at least one country in another WHO region Post peak period pandemic in most countries with adequate surveillance have dropped below peak levels Post pandemic period influenza activity have returned to the levels seen for seasonal influenza in most countries with adequate surveillance.

190. WHO Strategies For Influenza Pandemics Before pandemics WHO has network of 115 national influenza centres in 84 countries that- Continuously monitor influenza activity Report the emergency of any "unusual" influenza virus Detection of outbreaks The isolation of pandemic virus Engaging in fund-raising for research 197

191. WHO Strategies For Influenza Pandemics During pandemics- work for E arly warning system for outbreak Limiting or delaying the spread of the virus at the source Reducing the human infections Reducing morbidity, mortality and social disruption from the pandemic Conducting research to guide response measures http://www.who.int/csr/disease/influenza/en /

192. WHO Strategies For Influenza Pandemics During pandemics- work for I nternational coordination to ensure a rapid and effective response W ork together with international partners to monitor the pandemic Offers guidance tools and training to countries for pandemic management 199

193. Ecology Wild birds are the natural reservoir of influenza A viruses (Especially: shorebirds and waterfowl) Viruses are well adapted to these host birds Infection does not cause disease in wild birds Waterfowls are resistant to the disease induced by HPAI viruses also A ll HA and NA virus subtypes are found in aquatic birds http://www.nwhc.usgs.gov

194. Ecology Replicate in the intestinal tract of aquatic birds and are transmitted in the feces Transmission in aquatic birds is by the fecal-oral route http://www.nwhc.usgs.gov

195. Transmission From water birds to domestic poultry Infected birds shed virus in saliva, nasal secretions, and feces Direct contact with secretions Contaminated food, water, equipment and clothing Broken contaminated eggs may infect chicks in the incubator 202

196. Pathogenicity Why mutations usually occur in domestic poultry not in wild birds ? 203

197. Pathogenicity In domestic poultry- two forms of disease (Domestic poultry : chickens, ducks and turkeys) 1. Low pathogenic form(LPAI)- directly from wild birds M ild symptoms (ruffled feathers, a drop in egg production) E asily go undetected. 2. High pathogenic form(HPAI)- due to change during replication in the domestic poultry spreads very rapidly mortality up to 100%, often within 48 hours 204

198. Pathogenicity Pigs can serve as a ‘mixing vessel’ between avian and human influenza viruses Pig can be infected from both bird and human viruses T wo different viruses can recombine and give rise to new combinations- having mix genetic materials and capabilities of both parental viruses N ew virus can infect both human and birds http://www.nwhc.usgs.gov

199. Pathogenicity http://www.nwhc.usgs.gov

200. Transmission In Human From domestic poultry to human Same as from water birds to domestic poultry Infected birds shed virus in saliva, nasal secretions, and feces Direct contact with secretions Contaminated food, water, equipment and clothing Broken contaminated eggs may infect chicks in the incubator http:// www.who.int/csr/disease/influenza/en/transmission

201. Transmission In Human From place to place Bird migration Travel by infected people, along with contaminated luggage or clothing Transportation of infected poultry and poultry products http:// www.who.int/csr/disease/influenza/en/transmission

202. Transmission F rom person-to-person Influenza viruses from one ill person to another has been reported very rarely V iral transmission among human occur by aerosol Transmission of disease has not been observed from person-to-person www.cdc.gov/flu

203. Symptoms I.P. 2-5 days Influenza like symptoms Cough Sore throat Muscle ache High fever Eye infection Pneumonia Acute respiratory distress 210

204. Laboratory findings Leukopenia T hrombocytopenia E levated aminotransferase levels Hyperglycemia Elevated creatinine levels 211

205. Treatment Supportive therapy Supplemental oxygen Intubation/ventilation Fluid management Nutrition Specific therapy Antiviral drugs Antibiotics for bacterial super infections DHS - Acute Communicable Disease Control Program

206. Treatment Antiviral medications ( oseltamivir and zanamivir ) that : Reduce the severity and duration of symptoms Shorten the length of the illness Control outbreaks of the flu in population Reduce complications from the flu Resistant to amantadine and rimantadine 213

207. Prevention Prevent contact with the feces, saliva or respiratory secretions of infected birds by: C leaning hands constantly H and washing before eating E ating hygienic food G etting enough sleep and exercising help bolster the immune system 214

208. Immunization FDA approved first adjuvant vaccine for H5N1 avian influenza in April 2014 Egg based preparation Monovalent vaccine AsO3 as adjuvant Both adjuvant and vaccine in separate vial 215

209. Immunization Recommendations- For >18 year age people& at higher risk 2 IM doses, 21 days apart ADRs- local pain, headache, fatigue, Success rate- 18-64years- --91% 65 or more--- 74 % Not commercially available 216

210. Biosecurity Used in pandemics For both human & birds Definition : all procedures used to prevent the introduction of disease O bjectives : - Prevent the entry of disease - Control the spread of disease 217

211. Benefits Of Biosecurity Reduces the risk of disease Limits the spread of diseases Helps protect the public health Improves the overall flock health Reduces losses and improves profits 218

212. Summary Contagious disease of animals caused by H5N1 virus that normally infect birds Viral mutation has virtually always occurs in domestic poultry only Transmission of disease has not been observed from person-to-person Total 447 death in the affected countries No death in India till now Antiviral medications are oseltamivir and zanamivir 219

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