DR CHANDRA SEKHAR NAIDU GURAJALA

1. Dr. G CHANDRA SEKHAR NAIDU
MD Paediatrics

2. AMOEBIASIS
&
GIARDIASIS

3. HISTORY
1875 LOSCH – RUSSIAN.
Differentiated the amoebic dysentery from bacillary
dysentery by describing amoeba in the stool.
1887 KARTULIS – EGYPT.
Found amoeba in the pus from a liver abscess.
1881 COUNCILMAN AND COFFLEUR.
Described true bowel lesions and used the term
Amoebic Dysentery.
1903 SCHAUDINN.
Differentiated pathogenic and non pathogenic types
of amoeba.

4. Trends of Amoebiasis

5. ENTAMOEBA HISTOLYTICA

6. Amebiasis

7. • Third most common cause of death from the
parasitic disease. (after schistosomiasis , Malaria)
 480 Million people (world)
 12% of world’s population
 High risk groups
 Travellers, immigrants, immunocompromised
individual, pregnant women, Mental institutes,
prisons, Children in day care centres.
 Cyst carriers
 .
EPIDEMIOLOGY

8. Events on Amoebiasis

11. Amoebiasis causes Epithelial
damage

12. the intestinal lesion
Gut
Minute crypt lesion
Extends through the muscularis mucosa and submucosa.
“Flask shaped” ulcer
Thrombosis of blood vessels
“Toxic megacolon”
Irreversible coagulation necrosis of bowel wall.
PATHOLOGY

13. Risk
Factors
 People in developing countries that have
poor sanitary conditions
 Travellers
 People who live in institutions that have
poor sanitary conditions
 HIV-positive patients

14. Host Factor Contributions
 Several factors contribute to influence
infection
1 Stress
2 Malnutrition
3 Alcoholism
4 Corticosteriod therapy
5 Immunodeficiency

16. How the Amebiasis
Manifests
 Most cases of amebiasis have very mild
symptoms or none.
 More severe infection may cause fever,
profuse diarrhea, abdominal pain,
jaundice, anorexia, and weight loss.
 In severe cases, it can lead to
development of abscesses (pockets of
amoebae and inflammatory cells) in the
liver or, more rarely, the brain.

17. Clinical symptoms are Vague
 Wide spectrum, from asymptomatic
infection ("luminal amebiasis"), to invasive
intestinal amoebiasis (dysentery, colitis,
appendicitis, toxic mega colon,
amebomas), to invasive extra intestinal
amebiasis (liver abscess, peritonitis,
pleuropulmonary abscess, cutaneous and
genital amoebic lesions).

18. C LINIC AL FINDINGS
INTESTINAL AMOEBIASIS
Asymptomatic infection
Mild to moderate colitis (non dysenteric colitis)
Severe colitis (dysenteric colitis)
Localised ulcerative lesions of the colon
Localised granulomatous lesion of the colon
(amoeboma)

19. Extra intestinal Amoebiasis


The specimens are
obtained from Liver, lung,
or Brain biopsy samples
and subjected to routine
Histopathology ( H&E)
sections
Giemsa stained touch
preparations which will
revel Trophozoites in
extra intestinal lesions.

20. Amoebic Liver Abscess
 The pus in liver
abscess appear as red
Anchovy sauce like
appearance
 The material
aspirated is likely to
contain Trophozoites
and may be detected
by direct microscopic
examination

21.  Infective colitis
 Ulcerative colitis
 Colorrectal carcinoma
 Trichuris infection
 Balantidiasis
 Crohn’s disease
 Diverticulosis
 Ileoceacal TB

22. Trophozoites of E.histolytica

23. Trophozoites and Cystic
stages

24. Cystic stage - E.histolytica

26. Do we need culturing for
Diagnosis ?
 Trying to get the
amoeba to grow
outside the body is
very difficult and
unreliable, and is
therefore not
generally done

27. Immunological Tests are not
confirmatory of Acute
Infections
When the body is exposed
to an infection, the immune
system creates antibodies to
fight it off. These can be
detected with a blood test,
and provide evidence that
the person
has been infected with E.
histolytica.
Unfortunately, this test does
not distinguish between
past and present infection

28. Serological Diagnosis
 The serological become reactive in invasive
Amoebiasis
 1 Indirect Heamagglutination assay ( IHA )
 2 ELISA
 3 Latex agglutination test
 4 gel diffusion
 5 Counter current Imunoelectrphoresis
 Serological tests remain positive for several years ever after successful
treatment

29. Immunological Test
Indirect Haemagglutination
 Enzyme Immunoassay
 Indirect Immunoflorescence
 Latex Agglutination
 Gel diffusion
Sensitivity
60 % invasive Bowel disease 100 % with
Amoeboma

30. Emerging methods in
Diagnosis
 These are considered the
most useful tests for
detecting E. histolytica.
They test directly for the
parasite itself by exposing
some stool to a strip of
paper coated with
antibodies. The parasites
will stick to the antibodies
on the paper. The test
distinguishes E.
histolytica from other
parasites.

31. Clinical
presentation
Drugs of Choice Adult Dosage
Intestinal infection
1st Choice
Metronidazole
( or )
Tinidazole followed by
2nd Choice
Paramomycin
.
750 – 800 mg.t.i.d × 10
days
500 mg.t.i.d × 10 days
25 – 30 mg kg-1 day-1 in 3
doses × 7 – 10 days

32. PREVENTION
Health Education
Improved water supply
Chlorination – not effective
Amoebic cysts
Destroyed by
200 parts / 106 of Iodine 5 – 10 acetic acid.
Heating > 680C
Removed by
sand filtration
Boling for 10 minutes kill the cysts

33. Food safety
Thoroughly cook all raw foods.
*Reheat food until the internal
temperature of the food
reaches at least 167º F
Wash your hands before
preparing food, before eating,
after going to the toilet or
changing diapers,
after smoking or after using a
tissue or handkerchief.
*Thoroughly wash raw
vegetables and fruits before
eating.

34. Personal Hygiene



Wash hands thoroughly
with soap and hot
running water for at least
10 seconds after using
the toilet or changing a
baby's diaper.
Clean bathrooms and
toilets often. Pay
particular attention to
toilet seats and taps.
Avoid sharing towels or
face washers.

35. Vaccines
 Vaccines are being developed and tested
for the treatment of Amebiasis. The
vaccine is a modified version of the
proteins expressed on the surface of E.
histolytica. A study in rodents found that
the vaccine prevented the formation of
liver abscesses, but much more research
is needed to determine if these vaccines
are useful and safe in humans

36. GIARDIASIS

37. GIARDIASIS
Giardia is a microscopic parasite that causes
the diarrheal illness known as giardiasis.
Giardia is found on surfaces or in soil, food, or
water that has been contaminated with feces
from infected humans or animals.

38. Giardia can be spread in different ways, water
(drinking water and recreational water) is the
most common mode of transmission.
Giardia is protected by an outer shell that
allows it to survive outside the body for long
periods of time and makes it tolerant to
chlorine disinfection

39. Giardia usually spreads when Giardia
lamblia cysts within feces contaminate food
or water which is then eaten or drunk
Giardia is one of the most common
parasitic human diseases globally

40. Infection is more common in children
than in adults
Infection with Giardia intestinalis most
often results from:
 Fecal-oral transmission
 Ingestion of contaminated water 6

41. Contaminated food is a less common
etiology
G intestinalis is a particularly significant
pathogen for people with:
 Malnutrition
 Immunodeficiencies

42. Giardiasis does not have any race predilection
Giardiasis is slightly more common in males
than in females
Giardiasis affects people of all ages
Infection is rare during the first 6 months of life
in breastfed infants
infants and young children have an increased
susceptibility to giardiasis

43. RISK FACTORS
• Include:
Travel
Changing diapers
Eating food without cooking it
Owning a dog

44. • Predisposing factors to symptomatic
infection
Include :
 Hypochlorhydria
 Various immune system deficiencies
 Blood group A
 Malnutrition

45. GIARDIASIS
• Giardiasis usually represents a zoonosis with
cross-infectivity between animals and
humans. Giardia intestinalis has been isolated
from the stools of beavers, dogs, cats, and
primates

47. LIFE CYCLE:
STAGE 1:
The cysts are hardy and can survive several
months in cold water.
Infection occurs by the ingestion of cysts in
contamination of water or food or fecal-oral route.
STAGE 2:
In the small intestine, excystation releases
trophozoites (each cysts produce two
trophozoites).

48. STAGE 3:
Trophozoites multiply by longitudinal binary
fission, remaining in the lumen of the proximal
small bowel where they can be free or
attached to the mucosa by a ventral sucking
disk.
STAGE 4:
Encystation occurs as the parasites transit
towards the colon.
The cysts is the stage found most commonly in
non-diarrheal feces.

49. STAGE 5:
Because the cysts are infectious when passed
in the stool or shortly afterward , person to
person transmission is possible.
While animals are infected with giardia, their
importance as a reservoir is unclear.

50. Giardia life cycle
Giardia has one of the simplest life cycles of all
human parasites
The life cycle is composed of 2 stages:
(1) The trophozoite which exists freely in
the human small intestine
(2) The cyst, which is passed into the
environment.
No intermediate hosts are required.

51. The trophozoite form of G lamblia
The trophozoite form of G lamblia
⚫ Teardrop-shaped
⚫ Measures 9-21 micrometers long by
5-15 micrometers wide.
29

52. GIARDIA CYST

56. CLINICAL
PRESENTATION
39
Clinical signs and symptoms
 Diarrhea  Nausea  Low-grade fever
(infrequent)
 Malaise,
weakness
 greasy stools  Various neurologic
symptoms (e.g.,
irritability, sleep disorder,
mental depression, )
 Abdominal
distention
 Anorexia
 Flatulence  Weight loss
 Abdominal
cramps
 Vomiting  Urticaria

57. Diarrhea is the most common symptom of acute
Giardia infection, occurring in 90% of
symptomatic subjects
Abdominal cramping, bloating, and
flatulence occur in 70% of symptomatic
patients

58. Gastrointestinal manifestations
Abrupt onset (rare)
 a small number of persons develop abrupt onset
of :
 these symptoms last 3-4 days
• Explosive watery diarrhea • Vomiting
• Abdominal cramps • Fever
• Foul flatus • Malaise

59. Sub acute syndrome ( More common)
 After the symptoms of abrupt onset
 Most patients experience a more insidious onset
of symptoms, which are recurrent or resistant.
 Stools become mal odorous, mushy, and greasy
 Watery diarrhoea may alternate with soft stools or
even constipation

60. Upper GI symptoms:
often exacerbated by eating
 accompany stool changes
may be present in the absence of soft stools.
These include:
 upper and mid abdominal cramping
 nausea
 early satiety
 bloating
 substernal burning
 acid indigestion.
43
Gastrointestinal manifestations

61. Constitutional symptoms
Anorexia, fatigue, malaise, and weight
loss are common
Weight loss occurs in more than 50% of
patients
Chronic illness may occur
• Adults may present with long-standing
malabsorption syndrome
• children may present with failure to
thrive
44

62. Extraintestinal manifestations
Are rare
Include allergic manifestations such as:
 Urticaria
 Erythema multiforme
 Bronchospasm
 Reactive arthritis
 Biliary tract disease
The etiology is likely a result of :
 Host immune system activation
 Cross-reactivity/molecular mimicry.
45

63. Complications of giardiasis
May include the following:
Development of chronic illness with weight loss
Malabsorption syndrome in adults
Failure to thrive in children
Disaccharidase deficiency
Zinc deficiency in schoolchildren
Growth retardation 2
Persistent gastrointestinal symptoms 49

64. diagnosis
Stool examination
• Ideally, 3 specimens from different days
should be examined because of potential
variations in fecal excretion of cysts.
• G intestinalis is identified in 50-70% of
patients after a single stool examination and
in more than 90% after 3 stool examinations.
Stool ova and parasite (O&P) examination
aids in the diagnosis of giardiasis in 80-85% of
patients

65. The diagnosis
Stool antigen enzyme-linked immunosorbent assays
 These tests are best used as a screening test
in high-incidence settings such as:
• Day-care centers
• For identification of subjects during an
epidemic,
 They should not take the place of stool
microscopy.

66. diagnosis
Stool antigen enzyme-linked immunosorbent assay
(ELISA) may be helpful ,If the results from 3 OVA &
PARASITE tests are negative and giardiasis is still
suspected
Upper endoscopy with biopsies and duodenal
aspirate is a reasonable alternative

67. Differential diagnoses of Giardiasis
• Amebiasis • Food poisoning • Sprue
• Crohn disease • Irritable bowel
syndrome
• Strongyloidiasis
• Cryptosporidiosis • Lactose
intolerance
• Viral
gastroenteritis

68. Treatment
Generally, do not treat asymptomatic persons who
excrete the organism, except to :
 Prevent household transmission( e.g., from
toddlers topregnant women or topatients with
hypogammaglobulinemia or cystic fibrosis)
 Permit adequate treatment in individuals with
possible Giardia intestinalis –associated antibiotic
malabsorption who require oral antibiotic
treatment for other infections 54

69. Treatment
Metronidazole is the most commonly
prescribed antibiotic for this condition
Appropriate fluid and electrolyte
management is critical, particularly in
patients with large-volume diarrheal
losses 55

70. Prognosis
The prognosis for patients with giardiasis is
generally excellent.
Most patients are asymptomatic
Most infections are self-limited.
Giardiasis is not associated with mortality
except in rare cases of extreme dehydration,
primarily in infants or malnourished
children.

71. Prognosis
The prognosis for patients with giardiasis is
generally excellent.
 Most patients are asymptomatic
 Most infections are self-limited.
Giardiasis is not associated with mortality
except in rare cases of extreme dehydration,
primarily in infants or malnourished
children.

72. Prevention
Careful hand washing
 Infected persons and persons at risk
should carefully wash their hands after
they have any contact with feces
 Careful hand washing is important,
especially for caregivers of diapered
infants in day-care centers

73. Dr. G CHANDRA SEKHAR NAIDU
MD Paediatrics