Giardia Lamblia

Giardia
 Giardia lamblia is a flagellated protozoan that
infects the duodenum and small intestine.
 range from asymptomatic colonization to acute
or chronic diarrhea and malabsorption.
 more prevalent in children
 life cycle of G. lamblia is composed of 2 stages:
 trophozoites
 cysts
 Giardia
Lamblia
 EPIDEMIOLOGY
 usually occurs sporadically
 major reservoir for spread :water contaminated
with Giardia cysts
 Giardia cysts are relatively resistant to
chlorination and to ultraviolet light irradiation
 Boiling is effective for inactivating cysts.
 Person-to-person spread also occurs .
 Human milk contains glycoconjugates and
secretory IgA antibodies that may provide
protection to nursing infants.
 CLINICAL MANIFESTATIONS
 incubation period :1–2 wk
 clinical manifestations :asymptomatic . acute infectious
diarrhea, chronic diarrhea with failure to thrive and
abdominal pain or cramping.
 Symptomatic infections occur more frequently in
children than in adults.
 Most symptomatic patients : acute diarrhea. low-grade
fever, nausea, and anorexia;
 intermittent or more protracted course characterized by
diarrhea, abdominal distention and cramps, bloating,
malaise, flatulence, nausea, anorexia, and weight loss
develops
 CLINICAL MANIFESTATIONS
 stools may be profuse and watery and later
become greasy and foul smelling
 Stools do not contain blood, mucus, or fecal
leukocytes
 Varying degrees of malabsorption may occur.
 Abnormal stool patterns may alternate with
periods of constipation and normal bowel
movements.
 Malabsorption of sugars, fats, and fat-
soluble vitamins has been well documented
and may be responsible for substantial
weight loss.
 Giardiasis has been associated with growth
stunting and repeated Giardia infections
with a decrease in cognitive function in
children in endemic areas.
 Giardiasis should be considered in young children
in child care or in any person who has had contact
with an index case or a history of recent travel to
an endemic area who has persistent diarrhea,
intermittent diarrhea and constipation,
malabsorption, crampy abdominal pain and
bloating, failure to thrive, or weight loss
 DIAGNOSIS
 established by microscopy documentation of
trophozoites or cysts in stool specimens,
 3 stool specimens are required to achieve a
sensitivity of >90%.
 Stool enzyme immunoassay (EIA) or direct
fluorescent antibody tests are more sensitive
 aspiration or biopsy of the duodenum or upper
jejunum
TREATMENT
 should receive therapy :
acute diarrhea
failure to thrive
exhibit malabsorption
 Asymptomatic excreters generally are not
treated except:
 in specific instances such as in outbreak
control, for prevention of household
transmission by toddlers to pregnant
women and patients with
hypogammaglobulinemia or cystic fibrosis,
and in situations requiring oral antibiotic
treatment where Giardia may have produced
malabsorption of the antibiotic
 Tinidazole: >3 yr: 50 mg/kg/day once daily
 nitazoxanide
 Metronidazole: 15 mg/kg/day in 3 divided doses
for 5–7 days
 Second line alternatives:
furazolidone 6 mg/kg/day in 4 divided doses for
10 days
albendazole: >6 yr: 400 mg once a day for 5 days
paromomycin, and
quinacrine :6 mg/kg/day in 3 divided doses for 5
days
 PREVENTION
 Handwashing
 purify public water supplies adequately include
chlorination and filtration.
 Travelers to endemic areas are advised to avoid
uncooked foods that might have been grown,
washed, or prepared with water that was
potentially contaminated.
 Purification of drinking water can be achieved by a
filter or by brisk boiling of water for at least 1 min
Irritable Bowel
Syndrome
What is Irritable Bowel Syndrome(IBS)?

 A group of functional bowel disorders

 Chronic abdominal complaints without a structural or
biochemical cause
 Constitutes a major health problem with
gastrointestinal (GI) symptoms
 The cause of IBS is unknown.
 Affects up to ~20 % adults in the industrialized
world
 The condition is more frequent in women.
 The direct medical costs of IBS are ~ $ US 8 billion
in the US each year.
Symptoms of IBS

 Abdominal discomfort and pain

 Bloating, mucous in stools, diarrhea, constipation, or
alternating diarrhea and constipation
 Depression, anxiety or stress
 IBS can be subdivided into
 Diarrhea-predominant (IBS-D)
 Constipation-predominant (IBS-C)
 Alternating diarrhea and constipation
Subclassification of patients
 Supportive symptoms of IBS
1. Fewer than 3 bowel movements a week
2. More than 3 bowel movements a day
3. Hard or lumpy stools
4. Loose or watery stools
5. Urgency
6. Feeling of incomplete bowel movement
7. Passing mucus during a bowel movement
8. Abdominal fullness, bloating or swelling
 Diarrhea-predominant IBS (IBS-D)
 One or more of 2, 4 or 6 and none of 1, 3 or 5
 Constipation-predominant IBS (IBS-C)
 One or more of 1, 3 or 5 and none of 2, 4 or 6
Symptom Criteria for IBS
 Rome IV criteria
 Recurrent abdominal pain, on average
≥1 d/wk in the past 3 mo, related to ≥2 of
the following:
 Defecation
 Change in stool frequency

 Change in stool form (appearance)

 Criteria
should be fulfilled for the past 3
mo with symptom onset ≥6 mo before
diagnosis
Symptom Criteria for IBS
 Manning criteria
 Toestablish IBS diagnosis, patient must
meet ≥3 criteria:
 Pain relief with defecation, often
 Looser stool at pain onset, often

 More frequent stools at pain onset, often

 Visible abdominal distention

 Mucus per rectum

 Feeling of incomplete evacuation

What is the utility of the physical
examination?
 Physical exam usually normal in patients
with IBS
 Mildabdominal tenderness may be
present
 Symptoms that suggest other diagnoses:
 Fever, weight loss
 Lymph node enlargement
 Abdominal mass, hepatosplenomegaly
 Digital rectal examination
 Evaluate for dyssynergic defecation
 Rule out rectal cancer
Which diagnostic tests are useful?
 Lab tests
 CBC, complete metabolic panel, C-reactive protein
 Thyroid profile if suspicion for thyroid disease is high
 Test for celiac disease in nonconstipated patients with IBS

 Stool sample evaluation

 Check for occult blood
 Exclude C. difficile infection in IBS-D + recent antibiotics
 Check for ova and parasites based on travel history
 Fecal calprotectin measurement to identify inflammation

 Colonoscopy, other imaging: on case-by-

case basis
 Biomarkers: evidence and consensus don’t
support use
 Traditional therapies focused on
individual symptoms of IBS with
constipation Bloating and distention
Dietary modifications 
Abdominal pain / discomfort Antispasmodics 
Antispasmodics  Antiflatulants 
Tricyclics  Abdominal Digestive enzymes 
Analgesics  pain / Bloating / Antibiotics 
discomfort distention

Irregular Constipation
Bowel or Diarrhea
Habit
Fiber 
Laxatives 
Imodium 
None of these medications effectively treat the multiple symptoms of IBS. 
May exacerbate individual symptoms e.g., fiber and bloating; antispasmodics and constipation

16
 IBS: Symptomatic Therapy

Smooth muscle relaxants Smooth muscle relaxants

5-HT agonists/antagonists 5-HT agonists/antagonists
TCAs, SSRIs Antiflatulents
Abdominal
pain/ Bloating
discomfort

Altered bowel
function
CONSTIPATION
Fibres DIARRHEA
Osmotic agents Loperamide
5-HT4 agonists Cholestyramine
Prokinetics 5-HT3 antagonists

17
Inflammatory Bowel Disease
 Overview
– Ulcerative colitis and Crohn’s disease are two main
forms of IBD, can be differentiated on basis of
genetic predisposition, risk factors, and clinical,
endoscopic and histologic features
– Exact etiology of IBD is unknown, though thought
to be related to dysregulated mucosal immune
response to commensal gut flora in genetically
susceptible individuals
 Pathophysiology
• Exact mechanism for IBD not well understood,
though to be related to combination of factors in
gut, including:
– Damage to epithelial mucin proteins and tight
junctions,
– Breakdown of homeostatic balance between host’s
mucosal immunity and enteric microflora
– Genetic polymorphisms in toll-like receptors (TLRs)
– Disrupted homeostatic balance between regulatory
and effector T-cells
 Ulcerative colitis
Epidemiology
• Higher incidence than CD
– More commonly seen in North America and Europe
• Bimodal incidence pattern
– Onset 15-30 years or 50-70s year olds
• Genetic factors: Family history very important
– Ashkenazi Jews have 3-5x higher risk
• Environmental factors
– Smoking associated with paradoxically lower risk, milder disease
– Hx of prior GI infections, e.g. Shigella, Salmonella, Campylobacter,
during adulthood double risk of developing UC, thought to be 2/2
changes in gut flora triggering chronic inflammatory process
– Weak associations between NSAIDs, OCPs and increased risk of UC
– No data supports psychological stress as trigger for onset or relapse
 Ulcerative Colitis
Clinical Presentation
• Common presenting symptoms include rectal bleeding, diarrhea, urgency,
tenesmus, abdominal pain
– More rarely can see fistulas, weight loss, more common in CD
– In severe or advanced cases, patients may present with fever
• Clinical course characterized by alternating periods of remission and relapse
• Montreal classification used to categorize extent and severity of disease
– E1 (proctitis): inflammation limited to the rectum
– E2 (left-sided; distal): inflammation limited to the splenic flexure
– E3 (pancolitis): inflammation extends to the proximal splenic flexure
– S0 (remission): no symptoms
– S1 (mild): four or less stools per day (with or without blood), absence of systemic symptoms,
normal inflammatory markers
– S2 (moderate): four stools per day, minimum signs of systemic symptoms
– S3 (severe): six or more bloods per day, pulse rate of ≥90 beats per min, temperature ≥37·5°C,
ESR >30
• Extraintestinal manifestations are more commonly seen in UC than CD
– include aphthous oral ulcers, iritis/uveitis/episcleritis, seronegative arthritis, ankylosing
spondylitis, sacroiliitis, erythema nodosum, pyoderma gangreosum, autoimmune hemolytic
anemias and primary sclerosing cholangitis
 Ulcerative Colitis
Diagnosis
• Based on clinical symptoms confirmed by objective
findings from endoscopic and histologic examinations
• Initial w/u must r/o infectious and non-infectious
causes of diarrhea
• Endoscopic features
– loss of vascular pattern, erythema, granular and friable
mucosa, erosions, ulcerations and spontaneous bleedings
• Pathologic features
– distortion of crypt architecture, crypt abscess, infiltration
of lamina propria w/ plasma cells, eosinophils,
lymphocytes, lymphoid aggregates and mucin depletion
 Ulcerative Colitis
Treatment
• Treatment should be tailored to disease
activity and extent of disease activity
– 5-ASA drugs: E.g. mesalazine, sulfasalazine
– Corticosteroids
– Immunosuppresants: E.g. azathioprine, 5-
mercaptopurine
– Biologics: E.g. infliximab, adalimumab
 Ulcerative Colitis
Treatment
• Surgical treatment required in approximately 20-
30% of patients. Surgery is generally curative in
UC.
– Emergency: Life-threatening complications related to
fulminant disease unresponsive to medical treatment
– Urgent: Severe disease admitted to hospital and not
responding to intensive medical treatment
– Elective: Refractory disease intolerant to long-term
maintenance treatments or colorectal cancer.
 Ulcerative Colitis
Prevention/Screening
• UC patients at increased risk of colorectal cancer
– 2% after 10 years, 8% after 20 years and 18% after 30 years
• Screening colonoscopy beginning at 8 years after disease
onset
• Following initial colonoscopy, subsequent screening
depends on extent of disease
– Proctitis/proctosigmoditis: Follow specific age guidelines for
surveillance of colorectal cancer
– Left-sided colitis/pancolitis: Every 1-2 years
– UC w/ PSC: Annually from time of dx of PSC
• Risk factors for CRC
– Duration and extent of disease
– Endoscopic and histologic severity of inflammation
 Crohn’s Disease
Epidemiology
• Genetic factors
– Family hx well established as one of the strongest
risk factors for development for CD
• Environmental factors
– Lifestyle factors such as tobacco use, sedentary
lifestyle, exposure to air pollution, and
consumption of western diet
• Infectious factors
– CD often occurs after infectious gastroenteritis
 Crohn’s Disease
Clinical Presentation
• Unlike in UC, Crohn’s disease can affect any portion of the GI tract
• Common presenting symptoms
– abdominal pain, bloody or watery diarrhea, incontinence, fistulas and
perianal symptoms. Extracolonic GI involvement associated with
aphthous ulcers, dysphagia, upper abdominal pain and vomiting.
• Patients with CD may have hx of other autoimmune disorders,
• Montreal classification used to categorize CD
– L-classification: Defines extent of disease
• L1: Disease confined to terminal ileum
• L2: Disease confined to clon
• L3: Disease involving ileum and colon
• L4: Disease involving upper GI tract
• L4+L3: Disease involving upper GI tract and distal disease
– B-classification: Defines phenotype
• B1: Without stricture formation, non-penetrating
• B2: Stricturing
• B3: Penetrating
• B3p: Perinally penetrating
 Crohn’s Disease
Diagnosis
• Clinical diagnosis based on H&P findings with objective
findings from history and laboratory studies
• As with UC, must r/o important non-infectious causes
(IBS, Behcet’s syndrome) and infectious causes
(Yersinia, enteroviruses etc.) that mimic CD
• Endoscopy is gold standard for diagnosis
• Radiologic tests may assist in diagnosis
– CT/MRI enterography or enteroclysis
– Abdominal U/S
• Biomarkers can also be used
– CRP, lactoferrin and calprotectin
 Crohn’s Disease
Treatment
• All patients with CD should be counseled to quit smoking
• As with UC, initial medical treatment depends on
phenotype, disease activity, comorbidities and other
individual characteristics of patient
– In most cases, short course of antibotics, steroids, or anti-TNF
agent, e.g. infliximab, adalimumab, combined with thiopurines
or methotrexate for long-term maintenance
– 5-ASA derivatives, which are mainstay of UC, have shown to be
less useful in treatment of CD
• Superiority of combination of thiopurines and TNF blockers
• No current consensus on optimal length of therapy
• Unlike in UC, surgery is not curative in CD
 Crohn’s Disease
Prevention/Screening
• Regular screen for active infection
– tuberculosis, infections hepatitis, CMV, HIV and C.
difficile
• Colorectal cancer screening
– In patients with more than a third of colon affected
(Montreal classification L3), first screening
colonoscopy should occur 8 years after onset,
repeated every 1-2 years once remission achieved,
and every 1-3 years once normal.
– Patients with PSC should undergo annual screenings