Dysentery, shigellosis, bacillary dysentery, amoebic dysentery, loose or watery stool, blood in stool, giardiasis.

1. Dr. Faisal 2015 Batch
DUMC
Dysenteries
 Dysenteryreferstothe presence of grosslyvisible bloodinthe stoolsand diarrhoeawith
abdominal cramps,tenesmusandpassage of mucusinthe stools isconsequence of infectionof
the colon by eitherbacteriaoramoeba.
 There are 2 main formsof dysenteries—bacillaryandamoebic.
Bacillary Dysentery (Shigellosis)
INTRODUCTION
 Bacillarydysenteryismuch more commoninchildrenthanamebicdysentery.
 The bacteriacausingbloodydiarrheaare Shigellaspecies(S.dysenteriae,S.flexneri,S.boydii and
S. sonnei.),enteroinvasive andenterohemorrhagicE.coli,SalmonellaandCampylobacterjejuni.
 S. flexneri isthe commonestorganismreportedindevelopingcountriesand
 S. dysenteriaeisassociatedwithepidemicsof dysentery.
TRANSMISSION
 Infectionoccursbyfoeco-oral route andisseenwithpoorpersonal hygiene,indensely populated
areas,and withcontaminatedfoodandwater.The commonhouseflyplaysa role inspreadof
infection.
CLINICAL MANIFESTATION / CLINICAL FEATURES / SIGN & SYMPTOMS
 A childwithbacillarydysenterypresentswithfeveranddiarrhea.Diarrheamaybe wateryto start
with,butthenshowsmucusand bloodmixedwithstools.
 There istenesmus,whichreferstoineffectual defecationalongwithstrainingandsuprapubic
discomfort.
Grossly, earlyintestinal lesionsappearassmall areasof elevationonthe mucosal surface.In
advancedcases,typical flask-shapedulcershavingnarrow neckandbroadbase are seen.They
are more conspicuousinthe caecum,rectumandinthe flexures (Fig. 1).
Microscopically, the ulceratedareashowschronicinflammatoryreactionconsistingof
lymphocytes,plasmacells,macrophagesandeosinophils.The trophozoitesof Entamoeba are
seeninthe inflammatoryexudate andare concentratedatthe advancingmarginof the lesion.

2. Dr. Faisal 2015 Batch
DUMC
Intestinal amoebaecharacteristicallyhave ingestedredcellsintheircytoplasm.Oedemaand
vascularcongestionare presentinthe areasurroundingthe ulcers.
A. The luminal surface shows multiple
ulcers some of which are deep and are
flask-shaped with narrow neck and
broad base (arrow) containing necrotic
tissue and undermined margins.
B. Trophozoites of Entamoeba histolytica
are seen at the margin of ulcer (arrow).
COMPLICATION
 The illnessmaybe complicatedbydehydration,dyselectrolytemia,hemolyticuremicsyndrome,
convulsions,toxicmegacolon, intestinal haemorrhage,perforation&stenosis, rectal prolapse,
polyarthritisandiridocyclitis and,veryrarely,Shigellaencephalopathy.
TREATMENT
 Administrationof ORS,continuationof oral diet,zincsupplementation andantibiotics are the
componentsof treatment.
 Stool culture andsensitivityshouldbe sentfor before startingempirical antibiotics.Antimicrobial
agentsare the mainstayof therapyof all cases of shigellosis.Basedonsafety,low costand

3. Dr. Faisal 2015 Batch
DUMC
efficacy, ciprofloxacin(15mg/kg/day intwodivideddosesfor3days) has beenrecommendedby
WorldHealth Organization(WHO) asthe firstline antibioticforshigellosis.
 However,antimicrobial resistancetofluoroquinoloneshadincreasedsignificantlyfrom2002 to
2011 and onlyceftriaxonehasbeenshowntobe uniformlyeffective.Keepingthisinmind,
intravenous ceftriaxone (50-100 mg/kg/dayfor 3-5 days) shouldbe the firstline of treatmentin
a sick child.
 In a stable child,eitherciprofloxacinororal cefixime maybe given,butthe patientshouldbe
monitoredforclinical improvementwithin48hr ( decrease infever,stool frequencyandbloodin
stools).
 If no improvementisseenat48 hr, antibioticsshouldbe changedappropriately.
 Oral Azithromycin(10mg/kg/dayfor3 days) can be usedforshigellosisbutthe experience is
limited.
Amoebic Dysentery (Amebiasis)
INTRODUCTION
 Amebiasis is defined as infection with Entamoeba histolytica.
 Amebic dysentery is less common among children.
 The onset is insidious.
 Tinidazole or metronidazole is the drug of choice.
 Any young child presenting with blood in stools and persistent abdominal pain should be
suspected to have intussusception and evaluated accordingly.
 Clinical features of amebiasis range from asymptomatic colonization to amebic dysentery
and invasive extraintestinal amebiasis, occurring most commonly as liver abscess.
 It is more prevalent in the tropical countries and primarily affects the large intestine.
Infection occurs from ingestion of cyst form of the parasite. The cyst wall is dissolved in
the small intestine from where the liberated amoebaepass into the large intestine.
 Here, they invade the epithelium of the mucosa, reach the submucosa and produce the
characteristic flask-shaped ulcers.
EPIDEMIOLOGY

4. Dr. Faisal 2015 Batch
DUMC
 E. histolytica is thought to infect 10% of the world's population and 2-55% Indians.
However, these may be overestimates, because two morphologically identical,
genetically distinct but apparently nonpathogenic Entamoeba species, namely E. dispar
and E. moshkovskii, cause most asymptomatic cases.
 Amebic dysentery and extraintestinal amebiasis is associatedwith a high rates of
morbidity and mortality. It is less common in children, accounting for less than 3% of
diarrhea in children below 5 yr.
ETIOPATHOGENESIS
 An ingested cyst divides in the small intestine to form 8 trophozoites that colonize the
mucosa of the large intestine. Trophozoites cause tissue invasion and destruction with
little or no local inflammation, resulting in characteristic flask shaped ulcers in cecum,
transverse colon and sigmoid colon.
 Extraintestinal complications occur when trophozoites invade the bloodstream and
migrate through the portal circulation to lodge, most commonly, in the liver.
 Amebic liver abscess is usually single (95%) and more frequently involves the
posterosuperior part of right lobe of the liver.
 The abscess may regress, rupture or disseminate; transdiaphragmatic rupture may cause
amebic empyema and pulmonary amebiasis.
 Rare complications include amebic involvement of peritoneum, pericardium, pleura,
lungs, brain, genitourinary system and skin.
CLINICAL FEATURES
 Asymptomatic cyst passage is the most common manifestation of E. histolytica.
 In most cases the infection resolves spontaneously; uncommonly, amebic dysentery and
other invasive manifestations may occur later.
 After an incubation period varying from weeks to months, about 10% individuals
colonized with E. histolytica develop symptomatic disease.
 Amebic colitis presents as abdominal pain or tenderness (in 80%), with watery, bloody or
mucous diarrhea. Some may have only intermittent diarrhea alternating with
constipation. Fever is unusual.
 Occasionally, fulminant amebic colitis may occur, with profuse bloody diarrhea, fever,
widespread abdominal pain, diffuse tenderness and pronounced leukocytosis. Toxic

5. Dr. Faisal 2015 Batch
DUMC
megacolon, ameboma, cutaneous amebiasis and rectovaginal fistulae can occur as
complications of intestinal amebiasis.
COMPLICATIONS
Complications of intestinal amoebic ulcers (flask shape) are listed below.
1. Amoebic liver abscess
2. Amoebic hepatitis
3. Intestinal perforation
4. Intestinal haemorrhage
5. Formation of amoeboma which is a tumour-like mass.
 Amebic liver abscess, seen in about 1 % of infected individuals, may occur months to yr
after infection.
 While some individuals may have concurrent amebic colitis, more commonly, there are
no bowel symptoms.
 The child usually presents with fever with chills and rigors and right upper quadrant pain
of acute onset (<10 days).
 Examination reveals toxicappearance, right upper quadrant tenderness and
hepatomegaly; jaundiceis unusual (10- 15%).
 Cough along with dullness or crepitations in the right lung base may be present.
Complications include rupture into the pleura pericardium and superinfection with
bacteria.
DIAGNOSIS
 Diagnosis of amebic colitis is established by demonstration of motile trophozoites by
direct microscopic examination of fresh fecal sample.
 At least 3 stool specimens taken on consecutive days should be examined because the
test has poor sensitivity ( <60%; -90% with 3 fresh samples).
 Stool contains plenty of erythrocytes but few leukocytes, unlike bacillary dysentery,
where leukocytes are plentiful.
 Presence of ingested erythrocytes within trophozoites is pathognomonic for E.
histolytica. Presence of cysts of E. histolytica in stool samples is of no clinical significance
and should not be treated.
 Serological tests are routinelyemployedfordiagnosisof extraintestinal disease with E.
histolyticaespeciallyfordifferentiatingamebicfrompyogenicliverabscess.
They are positive in70-80% patientswithinvasive diseaseatpresentationandin>90% cases
beyondfirstweekof symptoms.

6. Dr. Faisal 2015 Batch
DUMC
 IgG antibodies persistforyrafterE. histolyticainfection,whereasthe IgMantibodiesindicate
presentorcurrent infection.
 Commonlyusedserologictestsinclinical practice are ELISA,IHA andIFA.Serological response as
detectedby ELISA becomesnegative6-12 monthsafterinfection.
 The IHA testis simple toperformandhasbeenshown tobe highlyspecific(-99%) andsensitive.
 The test maystay positive foraslongas 10 yr followingcompleterecovery,limitingitsutilityin
endemicareas.
 The IFA testisrapid,reliable,reproducibleand helpstodifferentiate amebicliverabscessfrom
othernonamebicetiologies.
 In case of a liverabscess chestradiographshowselevated diaphragmandpleural reactionon
the right side.
 Ultrasound,CT,MRI, or isotope scan can localize the abscess inmostcases. Leukocytosis
withouteosinophilia, mildanemia,raisedalkaline phosphatase,andahigherythrocyte
sedimentationrate (ESR) are commonlaboratoryfindingsinthese patients.
TREATMENT
 The practice of givingantiamoebicdrugsforall children presentingwithdiarrheashouldbe
stronglydiscouraged since amebiasisisrelativelyuncommoninyoungchildren. Metronidazoleis
the drug of choice fortreatingamebic colitis(Table 10.14).
 Alternativesinclude tinidazole, orindazoleandsecnidazole.Since metronidazoledoesnot destroy
the cysts,a luminal agent(paromomycin, iodoquinol,ordiloxanidefuroate)shouldbe usedto
eradicate colonization.
 Whenpossible,fulminantamebiccolitis,evenwithperforation,ismanaged conservatively, with
the additionof antibioticstodeal withbowelflora. Mostamebicliverabscesses,evenlarge ones,
can be curedwithoutdrainage.Mostpatientsshow a response totreatment(reducedfeverand
abdominal pain) within 72-96 hr.
 Individuals withamebicliverabscessshould alsoreceive aluminal agenttoeliminateintestinal
colonization.TherapeuticaspirationguidedbyCTinthe treatmentof uncomplicatedamebicliver
abscessis controversial.
 Large amebicliverabscesses(>300 ml) may benefitfromaspirationwithdecrease indurationof
hospital stayandfasterclinical improvementrecovery whencomparedtothose managed
medicallyalone.
 Abscesscavityresolvesslowlyoveraperiodof several months.
 Aspirationisreservedforindividualsinwhom diagnosisisuncertain(where pyogenicabscessor
bacterial superinfectionisaconcern),those whohave not respondedtometronidazoletherapy
(persistentfeverorabdominal painafter4 daysof treatment),individuals withlarge leftlobe

7. Dr. Faisal 2015 Batch
DUMC
abscesses(because of the riskof rupture intothe pericardium),size more than 8-10 cm
(suggestingimpendingrupture) andseverelyill patientswithan acceleratedclinical course and
large abscesses.
 Aspiration, percutaneous catheterdrainage,orboth,improve outcomes inthe treatmentof
amebicempyemaafterliverabscessrupture,andintreatmentof amebicpericarditis or
peritonitis.
Giardiasis
INTRODUCTION
 Giardiasis, caused by Giardia lamblia (also known as G. intestinalis or G. duodena/is), is a
major cause of diarrhea in children and in travelers.
EPIDEMIOLOGY
 The infection is endemic in developing countries with poor sanitation. Individuals with
malnutrition, humoral immunodeficiencies and cystic fibrosis are particularly susceptible.
Children appear to be more severely affected than adults.
ETIOPATHOGENESIS
 Giardia exists in two stages, cysts and trophozoites. Outside the human body it exists in
the form of cysts.
 Cysts are hardy, capable of surviving in cool, moist environments for up to 2 months and
in water that has been routinely chlorinated, but are destroyed by boiling for 10 min.
 Transmission of infection is through cysts, which may be ingested in contaminated water
or food or spread by direct person-to-person contact.
 Ingestion of 10-100 cysts is sufficient for causing infection.
 Low pH of the duodenum facilitates excystation and release of trophozoites.
Trophozoites colonizethe duodenum and proximal jejunum of the host, where they
attach to the intestinal brush border.
 It is believed that the infection causes diarrhea via a combination of intestinal
malabsorption and hypersecretion.

8. Dr. Faisal 2015 Batch
DUMC
 These effects cause malabsorption and maldigestion and in addition, may facilitate the
development of chronic enteric disorders, including inflammatory bowel disease and
irritable bowel syndrome.
CLINICAL FEATURES
 The incubation period after ingestion of cysts is 1-2 weeks.
 Most infections in both children and adults are asymptomatic.
 Symptomatic infections are more common in children than in adults and usually take the
form of acute diarrhea with sudden onset of explosive, watery, foul smelling stools, along
with nausea and anorexia; others may also have abdominal distension, flatulence,
epigastric cramps and mild fever.
 There is no blood or mucus in stools.
 The illness may last 3--4 days and is usually self limiting in normal immunocompetent
children.
 Variable degree of malabsorption may occur.
 Some patients may have a protracted course, with persistent or recurrent mild to
moderate symptoms such as brief episodes of loose foul smelling stools alternating with
constipation.
 Persistent diarrhea may be seen in 30-50% cases.
 A few children may develop chronic diarrhea, lactose and fat malabsorption and failure to
thrive.
DIAGNOSIS
 Diagnosis of giardiasis is established by microscopic examination of at least 3 fresh
specimens of stools collected on alternate days. There is no blood or leukocytes in stools.
Enzyme immunoassay (EIA) and direct fluorescent antibody test for Giardia antigens in
stools have been reported to have better sensitivity and require less expertise than
traditional microscopy.
 Where diagnosis is strongly suspected, duodenal aspirate or biopsy may yield high
concentration of Giardia when fresh wet mount is examined for trophozoites.

9. Dr. Faisal 2015 Batch
DUMC
 Where duodenal aspirate is negative, intestinal biopsy may be considered in presence of
features like lactose malabsorption or abnormal radiographic findings (edema or
segmentation in small intestine), or a suggestive setting like absent secretory IgA or
hypogammaglobulinemia.
TREATMENT
 All symptomatic cases-acute and persistent diarrhea, failure to thrive and malabsorption
syndrome-require drug treatment.
 Asymptomatic cyst carriers are not treated except in specific situations like for outbreak
control or for prevention of spread from toddlers to immunocompromised family
members.
 Treatment options are listed in Table 10.15.
TABLE 10.15: AGENTS FOR TREATMENT OF GIARDIASIS
Drug Dosage
Drugs of choice
Tinidazole
50 mg/kg (maximum 2 g) orally, single dose
Metronidazole
5-10 mg/kg (maximum 250 mg) orally q 8 hr for 7 days
Nitazoxanide
Age 1-3 yr: 100 mg orally q 12 hr for 3 days
Age 4-11 yr: 200 mg orally q 12 hr for 3 days
Age >11 yr: 500 mg orally q 12 hr for 3 days

10. Dr. Faisal 2015 Batch
DUMC
Alternative agents (drugs)
Albendazole
10-15 mg/kg (maximum 400 mg) orally once daily for 5 days
Mebendazole
200 mg orally q 8 hr for 5 days
Paromomycin*
10 mg/kg orally q 8 hr for 5-10 days
Furazolidone
1.5 mg/kg (maximum 100 mg) orally q 6 hr for 7-10 days
Quinacrine
2 mg/kg (maximum 100 mg) orally q 8 hrfor 5 days
*Has poor intestinal absorption; useful in treating giardiasis during Pregnancy "Monoamineoxidase inhibitor;
significant food and drug interactionsif used for >5 days