Giardiasis is caused by the intestinal parasite Giardia lamblia. It commonly causes epidemic and endemic diarrhea worldwide. The life cycle involves a trophozoite stage that colonizes the small intestine and a cyst stage that is passed in feces and can survive for months in the environment. Symptoms range from asymptomatic cyst passage to acute or chronic diarrhea. Diagnosis is made by identifying cysts or trophozoites in stool samples. Treatment involves antimicrobial drugs. Prevention focuses on proper water treatment and hygiene practices.

1. GIARDIASIS
M.Moghadami Internist, subspecialist of infectious disease
1

2. INTRODUCTION
 van Leeuwenhoek 1600
 Giardia lamblia (intestinalis and duodenalis )
1900s
 intestinal flagellates in the division Protozoa
 Human but other such as dog, cat, cow,
beaver, and sheep
2

3. • A common cause of epidemic and endemic
diarrhea in world
3

4. SPECIES
 Giardia lambelia in human
 Giardia muris ,G agilis, G microti, G psittaci
4

5. LIFE CYCLE: TROPHOZOITE
 freely living stage
 9 to 21 μm long
and 5 to 15 μm
wide
 Morphology
 Growth : biliary
lipids, a high
concentration of
cysteine, and low
oxygen tension
5

6. LIFE CYCLE: CYST
 smooth, oval, thin-walled
cysts 8 to 12 μm long
and 7 to 10 μm wide
 Encystation: cholesterol
starvation ,alkaline pH
 Excystation :gastric acid
and pancreatic enzymes
6

7.  Cyst resistance to cholorization
 3 month stay alive
 Production in terminal illeum
7

8. EPIDEMIOLOGY
 Giardia is distributed throughout the world. In
US G. lamblia has been demonstrated in 4%
to 7% of stool specimens, making it the most
commonly identified intestinal parasite.
 In resource-poor regions of the world,
Giardia is one of the first enteric pathogens
to infect infants, with peak prevalence rates
of 15% to 30% occurring in children younger
than 10 years.
8

9. 
‫کان‬ ‫کود‬
3
‫بزرگساالن‬ ‫برابر‬

‫خانه‬ ‫یتیم‬ ‫و‬ ‫مدارس‬ ‫و‬ ‫ها‬ ‫کودک‬ ‫مهد‬

‫زیر‬ ‫وکودکان‬ ‫بارداری‬ ‫در‬ ‫زنان‬
5
‫سال‬

‫انسان‬ ‫در‬ ‫تنها‬ ‫مخرن‬
9

10. 
‫شرقی‬ ‫آذربایجان‬ ‫در‬
( :
‫زاده‬ ‫شریعت‬ ‫دکتر‬ ‫مطالعه‬
)
6609
‫ترین‬ ‫شایع‬ ‫ژیاردیا‬ ‫نفر‬
15/2
%
‫و‬ ‫ارومیه‬ ‫در‬
43/8
%
‫نقده‬ ‫در‬
10

11. 110
‫لرستان‬ ‫دانشجو‬
(
‫زاده‬ ‫نایب‬ ‫دکتر‬ ‫مطالعه‬
)
8/4
%
‫و‬ ‫انگل‬ ‫به‬ ‫آلودگی‬
3.9
%
‫ردیا‬ ‫ژیا‬ ‫به‬ ‫آلودگی‬
‫مازندران‬ ‫روستا‬
:
10.2
%
‫آلودگی‬
11

12. ROUTES OF INFECTION
 contaminated water : Recreational
water ,Backpackers , water treated by a
faulty purification system,
 food borne transmissions
 person-to-person :young children in
daycare centers (30-50% cyst passer)
12

13. PATHOGENESIS
 Infection ingestion of as few as 10 to 25
cysts
 After excystation, colonize and multiply in
the upper small bowel.
 Adherence in gut is via the ventral disk, with
attachment at the brush border of
enterocytes .
13

14.  Avoidance of peristalsis
 Disruption of brush border cells
 Disacharidse defeciency
 Rarely invasion,enterotoxin,..
14

15. GI INVOLVMENT
 Duodenum: 82.5%
 Jejunum: 2,1%
 Stomach: 8.7%
 Ileum: 12.1%
 Colon: 0.4%
15

16. IMMUNE RESPONSE
 Important in clearing of infection
 Prevalence in developing countries is higher
in younger ages
 Humoral immunity
 Cellular immunity
 Inflammatory response enterocytes
damage
 Human milk
16

17. PREDISPOSITION
 common variable immunodeficiency and in
children with X-linked agammaglobulinemia
 gastric surgery and reduced gastric acidity
 Role of HIV Infection
17

18. 18

19. CLINICAL MANIFESTATIONS
19
 asymptomatic cyst passage
 acute self-limited diarrhea
 chronic syndrome of diarrhea,
malabsorption, and weight loss

20.  100 ingesting cysts, an 5% to 15%
asymptomatic cyst passers, 25% to 50%
symptomatic with an acute diarrheal
syndrome, and the remaining 35% to 70%
have no trace of infection.
20

21. ACUTE DIARRHEA
 acute onset of diarrhea, abdominal
cramps, bloating, and flatulence
 symptomatic for more than 1 week to 10
days
 severe illness
21

22. CHRONIC DIARRHEA
 profound malaise
 diffuse abdominal and epigastric discomfort
 Small volume ,greasy stool
 Weight loss
 Periodic diarrhea
 Malabsorption
 post-Giardia lactose intolerance
 As cause for growth retardation?
22

23. DIAGNOSIS
 should be considered in all patients with
prolonged diarrhea, particularly that which is
associated with malabsorption or weight loss
 OB & OP Examination:
Giardia should be identified 60% to 80% of
the time after one stool, and some report
over 90% identification after three stools
23

24. ANTIGEN ASSAYS
 85% to 98% sensitive and 90% to 100%
specific
 CWP-1 by ELISA, fluorescein-tagged
monoclonal antibodies ,….
24

25. SAMPLING OF THE DUODENAL CONTENTS
 the string test or Entero-Test (HDC
Corporation, Milpitas, CA),
 duodenal aspiration
 duodenal biopsy
25

26. TREATMENT
 Indication
 Drugs
 Pregnant ladies
26

27. PREVENTION
 proper handling and treatment of water used
for communities
 good personal hygiene on an individual basis
27

28. AMEBIASIS

29. ENTAMOEBA HISTOLYTICA
 Entamoeba species (histolytica and
dispar) close to lowest branch of
eukaryotic tree
 Although the organism was
originally thought to lack
mitochondria, nuclear-encoded
mitochondrial genes and a
remnant organelle have now been
identified.
 E. histolytica and E. dispar
trophozoites are morphologically
indistinguishable, ranging in size
from 10 to 60 μm, with an average
of 25 μm

30.  Pseudopod-forming, non-flagellated
protzoa
 Replicate by binary fission
 Most invasive parasite of the Entamoeba
group
 Only member that causes: Amebic colitis
& liver abscess

31. AMEBAS INTESTINALES
 Entamoeba
_E.histolytica (patogena)
_E.coli
_E.hartmani
_E.gingivalis(oral)

33.  Trophozoites of Entamoeba
histolytica (Trichrome stain).
Two diagnostic
characteristics:
Two of the trophozoites have
ingested erythrocytes, and
the nuclei have typically a
small, centrally located
karyosome, as well as thin,
uniform peripheral chromatin.

34. Free-living E. histolytica with
Ingested RBCs

35. EPIDEMIOLOGY
 worldwide incidence = 0.2-10%
 estimated that 10% of world’s
population may be infected
 50 million cases of invasive amebiasis/yr
 100,000 deaths/yr

36. Region Infection Disease Death
Africa 85 million 10 million 10-30
thousand
Asia 300 million 20-30 million 25-50
thousand
Europe 20 million 100 million minimum
America 95 million 10 million 10-30
thousand
total 650 million 150-200
million
40-110
thousand

37. EPIDEMIOLOGIC RISK FACTORS
Persons with lower socioeconomic status in endemic area, including those
with Crowding
Immigrants from endemic area
Institutionalized populations, especially developmentally and cognitively impaired
Promiscuous male homosexuals
malnourished individuals at any age
acquired immunodeficiency syndrome??

38. TRANSMISSION
 Faeces- mouth
 Contaminated water
 Contaminated meals
 Street vendors of meals

39. LIFE CYCLE
 A cyst that is excreted into the environment is ingested by a human host
though a fecally contaminated product. The cyst then undergoes excystation in
the small bowel, becoming a trophozoite. The trophozoite, attaches to the
colonic mucin and then reproduces by clonal expansion, most commonly in the
cecum.
 Encystment
 cysts may survive for as long as 48 hours at 20° to 25° C on foods and have
been found to remain viable in sewage and natural surface water, at 4° C, for 1
month.

40. PATHOGENESIS
• Adhesion (The trophozoite possesses a surface protein (lectin) that
recognizes the sugars galactose and N-acetylgalactosamine on the host
cell surface)
• Colitis results when the trophozoite penetrates the intestinal mucous
layer, which otherwise acts as a barrier to invasion by inhibiting amebic
adherence to the underlying epithelium and by slowing trophozoite
motility.
• killing of epithelial cells, neutrophils, and lymphocytes
• amoebapore, caspase 3,host inflammatory response

41. PATHOLOGY
 A spectrum of colonic lesions
ranging from nonspecific
thickening of the mucosa to the
classic “flask-shaped” ulcer may be
associated with amebic infection
 Liver abnormality :necrotic abscess
or periportal fibrosis, ascending
the portal venous system ,
proteinaceous debris rather than
white cells and is surrounded by a
rim of amebic trophozoites
invading tissue

44. HOST IMMUNITY
 IgA and IgG response to the lectin protein.
 Serum IgA antibody responses are found in subjects with asymptomatic E.
histolytica infection, but not during infection with E. dispar.
 Cell-mediated immune defense mechanisms probably have a role in limiting
invasive disease and resisting a recurrence after pharmacologic cure
 Cell-mediated responses have been described in patients with amebic liver
abscess.

45. CLINICAL MANIFESTATIONS
Intestinal Disease Extraintestinal Disease
Asymptomatic infection Liver abscess
Symptomatic noninvasive infection Liver abscess complicated by
Acute rectocolitis (dysentery) Peritonitis
Fulminant colitis with perforation Empyema
Toxic megacolon Pericarditis
Chronic nondysenteric colitis Lung abscess
Ameboma Brain abscess
Perianal ulceration Genitourinary disease

46. ASYMPTOMATIC INTESTINAL INFECTION
• Noninvasive intestinal infection may be established by confirmation of E.
histolytica in the stool in association with Hemoccult-negative stools, and
normal mucosa on colonoscopy
• In contrast to infection with E. dispar, asymptomatic infection with E.
histolytica is associated with a serum anti-amebic antibody response,
and frequently a stool antigen test will be positive .
• approximately 10% of patients will go on to manifest invasive
disease and most individuals will clear their infection within 18 months.
• Asymptomatic infection should be treated because of its potential to
progress to invasive disease.

47. INVASIVE INTESTINAL DISEASE
• Patients with amebic colitis typically present with a several-week history
of cramping abdominal pain, weight loss, and watery or bloody diarrhea.
The insidious onset and variable signs and symptoms make diagnosis
difficult, with fever and grossly bloody stool absent in most cases.
• Fulminant colitis : predisposition for occurring in malnourished, pregnant
women, recipients of corticosteroids, or very young patients. Such
patients are severely ill with fever, leukocytosis, profuse bloody mucoid
diarrhea, and widespread abdominal pain.
• Toxic megacolon : occurs in 0.5% of cases, and is a definite
complication of inappropriate corticosteroid therapy. Recognition is
important because these patients do not respond to drug therapy and
require colectomy

49. HISTOPATHOLOGY OF A TYPICAL FLASK-
SHAPED ULCER OF INTESTINAL
AMEBIASIS

50. AMEBOMA:
 Segmented mass of granulation tissue in the cecum or ascending
colon
 Occurs in 0.5% to 1.5% of patients with intestinal amebiasis
 Tender palpable abdominal mass
 Concurrent amebic dysentery present in 2/3 of patients
 “Apple-core” lesions on barium enema study
 Lesions resolve with anti-amebic chemotherapy
 Intestinal constriction occurs in the colon in <1% of patients

51. EXTRAINTESTINAL AMEBIASIS

52. LIVER ABSCESS
 can appear concurrently with colitis, but more
frequently there is no evidence or history of
recent intestinal infection by E. histolytica.
 Liver abscess can manifest with an acute
onset (less than 10 days) with abdominal
pain and fever or subacutely , with weight
loss being prominent and less than half the
patients having fever or abdominal pain.

53. LABORATORY FINDINGS IN LIVER ABSCESS
 leukocytosis in 80%
 mild anemia > 50%
 elevated alkaline phosphatase 80%
 Elevated transaminase levels in more aggressive
disease, and a
 Elevation erythrocyte sedimentation rate

54. LIVER ABSCESS COMPLICATION
Complications of amebic liver abscess may arise from rupture
of the abscess with extension into the peritoneum, pleural
cavity, or pericardium. Extrahepatic amebic abscesses have
occasionally been described in the lung, brain, and skin and
presumably result from hematogenous spread.

56. GROSS PATHOLOGY OF LIVER
CONTAINING AMEBIC ABSCESS

57. AMEBIC LIVER ABSCESSES

58. GROSS PATHOLOGY OF AMEBIC ABSCESS OF LIVER.
TUBE OF "CHOCOLATE" PUS FROM ABSCESS.

59. DIAGNOSIS OF INTESTINAL AMEBIASIS
• In developing countries, intestinal amebiasis is most commonly
diagnosed by identifying cysts or motile trophozoites on a saline wet
mount of a stool specimen. The drawbacks of this method include its low
sensitivity and false positive results owing to the presence of E. dispar or
E. moshkovskii infection.
• The diagnosis should ideally be based on the detection in stool of E.
histolytica specific antigen or DNA and by the presence of antiamebic
antibodies in serum.
• the trophozoites have ingested red blood cells, they may be assumed to
be E. histolytica and the patient should be treated. If, however, there is
no such distinguishing microscopic feature, a serum antibody test, stool
antigen test, or both should be utilized to confirm the diagnosis of E.
histolytica and not E. dispar infection, prior to initiation of treatment

61. THERAPY OF CYST PASSER
Type Efficacy (%)
Paromomycin, 30 mg/kg/day in 3 divided
doses for 5–10 days
85–90
Tetracycline, 250 mg qid for 10 days then
iodoquinol (Yodoxin), 650 mg tid for 20
days
95
Iodoquinol (diiodohydroxyquin, Yodoxin),
650 mg three times daily for 20 days

63. Therapeutic aspiration of an amebic liver abscess
is occasionally required as an adjunct to antiparasitic
therapy. Drainage of the abscess should be considered
in patients who have no clinical response to
drug therapy within five to seven days or those with
a high risk of abscess rupture, as defined by a cavity
with a diameter of more than 5 cm or by the presence
of lesions in the left lobe.