A 4 year old male child presented with failure to thrive, abdominal distension, pain and vomiting. The child's mother reported passing a 30cm long brown worm in stool 15 days ago. This suggests the child has ascariasis, an intestinal infection caused by the roundworm Ascaris lumbricoides. Ascariasis is highly prevalent in areas with poor sanitation and hygiene, infecting over 1 billion people worldwide. The worm's eggs pass in stool and become infective in soil, being ingested and causing symptoms like abdominal pain as the worms mature and migrate through the body. Diagnosis and treatment of ascariasis is important to prevent complications and further transmission.

1. AMOEBIASIS
Jagadish Prasad Mishra
Roll no-16
6th 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
Symptomatic group
Intestinal
Small % - invasive
amoebiasis
Mild abdominal
discomfort,
diarrhea to acute
fulminating
dysentery
Extraintestinal
Liver(liver
abscess), brain,
lung, spleen

5. Epidemiology
World
• Worldwide in distribution
• 3rd 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 μm 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 μm 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 107 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
• Direct 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%
• Severely ill with high fever
• Intestinal bleeding, perforation
• Paralytic 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-
I. Rupture from ALA into pleural space
II. Hepato-bronchial fistula with necrotic material in sputum
may mimic blood – trophozoites can be present
III. 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
Metastatic lesions in other organs

35. Samples :
I. Stool ( 3 consecutive samples)
II. Biopsy material from the ulcers (colonoscopy or
sigmoidoscopy)
III. Aspirate from liver abscess
IV. Serum
V. Pleural fluid
VI. Pericardial fluid
VII. 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-
I. Radiological examination
II. Radio isotope tracing of liver
III. Ultrasonogrphy of upper abdomen
IV. 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
Drug
Tinidazole
Metronidazole
Dose
2g/day
750mg(adult)
30mg/kg(children)
Frequency
tid
tid
Route
oral
Oral/iv
Duration
3 days
5-10
days

40. • Luminal infections and -(with above)
Treatment
Drug
Parmomycin
Iodoquinol
Dose
30mg/kg
650mg
Frequency
qid
tid
Route
oral
oral
Duration
5-10
days
20 days

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
Drug
Didohydroxyquin
Diloxanide furoate
Dose
650mg(adult), 30-
40mg/kg(children)
500mg
Frequency
tid
tid
Route
oral
oral
Duration
20 days
10 days

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

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

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.

59. 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.

60. 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

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

62. 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

63. 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

64. 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.

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

67. 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

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

69. Prevention
Primary 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.

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

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

72. 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.

73. 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

74. 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%

75. 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

77. Rod of Caduceus
RR

78. Rod of Asclepius

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

80. Also Known As….
• Guinea Worm
• Serpent worm
• Dragon worm
• Medina worm

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

82. What is this disease?

83. 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.

84. 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

85. 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

86. Guinea
• Guinea coast of West
Africa

87. Epidemiology

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

89. Guinea worm- Globally
Source: WHO website

90. Africa Map

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

92. Eradication efforts have reduced cases by 99%!

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

94. 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

95. In India

96. 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

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

98. 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

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

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

101. Strategies adopted by NCDC(contd…)
• The first was
– GW case management

102. 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

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

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

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

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

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

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

109. Life Cycle
Definitive host:
Man
Intermediate
host: Cyclops

111. 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

112. Inside Cyclops

113. 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

114. 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

115. Inside Man(contd…)

116. 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

117. Life Cycle of Guinea worm

118. How patient presents?

119. Patient presents with
• Patient presents with
– Allergic manifestation
– Blisters
– Or even the worm protruding
out

120. How to Diagnose?

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

122. What is the treatment?

123. There is no cure.

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

126. So the Caduceus or Asclepius?

127. So which is ours…?

128. Prevention is Better than Cure

129. Prevention
• Boreholes or hand dug
wells

130. Prevention: Filtering
• Filters cyclops out

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

132. Educating people

133. 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.

135. 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.

136. Sources(contd…)
• http://www.stanford.edu/class/humbio103/ParaSite
s2006/Dracunculiasis/history.html
• http://www.who.int/en/
• http://www.astdhpphe.org/infect/guinea.html
• http://ucdnema.ucdavis.edu/imagemap/nemmap/En
t156html/nemas/dracunculusmedinensis
• http://www.who.int/wer/2015/wer9019/en/

137. HOOKWORM
Mahesh ku. Sethi
Roll no.-19
MBBS

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

139. 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

140. 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 no 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

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

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

143. • 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

144. 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

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

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

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

148. Endemic index
• Chandler’s index:-based on the average
number of eggs per gram of stool
• Used in epidemiological studiesNo. 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

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

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

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

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

153. Epidemiological determinants
– Epidemiological determinants:-
III. 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.

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

155. Life cycle

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

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

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

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

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

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

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

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

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

165. 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. daily 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
Contraindicatio
ns
Age <2yr, pregnancy Age <1yr, kidney diseases, liver
dysfunctions

166. 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

167. • 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)

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

169. • 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

170. 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

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

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

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

175. 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

176. 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

177. 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

178. 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

179. Genetic Drift Vs Genetic Shift
179

180. 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

181. 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

182. 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

183. 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

184. 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

185. World Wide Deaths

186. World Wide Deaths

187. 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

188. 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

189. 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

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

191. 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

192. Outbreaks in India
2014 H5N1 outbreak in Kerala
• Occurred November 2014,
• Kuttanad, Alappuzha, Pathanamthitta & Kottayam
district
• Virus killed about 16,000 ducks
192

193. Outbreaks in India
Action taken by Govt.
• 41,000 persons were examined in Appuzha
• 7,000 persons were examined in Kottayam
• 3,000 persons were examined in Pathanamthitta
• 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

194. 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

195. 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

196. 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.

197. 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

198. WHO Strategies For Influenza Pandemics
During pandemics- work for
• Early 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/

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

200. 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
• All HA and NA virus subtypes are found in aquatic
birds
http://www.nwhc.usgs.gov

201. 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

202. 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

203. Pathogenicity
Domestic
poultry is not
a natural host
for virus
Degree of
adaptation of
virus for new
host is low
Viral mutation
has virtually
always occurs in
domestic poultry
only
Why mutations usually occur in domestic poultry not in wild
birds ?
203

204. Pathogenicity
In domestic poultry- two forms of disease
(Domestic poultry: chickens, ducks and turkeys)
1. Low pathogenic form(LPAI)- directly from wild birds
• Mild symptoms (ruffled feathers, a drop in egg
production)
• Easily 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

205. Pathogenicity
• Pigs can serve as a ‘mixing vessel’ between avian and
human influenza viruses
• Pig can be infected from both bird and human
viruses
• Two different viruses can recombine and give rise to
new combinations- having mix genetic materials and
capabilities of both parental viruses
• New virus can infect both human and birds
http://www.nwhc.usgs.gov

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

207. 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

208. 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

209. Transmission
From person-to-person
• Influenza viruses from one ill person to another has
been reported very rarely
• Viral transmission among human occur by aerosol
• Transmission of disease has not been observed
from person-to-person
www.cdc.gov/flu

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

211. Laboratory findings
• Leukopenia
• Thrombocytopenia
• Elevated aminotransferase levels
• Hyperglycemia
• Elevated creatinine levels
211

212. 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

213. 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

214. Prevention
Prevent contact with the feces, saliva or respiratory
secretions of infected birds by:
• Cleaning hands constantly
• Hand washing before eating
• Eating hygienic food
• Getting enough sleep and exercising help bolster
the immune system
214

215. 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

216. 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

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

218. 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

219. 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

220. “The pandemic influenza clock is
ticking. We just don’t know
what time it is.”
220