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CHAPTER 24 (A)
GASTROINTESTINAL
INFECTIONS
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Email: info@universitiespress.com
marketing@universitiespress.com
Phone: 040-2766 5446/5447
Part III
Microbiology as Applied to Infectious
Diseases

Dr Sonal Saxena, MD
Director Professor and Head of the Department of Microbiology
Maulana Azad Medical College,
New Delhi
and
Dr Amala A Andrews, MD
Maulana Azad Medical College,
New Delhi
UNIVERSITIES PRESS PVT LTD

INTRODUCTION
Gastrointestinal (GI) tract is colonised by normal flora which, along with mucosal
immunity, defend the host
Parasitic infections caused by protozoa and intestinal helminths are among the most
prevalent
Mechanism of disease production
Production of toxins
Invasion and multiplication

INTRODUCTION
Outcome of ingested pathogens
i) The pathogens produce primary pathology and disease manifestation in the gut, e.g.,
diarrheagenic Escherichia coli, Vibrio cholerae and Clostridium difficile
ii) A systemic infection is initiated in the gut, but pathology and disease are manifested
elsewhere in the body
Infections caused by Salmonella Typhi and Paratyphi A, S. schottmuller (Paratyphi B), hepatitis A
and E and polio

INFECTIONS OF
THE GIT
Gastroenteritis: Nausea, vomiting, abdominal
discomfort and loose motions (as seen in salmonellosis)
Diarrhea: Watery motions accompanied by a loss of
fluid and electrolytes; the small intestine is usually
affected (as seen with rotavirus and V. cholerae)
Dysentery: Inflammation of the large intestine,
accompanied by fever and abdominal cramps
associated with blood and mucus (pus) in stool
(Entamoeba histolytica, Shigella dysenteriae)
Enterocolitis: Affects both the large and small
intestine (Clostridioides difficile)
Food poisoning: This may be due to the ingestion of
a preformed toxin (as in clostridial infections) or due to a
toxin produced as a part of the pathogenesis of the
organism (e.g., staphylococcal food poisoning)

PATHOGENESIS
OF GI INFECTIONS
Source of gastrointestinal infection: Food
or potable water contaminated with
human or animal waste/feces (or other
environmental sources such as sewage)
Diarrhea:
Increase in fluid and electrolyte loss into
the lumen
Unformed liquid stool, which is sometimes
copious and watery
Fig. 24.1 Pathogenesis of GI
infections

TYPES OF DIARRHEA
Acute diarrhea: Predominant symptom of infective
gastroenteritis.
Chronic diarrhea is generally non-infectious
Traveller’s diarrhea
Diarrhea in children: Rotavirus and E. coli
GASTROENTERITIS
Inflammation of the stomach and intestines resulting from
bacterial invasion or toxins or viral infection
Manifests with vomiting and diarrhea

Table 24.1 Pathogenic mechanism of gastroenteritis

PATHOGENESIS
Small intestinal pathology:
Large volume, watery stools (enteritis), without pus or blood
Diagnosis based on stool examination with the unaided eye and
microscopy
Large intestinal pathology:
Frequent, small-volume stools with pus and/or blood
Diagnosis based on stool examination with the unaided eye and
microscopy
Dysentery:
Clinical condition of varying etiology
Characterised by the frequent passage of bloodstained, mucopurulent
stools
The two common types of dysentery are:
(i) Bacillary
(ii) Amoebic

ETIOLOGY
Table 24.2 Etiology of infective
gastroenteritis

FOOD POISONING
Acute manifestation of diarrhea (diarrheic type) or vomiting (emetic type)
Caused by toxins produced by microorganisms
Bacterial toxin-mediated food poisoning: Short incubation period since the toxins in the food
are preformed
i) Staphylococcus- and Bacillus cereus-related food poisoning
Incubation period of 1–6 hours
Diarrhea, abdominal cramps, nausea and vomiting are common symptoms

FOOD POISONING
ii) Food poisoning due to Clostridium perfringens
Incubation period of 8–14 hours
Caused by heat-resistant clostridial spores in tinned or processed food
Diarrhea, vomiting and abdominal cramps are the common features
iii) Botulism is a toxin-mediated disease caused by C. botulinum in
neonates and adults

FOOD POISONING
Fungal toxins or mycotoxins: Toxic metabolic products released by fungi, often
contaminate food.
Ingestion of such food results in disease
Aflatoxicosis results from the consumption of grains containing aflatoxins secreted by
Aspergillus flavus, which contaminates groundnuts, corn and peas
Ergotism results from the ingestion of rye contaminated with Claviceps purpurea

LABORATORY
DIAGNOSIS OF
GI INFECTIONS
Specimen collection
 Feces
 Rectal swab
 Outbreak of food
poisoning, the food
implicated, vomitus
and feces of the
patient
Fig. 24.2 Algorithm for the diagnosis of infective diarrhea (TCBS thiosulfate-citrate-bile
salts-sucrose agar; XLD—xylose lysine deoxycholate and DCA—deoxycholate citrate
agar)

LABORATORY DIAGNOSIS OF GI INFECTIONS
Transport:
Transport medium: Cary–Blair or Venkatraman–Ramakrishnan
For Vibrio cholerae: Alkaline peptone water
Microscopy
Wet preparation: To detect pus cells and RBCs, and ova, cysts or segments of adult
parasites
Saline and iodine preparation: To detect helminth ova, protozoan cysts and protozoan
trophozoites
Concentration techniques: Formol ether or salt floatation techniques done to increase the
positivity rate

Gram-stained smear: Has limited use in the diagnosis of GI infections
Presence of a large number of yeast cells in an immunocompromised host or infant
Presence of curved bacilli, suggestive of Vibrio
ZN stain: Modified acid-fast stain
For the identification of coccidian parasites like Cryptosporidium, Cystoisospora and
Cyclospora
Electron microscopy: For the identification of viruses

Culture of feces
Direct culture:
Non-selective media, e.g., MacConkey agar
Selective media, e.g., xyloselysine- deoxycholate (XLD) agar, deoxycholate citrate agar (DCA) or thiosulfate-
citrate-bile salt sucrose agar (TCBS) are used
Enrichment culture: To isolate pathogens if their number is small
Fresh feces are introduced into a liquid culture medium like selenite F broth, tetrathionate broth (incubated for
12–18 hours) or alkaline peptone water (6–8 hours)
Following this, a subculture is made on the solid culture medium used for direct plating

LABORATORY DIAGNOSIS
OF GI INFECTIONS
Isolated organism is identified by biochemical tests and
serotyping
Antibiotic sensitivity tests: For Shigella, Vibrio and
Salmonella isolates
Tissue culture: Done for epidemiological or research
purposes only
Serology: ELISA for the detection of E. coli O157: H7
(EHEC), Shiga toxin and C. difficile toxins
PCR: To detect Norwalk and other viral agents
Detection of enterotoxin and Rapid diagnostic tests
(RDT)

TREATMENT
Acute diarrhea: Fluid and electrolyte replacement
Viral diarrheas are self-limiting and may require only fluid and electrolyte
correction
Infective bacterial diarrheas (cholera) or dysentery (shigellosis) may
require appropriate antibiotics like ceftriaxone, ciprofloxacin and
tetracycline
Parasitic causes: metronidazole and tinidazole may be used to treat
individuals

CONTRAINDICATION OF ANTIBIOTICS IN GI INFECTIONS
They may increase the risk of hemolytic uremic syndrome in children
infected with E. coli O157, H7 (Shiga toxin-producing E. coli)
Prolonged use of antibiotics may also lead to the development of
resistance in the normal gut flora in addition to the pathogen
Antibiotics suppress the normal flora, allowing C. difficile or Candida to
overgrow, invade and cause necrotising enterocolitis
Viral diarrheas are NOT to be treated with antibiotics

CHAPTER 24 (B)
GASTROINTESTINAL
INFECTIONS
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Phone: 040-2766 5446/5447
Part III
Diseases

BACTERIAL CAUSES OF
GASTROINTESTINAL
INFECTIONS
This Photo by Unknown Author is licensed under CC BY-NC

SALMONELLA (NON-TYPHOIDAL SALMONELLAE)
Gram-negative bacteria belonging to the family Enterobacteriaceae and genus Salmonella
Salmonella gastroenteritis or food poisoning—zoonotic disease, the source of infection
being animal products
GIT infections may also be caused by non-typhoidal salmonellae
Most common species: S. typhimurium

SALMONELLA (NON-TYPHOIDAL SALMONELLAE)
Other common species:
 S. enteritidis, S. haldar
 S. heidelberg, S. agona
 S. virchow, S. seftenberg
 S. indiana, S. newport and S. anatum
Non-typhoid salmonellosis is a frequent infectious complication in systemic lupus
erythematosus (SLE)

EPIDEMIOLOGY
Infection via ingestion of contaminated water
and food—mainly poultry (including eggs and
egg products), meat, milk and milk products
Eating salads and undercooked meat and
meat products
Salads and other uncooked vegetables
contaminated by manure or handling
Cross-infection in hospitals

PATHOGENESIS
Incubation period of 24 hours or less
Diarrhea, vomiting, abdominal pain and fever are the main clinical
features
Subsides in 2–4 days
Typhoidal or septicemic type of fever

CLINICAL FEATURES
Salmonella gastroenteritis
Frequent passage of liquid or watery stool with increased water and
electrolyte loss
Abdominal pain, vomiting and fever
Self-limiting in most cases
In neonates and children  fluid and electrolyte loss might lead to
dehydration and electrolyte imbalance and may turn fatal unless treated
immediately

Feces culture
In outbreaks of food poisoning, culture of the article of food suspected to have been
contaminated also
TREATMENT
Uncomplicated, non-invasive Salmonella gastroenteritis: Antibiotics should not be used
Serious, invasive cases: Antibiotic treatment is needed
CONTROL
By adhering to personal and food hygiene

ANTIBIOTIC RESISTANCE IN SALMONELLA
Multiresistant salmonellae: important agents of hospital cross-infections
R factors conferring multiple drug resistance – first reported in England
in the 1960s
These resistant strains have become widely disseminated among
salmonellae
Vaccines do not protect against Salmonella gastroenteritis or
Salmonella septicemia

ESCHERICHIA COLI
Gram-negative, straight rods, measuring 1–
3 µm × 0.4–0.7 µm
Arranged singly or in pairs
Motile by peritrichous flagella.
Capsules and fimbriae are found in some
virulent strains
Fig. 24.3 (a) Gram-stained smear of E. coli gram-negative slender rods (Source: Dept. of
Microbiology, PIMS, Puducherry) and (b) a computer-generated 3D image of long, whip-like,
peritrichous flagellae of E. coli (Source: Centres for Disease Control and Prevention [CDC], Public
Health Image Library [PHIL] Image ID 21915)

ANTIGENIC STRUCTURE AND VIRULENCE FACTORS
Somatic antigen O, flagellar antigen H and capsular antigen K
Fimbrial or F antigens are also present
Two types of virulence factors: surface antigens and toxins
1. Surface antigens
Somatic antigen O (somatic lipopolysaccharide):
Has endotoxic activity and protects the organism from phagocytosis and the bactericidal
effects of complements
Normal colon strains belong to the ‘early’ O groups (1, 2, 3, 4, etc.)
Enteropathogenic strains belong to the ‘later’ O groups (26, 55, 86, 111, etc.)

K envelope antigen: Seen in strains causing neonatal meningitis and septicemia
Offer protection against phagocytosis
H antigen (flagellar antigen)
F antigens: Heat-labile
P fimbriae (seen in uropathogenic strains) bind specifically to the P blood group
substance on human erythrocytes and uroepithelial cells
Fimbriae are important in initial attachment and colonisation
Colonisation factor antigens (CFA) in enterotoxigenic E. coli. cause human diarrhea

2. Toxins
Two kinds of exotoxins—hemolysins and enterotoxins.
Hemolysins – not relevant in pathogenesis
CNF1 (cytotoxic necrotising factor-1) and siderophores are virulence factors in uropathogenic
E. coli and are important components of biofilm production and adhesion
Enterotoxins are important in the pathogenesis of diarrhea
Three types of E. coli enterotoxins
i) Heat-labile toxin (LT)
ii) Heat-stable toxin (ST)
iii) Verotoxin (VT), which is also known as Shiga-like toxin (SLT)

Heat-labile toxin (LT): resembles the cholera toxin
Has one A subunit (A for active) and five B subunits (B for binding)
The toxin binds to the GM1 ganglioside receptor and subunit A is activated to yield two
fragments: A1 and A2
A1 activates adenylyl cyclase in the enterocyte to form cAMP  increased outflow of water
and electrolytes into the gut lumen, with consequent watery diarrhea

ANTIGENIC STRUCTURE
AND VIRULENCE FACTORS
Heat-stable toxin (ST): Poorly antigenic
Two types of STs
 STA (acts by activating cGMP in the intestine)
 STB
 E. coli verocytotoxin or verotoxin
Cytotoxic effect on Vero cells (also known as
Shiga-like toxin [SLT])
Acts by inhibiting protein synthesis
Table 24.3 Methods for detecting ETEC-labile
(LT) and ETEC stable (ST) enterotoxins

CLINICAL
FEATURES
Diarrhea
Septicemia, neonatal sepsis and neonatal meningitis
(Chapter 20 and 23)
Urinary tract infection (Chapter 27)

DIARRHEA IS CAUSED BY SIX TYPES OF E. COLI
1. Enteropathogenic E. coli (EPEC)
Diarrhea in infants and children and usually produce institutional
outbreaks
E.g., 026:B6, 055:B5, 0111:B4, etc.
Non-invasive and do not produce enterotoxins
Plasmid-encoded protein, EPEC adherence factor (EAF) for adherence

2. Enterotoxigenic E. coli (ETEC): Two epidemiological entities are associated
i) Endemic diarrhea in developing tropical countries
Seen in all age groups
From mild, watery diarrhea to a fatal disease indistinguishable from cholera
ii) Traveller’s diarrhea
 In persons from non-endemic areas who visit endemic areas
06, 08, 015, 025, 027 and 0167
Adheres to intestinal mucosa by fimbriae called colonisation factor antigens
ETEC produce enterotoxins which may be either LT or ST or both

3. Enteroinvasive E. coli (EIEC): Resemble the Alkalescens–Dispar group
Invade interstitial epithelial cells as seen in shigellosis
Serogroups 028 ac, 0112 ac, 0124, 0136, 0143, 0114, 0152 and 0154
Molecular serotyping of clinical isolates - used to diagnose EIEC infection
HeLa or HEp-2 cell invasion in culture can also be used as a diagnostic test

4. Enterohemorrhagic E. coli (EHEC):
Produce two potent toxins, verocytotoxin (VT) and Shiga-like toxin (SLT)
Produce fatal hemorrhagic colitis and hemorrhagic uremic syndrome (HUS)
In young children and the elderly
Primary target - vascular endothelial cells
HUS- characteristic renal lesion is capillary microangiopathy
Serotype O157:H7 or rarely, O26:H1 are associated with EHEC diarrhea and its complications

5. Enteroaggregative E. coli (EAEC):
Associated with persistent diarrhea
Bacteria aggregate in a ‘stacked brick’ formation on HEp-2 cells or glass
Most of them are O-untypable, many are H-typable

6. Diffusely adherent E. coli (DAEC):
Defined by a pattern of diffuse adherence (DA), in which the bacteria uniformly cover the entire
cell surface
Less well-established as pathogens
May cause diarrhea in children above 12 months of age

LABORATORY
DIAGNOSIS
Mere isolation from stool
samples does not confirm
its role in the causation of
disease
Specific tests are
required to identify
diarrheagenic E. coli
Table 24.4 Characteristics of diarrheagenic E. coli and methods to detect
them

PREVENTION
AND
TREATMENT
Antibiotic treatment is not indicated for E. coli
diarrhea
Personal hygiene and food safety for
prevention
No vaccines available

VIBRIO CHOLERAE
Slender, gram-negative, curved bacilli
Causes cholera
CLASSIFICATION
Based on their requirement of sodium
chloride
i) Halophilic: V. parahaemolyticus, V.
alginolyticus, V. vulnificus
ii) Non-halophilic: Vibrio cholerae
Fig. 24.4 Vibrio cholerae: (a) comma-shaped gram-negative rods
and (b) digitally-enhanced photomicrograph of Vibrio cholerae
stained by Leifson flagella stain visualised under 320 ×
magnification showing polar flagella (Source: [a] Department of
Microbiology, Pondicherry Institute of Medical Sciences, Puducherry
and [b] CDC, PHIL, Image ID 1034)

VIBRIO CHOLERAE
Biotypes of Vibrio
• Based on a few biochemical
properties
• Two biotypes - classical and El Tor
Serotypes
• Based on minor surface antigenic
characteristics, classical and El Tor
biotypes of cholera vibrios were
classified as Ogawa and Inaba
• Serotype Hikojima: Agglutinated by
both Ogawa and Inaba antisera
Fig. 24.5 Gardner and Venkatraman’s
classification of virbrios (updated)

VIBRIO CHOLERAE
The non-O-1 vibrios (the non-agglutinating
vibrios) have been classified up to 139
serogroups; O-139 causes epidemics of
cholera
Typing
Phage typing
Molecular typing
Pathogenesis
Toxin (cholera toxin)-mediated action
Cholera toxin (CT) is a protein with six units—
one A unit surrounded by five B subunits
Table 24.5 O serotypes of cholera
vibrios

VIBRIO CHOLERAE
B (binding) units attach to the GM1 ganglioside receptors on the surface of jejunal
epithelial cells
The A (active) subunit dissociates into A1 and A2 fragments in the enterocyte
A1 fragment causes prolonged activation of cellular adenylate cyclase and the
accumulation of cAMP  outpouring of intracellular electrolytes—Na, Cl and K—and
large quantities of water into the small intestinal lumen, leading to watery diarrhea
The toxin also inhibits the intestinal absorption of sodium and chloride by the
microvilli

VIBRIO CHOLERAE
Fig. 24.6 Attachment of subunit B to GM1 ganglioside on epithelial
cells and entry of subunit A of the cholera toxin into the intestinal
epithelial cells, leading to hypersecretion of sodium chloride and
water (Source: Jessica Brochu, CC BY-SA 4.0, via Wikimedia
Commons)
 All clinical manifestations and complications
in cholera are due to massive water and
electrolyte depletion
 Cholera toxin (CT)can be toxoided
 Lipopolysaccharide O antigen (LPS and
endotoxin): Reason for immunity induced by
killed vaccines
Immunity
 Local immunity is conferred by
coproantibodies
 IgG, IgM and IgA
 Natural infection confers immunity, for 6–12
months

EPIDEMIOLOGY
Cholera occurs as sporadic, endemic, epidemic or pandemic
Natural habitats of cholera vibrio: saline waters of coastal seas and brackish estuaries
During the inter-epidemic periods- vibrio persists as continuous subclinical or mild
infection
Epidemiology of El Tor: Less severe illness than classical cholera
Mortality is low and the carrier rate high
Endemic in some areas and Periodic epidemics
In India, the classical vibrio has been replaced by El Tor

CLINICAL FEATURES OF CHOLERA
Incubation period : less than 24 hours to about five days
Mild diarrhea and vomiting in 1–3 days or abruptly with sudden, massive diarrhea
Rice water stool: Colourless, watery fluid with flecks of mucus
Complications are muscular cramps, renal failure, pulmonary edema, cardiac
arrhythmias and paralytic ileus
Rapidly fatal disease to a transient, asymptomatic colonisation

Specimen: Stool or rectal swabs
Preserve the specimen at 4°C or in an appropriate holding medium like VR fluid or
Cary–Blair medium for long periods
Microscopy
Characteristic darting motility of the vibrio and its inhibition by specific antiserum can
be demonstrated
Under a dark-field or phase-contrast microscope
Ideally after enrichment for six hours

Culture:
Growth is better in an alkaline medium, the range of pH being 6.4–9.6 (optimum being
8.2)
blood agar: Colonies are initially surrounded by a zone of greening, which later becomes
clear due to hemodigestion
Special media
Holding or transport media:
Venkatraman– Ramakrishnan (VR) medium: pH to 8.6–8.8
Cary–Blair medium: pH of 8.4
Autoclaved seawater

ii) Enrichment media (can also be used as transport
media): Alkaline peptone water (APW): pH of 8.6
iii) Media for culture and isolation:
Thiosulphate citrate- bile salt-sucrose (TCBS)
medium
Alkaline bile salt agar (BSA)—at pH 8.2
Monsur’s gelatin taurocholate trypticase tellurite
agar (GTTA): Cholera vibrios produce small, translucent
colonies with a greyish-black centre and a turbid halo
Fig. 24.7 Yellow colonies on TCBS
(Source: Department of Microbiology,
Pondicherry Institute of Medical
Sciences, Puducherry)

LABORATORY
DIAGNOSIS
Identification: Vibrio colonies identified by
performing the ‘string test’ in 0.5% sodium
deoxycholate saline on a slide.
A ‘string’ is formed by DNA material that is
released from the vibrios as a result of the
lysis of the cells by sodium deoxycholate
Serogrouping: Agglutination with cholera
O subgroup
Fig. 24.8 String test used to differentiate Vibrio
spp. From Aeromonas spp. and Plesiomonas

LABORATORY
DIAGNOSIS
Testing water quality
Two methods
i) Enrichment method:
 900 mL of the water to be tested is added to 100 mL ten-
fold concentrated peptone water at pH 9.2
Incubated at 37°C for 6–8 hours
Enriched a second time before it is plated on cholera-
specific selective media
ii) Filtration technique:
the water to be tested is filtered through a millipore
membrane
The membrane is then placed directly on the surface of a
selective medium and incubated
Colonies appear after overnight incubation
Sewage should be diluted in saline, filtered through gauze
and treated as was described for water

PREVENTION
i) Parenteral vaccines: Killed suspensions of V. cholerae—as subcutaneous or
intramuscular injection
ii) Oral vaccines
1. Killed oral whole cell vaccines
2. Live oral vaccines with classical, El Tor and O-139 strains, with their toxin genes
deleted
Two doses of the vaccines are required for full protection (minimum 1 week and
maximum 6 weeks apart)
Three doses are required for children aged 2–5 years (minimum 1 week and
maximum 6 weeks apart)

TREATMENT
Adequate replacement of fluids and electrolytes using oral rehydration solution (ORS)
Antibacterial therapy
Doxycycline is recommended as the first-line treatment for adults
azithromycin is recommended as first-line treatment for children and pregnant
women

VIBRIO MIMICUS
Infection acquired by eating seafood, especially oysters
The disease is self-limiting
Clinical manifestations resemble those caused by V. parahaemolyticus

HALOPHILIC VIBRIOS
Vibrios that have a high requirement of sodium chloride
Their natural habitats are seawater and marine life
• V. parahaemolyticus
• V. alginolyticus
• V. vulnificus
Halophilic vibrios known to cause human disease

Resembles the cholera vibrio except that it is capsulated and shows bipolar staining
Produces peritrichous flagella when grown on solid media and polar flagella in liquid
cultures
Grows only in media containing NaCl; tolerates salt concentrations up to 8%
On TCBS agar, the colonies are green; string test is positive
Differentiated from V. cholerae by various biochemical reactions
Three antigenic components have been recognised—somatic O, capsular K and flagellar H antigens
Kanagawa phenomenon: Hemolysis in special high-salt blood agar (Wagatsuma agar)
Only the Kanagawa positive strains are pathogenic
VIBRIO PARAHAEMOLYTICUS

PATHOGENESIS
V. parahaemolyticus causes food poisoning associated with marine food
Acute diarrhea and enteritis
Wound infections, sepsis are rare
TREATMENT
Infection is usually self-limiting
In severe cases of gastroenteritis, doxycycline is the antibiotic of choice
Uncomplicated wound infections, minocycline or doxycycline may be used

VIBRIO ALGINOLYTICUS
Resembles V. parahaemolyticus
Associated with infections of the eyes, ears and wounds in human
beings exposed to seawater

VIBRIO VULNIFICUS
VP-negative and ferments lactose but not sucrose
Salt tolerance of less than 8%
It causes two types of illnesses:
1. Wound infection following contact of open wounds with seawater
2. septicemia with high mortality: In immunocompromised hosts,
particularly those with liver disease
Following the ingestion of the vibrio, usually in oysters
Does not cause gastrointestinal manifestations; it enters the bloodstream

AEROMONAS AND
PLESIOMONAS
Rarely associated with diarrhea
Aeromonas hydrophila: Causes diarrhea and some
pyogenic wound infections in humans
Plesiomonas shigelloides: Causes diarrheal disease
Both these are oxidase-positive, polar flagellated, gram-
negative rods and may be mistaken for vibrios
They may be differentiated from vibrios by biochemical
tests such as utilisation of amino acids
This Photo by Unknown Author is licensed under CC BY-NC-ND

SHIGELLA
Short, gram-negative rods
Non-motile, non-sporing and non-capsulated
S. dysenteriae type 1 forms a toxin (Shiga toxin):
Exotoxin produced by a gram-negative bacillus
This Photo by Unknown Author is licensed under CC BY-SA

SHIGELLA
Antigenic structure
One or more ‘major’ antigens and a large number of ‘minor’ somatic O antigens
Some strains possess K antigens
Resistance
Shigellae are killed at 56°C in one hour and by 1% phenol in 30 minutes
In ice, they last for 1–6 months
S. sonnei is, in general, more resistant than the other three species S. dysenteriae, S. flexneri
and S. boydii

PATHOGENICITY
Most potent pathogen among the enteric bacteria
Infective dose is as low as 10–100 bacilli
Three types of toxic activity have been demonstrated in Shigella culture filtrates:
1. Neurotoxicity
2. Enterotoxicity: Two new Shigella enterotoxins
ShET-1 and -2: the former confined to S. flexneri 2a and the latter more widespread
S. dysenteriae type 1 forms an exotoxin, ShET-2, which induces inflammation of the epithelial
cells

PATHOGENICITY
3. Cytotoxicity:
 Shigella produces cytopathic changes in
cultured Vero cells
Shiga toxin appears to be the same as
verotoxin (or the Shiga-like toxin of E. coli –
VTEC)
The pathogenic mechanisms of shigellae
resemble those of enteroinvasive E. coli and
are as follows:

PATHOGENICITY
Invasive property of the bacillus can be demonstrated by its ability to penetrate
cultured HeLa or HEp-2 cells.
This property is attributed to the outer membrane protein called virulence marker
antigens (VMA)
The detection of VMA by ELISA serves as a virulence test for shigellae

EPIDEMIOLOGY
Human beings are the only natural hosts
Transmission of infection is through contaminated fingers, food and water and flies and
fomites such as door handles, water taps and lavatory seats
In young male homosexuals, transmission is a part of the gay bowel syndrome

CLINICAL FEATURES
Bacillary dysentery
Short incubation period (1–7 days, usually 48 hours)
Frequent passage of loose, scanty feces containing blood and mucus, along with
abdominal cramps and tenesmus, fever and vomiting
Complications:
In children and immunocompromised patients
Arthritis, toxic neuritis, conjunctivitis, parotitis and, in children, intussusception
Hemolytic uremic syndrome

Specimen: Feces
Enrichment media: Selenite F broth or Salmonella–Shigella (SS) broth
Microscopy: Plenty of pus cells with RBCs seen
Cultural characteristics
 Aerobes and facultative anaerobes
 On deoxycholate citrate agar (DCA) and xylose lysine deoxycholate (XLD), they form red
(alkaline) colonies
 Biochemical reactions: These help to differentiate the species of Shigella
 Identification by specific antisera: Confirmation by slide agglutination

Treatment
Uncomplicated shigellosis is a self-limiting
condition
In acute cases, particularly in infants and young
children:
Oral rehydration
Fluoroquinolones (ciprofloxacin) or
cotrimoxazole may be given empirically
Control
Improving personal and environmental
sanitation
Fig. 24.9 Red colonies of Shigella sonnei on XLD agar
(Source: CDC, PHIL, Image ID 17191)

CHAPTER 24 (C)
GASTROINTESTINAL
INFECTIONS
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Phone: 040-2766 5446/5447
Part III
Diseases

BACTERIAL CAUSES OF
GASTROINTESTINAL
INFECTIONS
This Photo by Unknown Author is licensed under CC BY-ND

CAMPYLOBACTER
Slender, spirally curved, gram-negative rods, 0.2–0.5 µm
thick and 0.5–5 µm long
They are typically comma-shaped but may occur as ‘S’ or
multispiral chains
Motile with a single unsheathed polar flagellum at one or
both poles
Growth occurs under microaerophilic conditions
Do not ferment carbohydrates but are strongly oxidase-
positive

RESISTANCE
C. jejuni, C. coli and C. lari are thermophilic and do not grow at 25°C
Plates are incubated at 42°C in an atmosphere of 5% oxygen, 10% carbon dioxide
and 85% nitrogen
Causing diarrheal disease: C. jejuni, C. coli, C. lari
Causing extraintestinal infection: C. fetus
Causing abscess: C. sputorum, C. conciscus
C. jejuni infection is zoonotic, the source being food of animal origin, especially raw
milk

PATHOGENICITY
C. jejuni is the most common bacterial cause of diarrheal disease in many developed
countries
Disease is mainly confined to children
Infection occurs by ingestion
C. jejuni is an invasive pathogen involving the mesenteric lymph nodes

CLINICAL FEATURES
Incubation period is 1–7 days
Fever, abdominal pain and watery diarrhea
Stool contains leukocytes and blood
The disease is usually self-limiting

Isolation of the Campylobacter from feces
Microscopy:
Direct microscopy by phase-contrast or dark-field microscopy: darting or tumbling
motility of the spiral rods
Stained smears: To demonstrate the small, curved rods
Culture: Feces or rectal swabs are plated on selective media
Cary–Blair transport medium
Culture media: Skirrow’s, Butzler’s and Campy BAP selective media
Colonies are nonhemolytic, grey or colourless, moist and flat or convex

TREATMENT
Fluid and electrolyte replacement
When needed, erythromycin is the best antibiotic
This Photo by Unknown Author is licensed under CC BY

HELICOBACTER
Gram-negative spiral rod
Motile by a unipolar tuft of lophotrichous flagella
Grows on chocolate agar or Campylobacter media under microaerophilic conditions
Produces abundant urease
This property has been used as a rapid test on gastric biopsy samples.
Helicobacter does not metabolise carbohydrates or reduce nitrate.
This Photo by Unknown Author is licensed under CC BY

EPIDEMIOLOGY
Sole source of H. pylori is the human gastric mucus
The exact mechanism of transmission is not clear, but it is likely to be oral–oral or fecal–oral
Poverty, overcrowding and poor hygiene favour transmission
Seen globally, with a prevalence of 30–60 per cent

PATHOGENICITY
Virulence factors of H. pylori
Vacuolating cytotoxin A
Cytotoxin-associated gene A
Urease enzyme
Outer membrane proteins
Lipopolysaccharide
Motility also help in pathogenesis
Bacteria do not invade the mucosa;
Gastric antrum is the commonest site of
colonisation
Fig. 24.10 Helicobacter pylori interact with gastric
mucosa and colonise (Source:
https://openstax.org/books/
microbiology)

CLINICAL FEATURES
Mild acute gastritis
Following this, organism persists as an asymptomatic coloniser, though
chronic superficial gastritis may be demonstrable histologically
Peptic ulcer disease
Chronic atrophic gastritis
Infection is a risk factor for gastric malignancies such as
adenocarcinoma and ‘mucosa-associated lymphoid tissue’ (MALT)
lymphomas

1. Invasive tests (endoscopic biopsy of gastric mucosa)
i) The tissue is subjected to rapid urease test
ii) Part of the tissue is sent for examination by microscopy and
culturesilver staining or Gram staining is positive for spiral bacilli
Culture requires an enriched medium and microaerophilic
conditions
2. Non-invasive tests:
IgM and IgG ELISA may be used for seroepidemiological studies
in the community
Fig. 24.11 Helicobacter
pylori gastritis—silver stain

3. Rapid tests: Several rapid immunochromatographic cassette and dipstick methods
for bedside testing for antigens or antibodies in stool, gastric aspirate or blood
4. ‘Urease breath test’:
The subject drinks a carbon isotope-labelled urea solution
This isotope can be detected in the breath
This method is sensitive and reliable but needs isotope assay facilities

TREATMENT
Indications are an active peptic ulcer disease or past history of peptic ulcer without
documented cure
H. pylori is sensitive to several antibiotics and bismuth salts
The standard treatment is a combination of bismuth subsalicylate, tetracycline (or
amoxicillin) and metronidazole for two weeks
The first-line treatment consists of clarithromycin, amoxicillin and metronidazole—
BID 14 days, clarithromycin (500 mg), amoxicillin (1 g) or metronidazole (500 mg
TID)

TREATMENT
Bismuth, tetracycline and a nitroimidazole for 10–14 days is the second
line of treatment
An alternative schedule uses a proton pump inhibitor like omeprazole
and clarithromycin
Treatment is indicated only for H. pylori-related gastric or duodenal
ulceration and not for asymptomatic colonisation
Drug resistance and recurrence are frequent

CLOSTRIDIOIDES DIFFICILE
Most common cause of healthcare-associated
diarrhea in many developed countries
Infections follow the use of broad-spectrum antibiotics
like clindamycin, ampicillin or fluoroquinolones, to which
the organism is resistant
The clinical entity of C. difficile infection is known as
pseudomembranous colitis
Associated with acute colitis and bloody or watery
diarrhea
20–25% of cases of antibiotic-associated diarrhea
are due to C. difficile

PATHOGENESIS
Two high-molecular-weight exotoxins, A and B
Toxin A: Potent enterotoxin that attaches to gut
receptors; it may also be cytotoxic
Toxin B is a cytotoxin
The toxin genes of Clostridiodes are present on a
chromosomal pathogenicity island
Fig. 24.12 Overgrowth of C. difficile and pseudomembrane
formation (Source:
https://openstax.org/books/microbiology)

Colonoscopy shows microabscesses
Culturing of stool specimens on selective media for epidemiological purposes
Cycloserine, cefoxitin fructose agar (CCFA)
Cysteine, cefoxitin yeast extract agar (CCYA)
Detection of toxins A and/or B in stool by ELISA is the mainstay of diagnosis
Demonstrated in the feces by its characteristic effect on Hep-2 or/and human diploid cell
cultures
Neutralisation by the C. sordellii antitoxin
Molecular methods
lateral flow assay: To detect C. difficile toxins and glutamate dehydrogenase in stool samples

PREVENTION AND TREATMENT
Prevented by restricting the use of antibiotics associated with C. difficile
outbreaks
The condition is treated by discontinuing the antibiotic causing the disease and
instituting vancomycin or metronidazole
Fecal transplant: To treat recurrent C. difficile colitis

AGENTS
ASSOCIATED
WITH FOOD
POISONING

STAPHYLOCOCCUS
AUREUS
Produces a potent exotoxin
(enterotoxin), which causes food
poisoning
Nausea, vomiting and diarrhea 2–6
hours after consuming food
contaminated by the preformed toxin
The toxin is relatively heat-stable
Meat, fish and milk and milk
products - common foods
responsible for the infection
The source of infection is usually
a food handler who is a carrier
This Photo by Unknown Author is licensed under CC BY-SA-NC

STAPHYLOCOCCUS AUREUS
Self-limiting illness with recovery in a day or two
Eight antigenic types of staphylococcal enterotoxin—enterotoxins A, B, C1–3, D, E and H
Type A toxin is responsible for most cases
Toxin directly acts on autonomic nervous system to cause the illness
The toxin is antigenic and is neutralised by the specific antitoxin
serological tests such as latex agglutination and ELISA - for the detection of the toxin

CLOSTRIDIUM BOTULINUM
Causes botulism, a paralytic disease that usually presents in the form of food
poisoning
C. botulinum is motile
Produces subterminal, oval and bulging spores which are are heat- and radiation-
resistant
Although the infection occurs via the gastrointestinal tract or wounds (wound
botulism), the disease is manifested as a neurological condition

CLOSTRIDIUM PERFRINGENS
Some strains of C. perfringens type A produce heat-labile enterotoxin which causes
food poisoning
It is similar to the enterotoxins of V. cholerae and enterotoxigenic E. coli
Caused by cold or warmed-up meat dish
In the intestines, their spores produce the enterotoxin
Incubation period: 8–24 hours
Abdominal pain, diarrhea and vomiting

Isolating heat-resistant C. perfringens type A from feces is not of much
value
Isolation from food is attempted
TREATMENT
The illness is self-limiting, and recovery occurs in 24–48 hours

OTHER
INFECTIONS
CAUSED BY C.
PERFRINGENS
Gangrenous appendicitis
Necrotising enteritis
Biliary tract infection
Endogenous gas gangrene of intra-abdominal origin
Brain abscess and meningitis
Panophthalmitis:
Thoracic infections:
Urogenital infections
Septic abortion

BACILLUS CEREUS
Important cause of food poisoning
Widely distributed in nature
Readily isolated from soil, vegetables and
a wide variety of foods including milk,
cereals, spices, meat and poultry
Generally motile but non-motile strains
may occur
Not capsulated and not susceptible to
gamma phage

BACILLUS CEREUS
Two types of food poisoning have been associated with B. cereus:
1. Diarrheic type
2. Emetic type
Diarrheal type
Associated with a wide range of foods including cooked meat and vegetables.
Characterised by diarrhea and abdominal pain
Incubation period: 8–16 hours
Vomiting is rare
Caused by serotypes 2, 6, 8, 9, 10 or 12

BACILLUS CEREUS
Emetic type
Associated with the consumption of cooked rice, usually fried rice from Chinese
restaurants
Acute nausea and vomiting, 1–5 hours after the meal
Diarrhea is not common
Caused by serotypes 1, 3 or 5
The emetic toxin is produced only when B. cereus is grown in rice but not in other media

TREATMENT
Both types of the illness are mild and self-limiting, requiring no
specific treatment
 Special selective media are
useful in isolating B. cereus from
feces and food sources
 Mannitol egg yolk phenol red
polymyxin agar (MYPA) and
 Polymixin-pyruvate mannitol
bromothymol blue agar
(PEMBA)
 The presence of 105 or more
bacteria per gram of specimen is
diagnostic

Table 24.6 Summary of bacterial
infections of the GI tract

Table 24.6 Summary of bacterial
infections of the GI tract (continued)

CHAPTER 24 (D)
GASTROINTESTINAL
INFECTIONS
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Phone: 040-2766 5446/5447
Part III
Diseases

FUNGAL AGENTS
ASSOCIATED WITH FOOD
POISONING

INTRODUCTION
Many fungi form poisonous substances
Mycotic poisoning is of two types:
1. Mycotoxicosis, in which fungal toxins contaminate food, which on
ingestion, cause infection
2. Mycetism, in which the ingestion of the fungus causes toxic effects

Mycotoxicos
es
Diseases caused by the toxic metabolic products
released by fungi and result from the ingestion of food
contaminated with mycotoxins (fungal toxins)
Examples are aflatoxicosis and ergotism
Mycotoxins are natural products produced by fungi and
found in some articles of food
The fungus does not necessarily have to be present in
the tissues to exert its pathogenic effect
There is no invasion of tissues by the fungus

Table 24.7 Important mycotoxins and their sources

AFLATOXIN
Aspergillus flavus secretes aflatoxin B1
Aspergillus parasiticus secretes aflatoxins B1, B2, G1 and G2
Frequently present in mouldy foods, particularly in groundnuts, corn and
peas
Highly toxic to animals and birds as well as human beings
Cause hepatomas in ducklings and rats, and has possible carcinogenic
effect in human beings

ERGOT ALKALOIDS
Ergotoxicosis (ergotism) is caused by the toxic alkaloids
produced by the fungus Claviceps purpurea, which
grows on the fruiting heads of rye
Trichothecenes are toxins produced by certain species
of Fusarium
Zearalenone is a toxin produced by Fusarium
graminearum; animals that consume grains
contaminated with this toxin may develop symptoms
and signs mimicking an estrogenic disorder

MYCETISM
Ingestion of poisonous mushrooms
Mycetism may cause gastrointestinal disease, dermatitis or death
Claviceps species—ergot poisoning
Coprine species—coprine poisoning
Inocybe species—muscarine poisoning
Hallucinogenic agents (d-lysergic acid, psilocybin) produced by the
Psilocybe species and other fungi

VIRAL AGENTS
ASSOCIATED WITH
GASTROENTERITIS

ROTAVIRUS
Group of RNA viruses of the family Reoviridae
Double-stranded RNA in 9–12 segments
Non-enveloped and resistant to lipid solvents
The family contains three genera:
Reovirus
Orbivirus
Rotavirus

ROTAVIRUS
Rotaviruses resemble cartwheels
Complete or double-shelled virus; measures about 70 nm in diameter and has a smooth
surface. It has a double-stranded RNA with a genome in 11 segments
Incomplete or single-shelled virus is smaller, measuring about 60 nm, with a rough surface that
has lost the outer shell
‘Empty’ particles without the RNA core are also seen
Rotaviruses are the most common cause of diarrheal disease in infants and children
Adult diarrhea rotavirus (ADRV) is also reported

CLASSIFICATION
Rotaviruses are classified into antigenic groups (A to G) based on the antigenic epitopes of the
internal structural protein (VP6)
Group A strains cause the majority of human infections in children
PATHOGENESIS
Transmitted by the fecal–oral route
Virus infects the mature enterocytes in the upper and middle part of the villi of small intestine
Destruction of the villi leads to copious diarrhea

CLINICAL
FEATURES
Incubation period is 2–3 days
Vomiting and diarrhea occur with little or no fever
Stools are usually greenish-yellow or pale, with no
blood or mucus
Disease is self-limiting, and recovery occurs within 5–
10 days
Mortality is low

EPIDEMIOLOGY
Commonest cause of diarrhea in infants and children the world over
Infection rate more in winter months
Produces large epidemics of diarrhea
Infection occurs in children below the age of five years but is most
frequent between 6 and 24 months of age

The virus can be detected in stool filtrates by enzyme immunoassays (EIA) and
immune electron microscopy (IEM)
Culture: Human rotavirus does not grow readily in cell cultures, but some strains have
been adapted for serial growth in tissue cultures
Serological techniques: IgM and IgG antibodies demonstrated in the blood of infected
children by ELISA
Genotyping can be done by polymerase chain reaction (PCR), which is a sensitive
detection method

TREATMENT
Rehydration is all the treatment that is needed.
PROPHYLAXIS
Rotavirus vaccines are in use in 23 countries
RotaTeq (RV5): Composed of five rotavirus strains
Rotarix (RV1): Attenuated human rotavirus that contains representatives of the most frequently
circulating rotaviruses

OTHER DIARRHEAGENIC VIRUSES
Calicivirus
Group of important viruses that cause gastroenteritis in humans
The most important virus in this group is the Norovirus whose
prototype is the Norwalk virus

NORWALK
VIRUS
Epidemic of gastroenteritis affecting school children
and teachers in Norwalk
Belongs to family Caliciviridae
Small, round RNA viruses with 32 cup-shaped
depressions on their surface
Epidemics of diarrhea associated with the
consumption of raw oysters
Virus demonstrated in feces by electron microscopy
Antibodies to the virus can be detected by immune
electron microscopy and radioimmunoassay

ADENOVIRUS
Outbreaks of diarrhea in children
More often in the summer months
Types 40 and 41
Can only be grown with difficulty in tissue culture

ASTROVIRUS
Star-shaped, isometric particles measuring 28 nm
Associated with some epidemics of diarrhea in children

CORONAVIRUS
These viruses are well-established causes of acute diarrhea in calves, piglets and
dogs and have been observed in human feces also
Though diarrhea is often observed in coronavirus respiratory infections, their
relation to diarrhea is uncertain

PARASITES CAUSING
INFECTIONS OF
GASTROINTESTINAL TRACT

Majority of intestinal parasitic
infections are asymptomatic
Parasites causing diarrhea
commonly are Giardia
duodenalis (Giardia intestinalis
or G. lamblia), Cryptosporidium
parvum and Entamoeba
histolytica
E. histolytica causes diarrhea
with blood (dysentery) and
other complications.

GIARDIA DUODENALIS (SYN. GIARDIA
INTESTINALIS OR G. LAMBLIA)
Giardiasis is the most common parasitic disease
Giardia lamblia is a flagellated intestinal protozoon
Causes chronic diarrhea with malabsorption
Giardia resides in the duodenum and upper jejunum

MORPHOLOGY
CYST
Oval and measures 11–14 × 7–10 μm
Immature cysts may have two nuclei, but a fully mature cyst is quadrinucleate—the four
nuclei are seen at one end in pairs
TROPHOZOITE
Pear-shaped
Bilaterally symmetrical structure that measures about 10 × 15 μm exhibits a ‘falling leaf’
motility
It resembles a tennis racket and has a sucking disc on its concave ventral surface
The parasite has four nuclei and two parabasal bodies present on axostyles

LIFE CYCLE
 Requires single host
 Humans acquire the
infection by ingesting
mature cysts with food or
water
 A large number of
trophozoites may be
excreted during the acute
stage
 Later, once stool loses
moisture and becomes
formed, cysts are excreted
Fig. 24.14 Morphology and life cycle of
Giardia

CLINICAL FEATURES
Ingestion of as few as 10 cysts is sufficient to cause infection in humans
Person-to-person transmission occurs where fecal hygiene is poor
Incubation period: 1–3 weeks
More than 50% of infections are asymptomatic
Acute presentation: Mild diarrhea to severe malabsorption syndrome
Loose motions are foul-smelling and contain mucus without blood
Chronic presentation: Intermittent or recurring
Foul-smelling diarrhea with weight loss due to malabsorption syndrome
-Extraintestinal manifestations such as urticaria, anterior uveitis or arthritis

Stool microscopy shows characteristic oval cysts of Giardia; trophozoites may be seen in
acute infection
Repeated samples may be requested since excretion of cysts is variable
Entero string test: To collect trophozoites
Endoscopic biopsy: From the duodenum or upper jejunum may show trophozoites
attached to microvilli.
Antigen detection from stool by ELISA or immunochromatographic test (ICT)
Serology: Antibodies can be detected by ELISA and immune fluorescence assay
Molecular detection: PCR can be used to diagnose giardiasis

TREATMENT
Drug of choice to treat giardiasis is metronidazole
Alternatively, tinidazole or albendazole can also be used
It is important to eradicate the carrier stage, particularly in food handlers
Cysts are resistant to chlorine and can be removed from drinking water
by filtration

COMMENSAL
FLAGELLATES OF
THE INTESTINE
Found in the caecum as harmless commensals
Are not known to cause any disease in humans
Chilomastix mesnili
Retortamonas intestinalis
Enteromonas hominis

DIENTAMOEBA
FRAGILIS
Commensal
Known to cause intermittent diarrhea, flatulence
and abdominal cramps in some people
Majority of cases are asymptomatic
Exists as small (5–12 µm) trophozoites with 1–2
nuclei; it does not have a cystic stage

OPPORTUNISTIC SPOROZOA THAT CAUSE DIARRHEA
Intestinal sporozoa are known to cause chronic diarrhea in immunosuppressed
conditions such as HIV infections
Cryptosporidium
Cystoisospora (previously known as Isospora)
Sarcocystis
Cyclospora

CRYPTOSPORIDIUM
Zoonotic parasite occurring worldwide
Cause severe, debilitating and chronic diarrhea in HIV-infected patients
Two species are known to cause infections in humans: C. parvum and C.
hominis
C. parvum is zoonotic and is seen commonly in rural areas
It can spread from infected animals to humans

Fig. 24.15 Oocysts of intestinal sporozoans:
(a) Cryptosporidium and (b) Cystoisospora
(Source: CDC, DPDx)

LIFE CYCLE
Parasite resides in the
intracellular region, just
within the brush border
cells of the intestinal
epithelium
Infection occurs by the
ingestion of sporulated
thick-walled oocysts
They are resistant to
chlorination
Fig. 24.16 Life cycle of
Cryptosporidium

CLINICAL FEATURES
Incubation period of 1–2 weeks
In immunocompetent host: Infection is often asymptomatic or may occur as self-
limiting, watery non-bloody, frothy diarrhea a few times daily
In immunosuppressed patients: Chronic, persistent and profuse diarrhea with
abdominal pain
 This leads to water and electrolyte loss, causing severe weight loss and wasting
Extraintestinal infections such as respiratory tract infections and pancreatitis develop
in severe immunosuppression

TREATMENT
Nitazoxanide 500 mg twice daily for three days is the drug of choice
Azithromycin and clarithromycin have proven effective in some cases

CYSTOISOSPORA
Cystoisospora belli was formerly known as Isospora belli
LIFE CYCLE
Cystoisospora require a single host for their life cycle
Infection is acquired by the ingestion of sporulated
mature oocysts
These oocysts release sporozoites, which enter cells
of the small intestine and multiply asexually
Immature oocysts bearing a single sporoblast are
liberated

LIFE CYCLE
These sporulate outside the cell in 1–2 days to become mature infective C. belli
These may enter intestinal cells to restart the cycle or develop into sexual forms
(microgamete and macrogametes)
Fertilisation results in the formation of oocysts
These oocysts are passed in the stool and become infectious after they sporulate
Each sporulated mature oocyst contains two sporocysts, each of which contains four
sporozoites

CLINICAL FEATURES
Acute-onset, watery diarrhea with fever and abdominal pain that can
last for days or months
Infection is self-limiting in immunocompetent persons but could last for
months in HIV-infected/immunosuppressed person
TREATMENT
Trimethoprim–sulfamethoxazole four times daily for 10 days is the first
line of treatment
For HIV-infected patients, it is given three times daily for three weeks

SARCOCYSTIS
Rare cause of diarrhea in immunosuppressed persons
Human beings are the definitive hosts of Sarcocystis hominis and S. suihominis
Pigs and cattle are the intermediate hosts for Sarcocystis suihominis and S. hominis respectively
Morphology: Sarcocystis exists in three morphological forms:
Oocyst: Contains two sporocysts, each of which contains four sporozoites
Sporocyst: contains four sporozoites each; both oocysts and sporocysts can be passed in stool
Sarcocyst: Found in the muscles of pigs and cattle; tiny compartments containing many bradyzoites
are seen in the sarcocyst

LIFE CYCLE
The intermediate host acquires infection by ingesting oocysts
with contaminated food or water
Sporocysts form schizonts in the endothelium and in the
bloodstream
They subsequently release merozoites, which migrate to
skeletal and cardiac muscles where they develop into
sarcocysts
Humans (definitive hosts) gets infected when they consume
improperly cooked meat or pork containing sarcocysts, which
release bradyzoites in the intestine
These bradyzoites develop into microgametes and macrogametes
A zygote is formed after fertilisation and matures into a sporocyst
and sporulated oocyst
Both are released in the intestinal lumen and passed with stools

CLINICAL FEATURES
Disease in humans is usually self-limiting
Fever, nausea, diarrhea or pain abdomen
Muscle aches, myositis and muscle weakness may be present in muscular
sarcocystosis

CYCLOSPORA
Cyclospora cayetanensis is transmitted by the ingestion of oocysts with food and water
Cause diarrhea of varying severity in travellers and immunosuppressed persons
Most cases are asymptomatic
Some patients develop diarrhea, flu-like symptoms, flatulence and belching
Prolonged diarrhea, anorexia and weight loss
Infective form is the oocyst
The mature oocyst contains two sporocysts, each with two sporozoites
The life cycle of Cyclospora is very similar to that of Cryptosporidium species

LABORATORY
DIAGNOSIS OF
DIARRHEA
SUSPECTED TO BE
CAUSED BY
INTESTINAL
SPOROZOA
 Patient must be investigated for HIV and CD4 counts
 Stool and biopsy samples of the small intestine are the
specimens of choice
 Direct microscopy of stool sample
 Wet mount: Characteristic refractile cysts of the parasite
 Modified acid-fast staining to visualise oocysts
 Auramine, safranin and lactophenol cotton blue stains to
visualise cysts
 Autofluorescence under UV light for Cyclospora and
Cystoisospora but is not useful for visualising
Cryptosporidium
 Direct fluorescent antibody staining can be used to detect
Cryptosporidium oocysts and is more sensitive than acid-
fast staining
 H & E stain of biopsy material: Cystoisospora and
Cryptosporidium can be detected in the small intestine

LABORATORY DIAGNOSIS OF DIARRHEA SUSPECTED TO BE
CAUSED BY INTESTINAL SPOROZOA
Antigen detection in stool: Both ELISA and immunochromatographic tests to detect C.
parvum-specific coproantigen in stool
Serology: Antibody detection can be done by ELISA to detect IgG and IgM antibodies to
Cryptosporidium in the patient’s serum
Molecular diagnosis: PCR is available to detect Cryptosporidium, Cyclospora and
Cystoisospora

Table 24.8 Microscopic characteristics of oocysts of intestinal sporozoa

PARASITES CAUSING
DYSENTERY
Entamoeba histolytica and Balantidium coli are
the most prominent causes of parasitic dysentery
Are motile with the help of pseudopodia
Table 24.9 Amoeba causing disease in humans

ENTAMOEBA HISTOLYTICA
Resides in the large intestine
Causes mild dysentery to life-threatening amoebic liver abscess
Infections are commonly seen in areas with poor sanitation and poor or contaminated
water supply

MORPHOLOGY
Three morphological forms
Trophozoite: This is the motile form of E. histolytica
Has pseudopodia, which act as organs of locomotion
Precyst: Smaller than trophozoites and are uninucleate and oval with blunt pseudopodia
Cysts: These are small, round structures
Develops from uninucleate structures to those with 1–4 nuclei.

LIFE CYCLE AND
PATHOGENESIS
Requires only one host for
its life cycle
Infection is acquired by the
ingestion of mature
quadrinucleate cysts that are
passed in the feces of
infected persons including
asymptomatic carriers
Fig. 24.17 Morphological forms and life cycle of
amoeba

PATHOGENESIS
Intestinal amoebiasis: Amoebae invade the colonic epithelial cells and lyse them
Classic ‘flask-shaped’ ulcer
Amoeboma: Tumour-like lesion in the lumen of the large intestine
Liver abscess: Lysis of liver cells and thrombus formation leads to the formation of
an abscess
‘Anchovy sauce pus’
Trophozoites are resistant to complement-mediated lysis; Entamoeba can cause
satellite lesions in various organs

CLINICAL FEATURES
Majority of infected patients are asymptomatic; cyst may be seen in stool samples without
any clinical manifestations
Intestinal amoebiasis: From mild diarrhea to dysentery.
Patients with liver abscess: Fever, right quadrant abdominal pain, hepatomegaly and altered
bowel movements
Satellite symptoms develop due to effusions or spread from the liver
These can present with pleuritis or peritonitis

Table 24.10
Differentiation
between
bacillary and
amoebic
dysentery

LABORATORY
DIAGNOSIS
Samples include stool, aspirate from liver abscess and biopsy
specimen obtained after sigmoidoscopy
Microscopy for cyst or trophozoites: Saline and iodine
mount of freshly passed stool: characteristic quadrinucleate
cysts and trophozoites
Culture: In xenic and axenic media
Examples of the xenic media used for the culture of Entamoeba
spp. include modified Boeck and Drbohlav medium and egg
diphasic medium
Isoenzyme analysis
Serology: Detection of antibodies by ELISA
Fecal antigen detection assays
Molecular diagnostics: PCR or DNA probes

TREATMENT
AND CONTROL
Drug of choice: Metronidazole
Other alternatives include
iodoquinol and diloxanide furoate
Good hygiene, adequate
sanitation measures, availability of
clean drinking water and
education regarding washing of
fruits and vegetables before
consumption help in the control of
infection

COMMENSAL, NON-PATHOGENIC AMOEBAE
Exist in the intestines of human beings without causing any disease
Their cysts or trophozoites may be passed in stool and need to be differentiated from those
of Entamoeba histolytica
Entamoeba dispar
E. hartmanni
Endolimax nana
Entamoeba coli

Table 24.11 Amoebae causing disease in humans

BALANTIDIUM
COLI
Ciliated organism
Pigs are its natural reservoirs,
while humans are its incidental
hosts
Upon ingestion, the cyst excysts
in the small intestine, releasing
ciliated trophozoites
These reach the large intestine
and multiply in its mucosal lining
Trophozoites encyst, and the
cysts are passed in feces
Fig. 24.18 Cyst and trophozoite of Balantidium

Microscopic examination of stool reveals characteristic trophozoites and
cysts
TREATMENT
The drug of choice is tetracycline
iodoquinol and metronidazole are the alternative antimicrobials
Prevention and control measures are similar to those recommended for
amoebiasis

CHAPTER 24 (E)
GASTROINTESTINAL
INFECTIONS
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Phone: 040-2766 5446/5447
Part III
Diseases

Intestinal
Nematode
Infections
MOST COMMON INFECTIONS
WORLDWIDE

ASCARIS
LUMBRICOIDES
(ROUNDWORM)
Largest nematode that resides in the small intestine.
Infection more common in children
Morphology
Adult, larva (four stages) and egg stages
Egg:
The fertilised egg (infectious form) is round or oval
and around 90 × 45 µm in size
It is surrounded by a thick, albuminous coat containing
a large, unsegmented ovum of granular mass. It floats
in the saturated salt solution
The unfertilised egg is elongated and bears a thin
and scanty coat which encloses a thin, unsegmented
ovum
It does not float in the saturated salt solution
Both types of the egg are bile-stained and appear
brown in saline mounts

LIFE CYCLE
 Humans acquire the
infection by ingesting
fertilised eggs
 Containing stage 2
rhabditiform larvae
UNIVERSITIES PRESS PVT LTD Fig. 24.19 Morphology and life cycle of

CLINICAL FEATURES
Most cases are asymptomatic
In children, malnutrition and growth retardation
Complications: Pain abdomen, intestinal obstruction, perforation,
intussusception or volvulus
The migration of adult worms through the biliary tract can cause biliary
colic, cholecystitis, cholangitis and pancreatitis
Allergic manifestations such as fever, urticaria, angioneurotic edema and
conjunctivitis can occur

CLINICAL FEATURES
Löffler’s syndrome
The migration of larvae through lungs, usually 10–12 days of ingestion of eggs, can result in an
irritating, non-productive cough and burning substernal discomfort that is aggravated by
coughing or deep inspiration.
Mild fever with eosinophilia develops, which subsides slowly over weeks
Chest X-rays: Features of eosinophilic pneumonitis

TREATMENT
Drug of choice is albendazole 400 mg once or mebendazole 100 g twice
daily for three days or 500 mg once
Alternatives are ivermectin (150–200 μg/kg), nitazoxanide or pyrantel
pamoate
Pyrantel pamoate can be given safely in pregnancy while others are
contraindicated
Control measures such as health education, improved sanitation and
not using human feces as a fertiliser are critical

HOOKWORMS (NECATOR AMERICANUS
AND
ANCYLOSTOMA DUODENALE)
Necator americanus, the ‘New World’ hookworm
Ancylostoma duodenale, the ‘Old World’ hookworm
Important cause of iron deficiency anemia
In India, N. americanus is more common in southern India

MORPHOLOGY
Adult: Anterior end of the worm is bent like
a hook
Mouth parts of the worm are well
developed with teeth in Ancylostoma
duodenale and cutting plates in Necator
americanus
Eggs: They are oval, about 60 × 40 µm in
size
Non-bile stained within a clear hyaline shell
containing a segmented ovum
There is clear space between the shell and
the ovum
Fig. 24.20 Egg and larva of
hookworm

Table 24.12 Differences between Necator americanus and Ancylostoma duodenale

LIFE CYCLE
Require only a single host for their life cycle
immature hookworm eggs are excreted by infected
persons in their stool
L3 larva enters humans by penetrating skin
Humans can get infected while walking barefoot in fields,
on grass and on damp soil
Autoinfection may also occur
Fig. 24.21 Life cycle of hookworms

CLINICAL FEATURES
Majority are asymptomatic
Acute infections: A maculopapular rash with itching at the site of entry of larva
Allergic symptoms
Non-specific complaints such as nausea, abdominal pain and diarrhea
Eosinophilia and elevated IgE
Chronic infections: Signs and symptoms of iron deficiency anemia and
malnutrition
Complications of anemia such as edema and congestive heart failure are
reported

TREATMENT
Albendazole 400 mg orally single dose
Mebendazole 500 mg BD for three days
Pyrantel pamoate 11 mg/kg for three days
Anemia needs to be corrected with iron and dietary supplements
PREVENTION
Personal hygiene
Use of appropriate footwear and health education
Mass drug administration programmes

TRICHURIS TRICHIURA (WHIPWORM)
Infection is acquired during childhood
Usually associated with mixed infections with roundworm
Morphology
Adult: The posterior end is about 2/5th of the total length and is thick like the
handle of a whip, while the anterior end is thin and slender (hence the name
‘whipworm’)
Eggs: The eggs are bile-stained, brown, barrel-shaped
Approximately 55 × 25 µm in size
They have characteristic bipolar mucus plugs
The eggs float in a saturated solution of common salt

LIFE CYCLE
Humans get infected
upon ingesting
embryonated eggs
present in contaminated
food or water or via
fomites or hands
Produce large number of
eggs within large intestine
of humans, which are
excreted in stools
whipworms

CLINICAL FEATURES
Majority of infections are asymptomatic
In heavy infections
 Vague abdominal pain, anorexia, flatulence, fever, nausea and
vomiting
 Dysentery syndrome (abdominal cramps, tenesmus and loose
motions with large amounts of mucus and blood)
Complications: Recurrent rectal prolapse, growth retardation and
cognitive impairment in children

Microscopic examination of stool demonstrates barrel-shaped ova of T.
trichiura which are bile-stained
TREATMENT
Albendazole (400 mg single dose) or mebendazole 100 mg BD for three
days.

ENTEROBIUS VERMICULARIS
(PINWORM)
Also known as threadworm
MORPHOLOGY
Adult: Tiny, thread-like and whitish worms;
reside in the large intestine
Eggs: Typically planoconvex, colourless
and walled; each egg contains a tadpole-
shaped larva inside and floats in the
saturated salt solution

LIFE CYCLE
Humans are the only hosts
They acquire infection by ingesting
the fully developed embryonated egg
Autoinfection is also common
The gravid female migrates to the
anus to lay eggs on the perianal skin
Eggs are usually laid at night and
cause itching
Fig. 24.23 Adult pinworm, egg and life cycle of
Enterobius

CLINICAL FEATURES
Asymptomatic clinically
In children, the pathognomonic sign is intense itching in the perianal region, especially
at night
Examination shows excoriation of perianal skin, which may also result in a secondary
bacterial infection

STRONGYLOIDES
STERCORALIS
Majority of cases are seen in Southeast Asia, South America
and Africa
Exists in the free-living state as well as a parasite
Female worm lives in the duodenum and the upper part of
the jejunum
Male worms are never found in humans
Reproduction by parthenogenesis—a natural form of
asexual reproduction, in which fertilisation by males is not
necessary

MORPHOLOGY
Parasitic females are tiny—about 2–3 mm long
Free-living females are even smaller—1–2 mm long.
Eggs immediately hatch into larvae (ovo-viviparous).
LIFE CYCLE
Rhabditiform larva is passed in the feces of infected persons
This larva moults twice and develops in the soil to form an L3 larvae
Humans get infected when the L3 larva penetrates their skin

 Larva enters blood circulation
and reaches the right side of
the heart, then the lungs and
finally, the alveoli
 These ascend the trachea and
are swallowed
 Subsequently, the worms
reach the intestine, where
they moult again to develop
into adults
 Autoinfection and
hyperinfection occurs
Strongyloides
LIFE CYCLE

CLINICAL FEATURES
50% of infected individuals are asymptomatic
Larva currens or racing larva: Rashes and rapidly migrating, linear, itchy lesions at the
site of entry of the larva; these can be located on the thighs, buttocks or feet
Hyper-infection syndrome and disseminated strongyloidiasis:
Seen in immunosuppressed or HIV patients or in individuals who have high steroid
intake
Invasion of other organs by the parasite can be seen in the liver, kidneys or meninges
It is potentially fatal if untreated

Sample: Stool
Microscopy
A freshly prepared stool sample in saline preparation shows actively motile larvae
Eggs may be seen only in hyper-infection syndrome
Serology: Antigen-capture ELISA for the detection of antigens in stool samples
Molecular detection: Real-time PCR
Other tests: Eosinophilia and elevated IgE may be present

TREATMENT
Drug of choice for strongyloidiasis is ivermectin
200 mg/kg for two days
The treatment is extended up to seven days in
hyper-infection
Other drugs which may be given are
thiabendazole (25 mg/kg BD) or albendazole (400
mg BD for two weeks)

TOXOCARA
Causes migration of larva in visceral organs called visceral larva migrans (VLM)
Primarily caused by Toxocara species (Toxocara canis and T. catis) but may also be seen
in infestation with hookworms of animals
Organisms causing VLM:
Toxocara canis
T. catis
Angiostrongylus species
Gnathostoma spinigerum
Anisakiasis species

TOXOCARA
More common in children
Morphology is similar to that of other
nematodes
Once ingested by humans, embryonated
eggs release larvae in the small intestine
which are carried by portal circulation to the
liver
In humans, the larva is not able to develop
further and get fibrosed
Patients present with liver or lymph node
enlargement
larva can sometimes reach the eye (ocular
larva migrans)  diffuse pan-uveitis and
retinal detachment on unilateral vision loss
can occur

ELISA is used for the detection of antibodies to Toxocara
TREATMENT
The drug of choice is albendazole for five days

Angiostrongylus cantonensis (rat lungworm): Can migrate to the central nervous
system or eye
Abdominal angiostrongyliasis: Caused by other species of Angiostrongylus; worm
localises in the arteries of the intestine and lays egg
Gnathostoma spinigerum
Can cause invasive masses in the eye and brain
Eosinophilic meningitis and cutaneous migratory swellings may be seen
Anisakiasis causes abdominal infections accompanied by eosinophilia

INTESTINAL
CESTODE
INFECTIONS
Adult cestodes residing in the intestine are
Taenia saginata
Taenia solium
Hymenolepis nana and H. dimunita
Diphyllobothrium

TAENIA SAGINATA AND T. SOLIUM
Taenia saginata (beef tapeworm)
Causes intestinal taeniasis
Infection is acquired by the ingestion of beef
containing encysted larvae
Humans act as definitive hosts
Cattle are the intermediate hosts
T. solium (pork tapeworm)
Cause intestinal as well as cysticercosis in
humans
Acquired by eating undercooked pork.
Intermediate hosts are pigs
Humans act as both intermediate and
definitive hosts in cysticercosis

Table 24.13 Differences between T. saginata
and T. solium

MORPHOLOGY
Adult
Resides in the small intestine
The scolex or head of the worm contains four cup-like suckers that help in attachment
The segment or strobila may be immature, mature or gravid
Eggs:
Are round about 30–40 μm in diameter
Acid-fast and double-walled, enclosing an embryo with six hooklets

LIFE CYCLE IN HUMANS
Humans get infected by ingesting the larval stages of the worm, which are found in
undercooked beef
The larvae are released in the small intestine; attach to the intestinal mucosa
Larvae develops into adult
Fertilisation occurs in the same segment, which becomes filled with eggs (gravid segment)
The eggs are released in stools

LIFE CYCLE IN
CATTLE
Eggs are ingested by cattle and subsequently hatch into
oncospheres.
The oncosphere penetrates the intestinal wall and reaches
skeletal muscles where it changes into a bladderlike sac
filled with larvae
This is known as cysticercus bovis

LIFE CYCLE
The life cycle of T. solium differs from that of T.
saginata in few aspects:
The intermediate host is a pig and hence the infection
is acquired by eating undercooked pork
Autoinfection can occur as eggs released in stool can
re-enter via contaminated hands or by reverse
peristalsis
Humans can act as the definitive as well as the
intermediate hosts in T. solium
Cysticercosis in humans is caused by the larval forms
of Taenia solium. The cysts show a predilection for the
central nervous system (causing neurocysticercosis or
NCC), subcutaneous tissue, skeletal muscles and eyes

Fig. 24.25
Morphology
and life
cycle of
Taenia

TAENIA
Clinical features of intestinal taeniasis
Mostly asymptomatic
Vague abdominal discomfort, weight loss, diarrhea and
pruritis in the anal region
Patient may pass proglottids in his feces, which may
be the only sign of infestation
Clinical features of cysticercosis
The presentation depends on the site of the lesion

Clinical features of ocular cysticercosis
Ocular cysts
Diplopia, proptosis, loss of vision and slow-growing inflammatory nodules
Clinical features of subcutaneous cysticercosis
Usually asymptomatic and may just present as palpable nodules
Clinical features of muscular cysticercosis
May be asymptomatic
Sometimes, myositis with accompanying fever and eosinophilia

• Eggs of both types of Taenia are morphologically similar, but only T. saginata eggs
are acid-fast
• They are bile-stained and float in a saturated salt solution
• Proglottids may be present in stool sometimes
Stool examination: To detect eggs
Antigen detection: ELISA
Species-specific diagnosis can be made using PCR

HYMENOLEPIS NANA
Dwarf tapeworm
Smallest tapeworm to infect humans
The most common tapeworm, with worldwide distribution
Morphology
Adult
Egg: The egg is non-bile stained, double-shelled, round to oval and about 30–50 µm in
size
Inner membrane has two polar thickenings, giving rise to 4–8 polar filaments
Yolk granules fill up the space between the two membranes
Larva: The larva is a solid structure with a fully developed scolex and is called a
cysticercoid

LIFE CYCLE
 Humans are the sole hosts
infected upon ingesting eggs or
infected insects
 The cysticercoids within the
insect remain viable and are
infective
 Autoinfection can also occur
with eggs released in the small
intestine
Fig. 24.26 Morphology of Hymenolepis
nana

CLINICAL
FEATURES
 Asymptomatic infections
 Symptomatic: Persistent abdominal
pain, headache, dizziness, anorexia or
diarrhea
 Heavy infection may be seen in
malnourished and
immunosuppressed individuals
Fig. 24.27 Life cycle of H. nana

Wet mount of stool sample: Characteristic H. nana eggs
TREATMENT
Praziquantel is the drug of choice and is given as a single oral dose

HYMENOLEPIS
DIMINUTA
Zoonotic tapeworm of rodents (‘rat tapeworm’)
The clinical presentation, diagnosis and treatment of H. diminuta
are similar to those of H. nana, but with the following differences
Human infection is rare and occurs due to the ingestion of
infected insects
The adult is larger; the scolex has no hooks
The eggs are larger and without polar filaments; they are not
infectious by the person-to-person route
The intermediate host of H. diminuta is an insect and the
definitive host is a rodent

DIPHYLLOBOTHRIUM LATUM
Largest known parasite to infest the human intestine
It is also known as fish tapeworm
Morphology
Adult: Lives in the small intestine head has two longitudinal grooves (bothria)
Eggs: These are oval, measuring about 60 µm x 40 µm in size, and operculated
with a knob at one end; freshly passed eggs are unembryonated. Later, they develop
a hexacanth oncosphere lined by a ciliated epithelium.
Larva: Three larval stages are present; the first stage (L1) is called the coracidium,
the second stage is procercoid and the third stage larva is known as the plerocercoid
larva

LIFE CYCLE
 Fresh or saltwater
Cyclops or Diaptomus
are the first
intermediate hosts
 Fish are the second
intermediate hosts
 Humans get infected
after eating
undercooked fish
containing plerocercoid
larvae
Fig. 24.28 Morphology and life cycle of D. latum

Clinical features
Most infections are asymptomatic
Symptoms range from minor complaints such as abdominal pain, vomiting, weakness and weight loss to acute
abdominal presentation
Vitamin B12 absorption reduced (megaloblastic anemia)
Diagnosis
Wet mount of stool - characteristic operculated, bile-stained eggs
proglottids may be seen in stools
Treatment
Praziquantel is the drug of choice
Alternatively, niclosamide can be given

INTESTINAL TREMATODES
Hermaphrodite, leaf-like, flat and unsegmented worms varying in length from 1 mm to several
cm
Life cycles are complex, often requiring two intermediate hosts
The primary host is a vertebrate
Intermediate host, in which asexual reproduction occurs, is usually a mollusc

FASCIOLOPSIS
BUSKI
Giant intestinal fluke
Morphology
Adult: It is dark red, fleshy,
leaf-shaped
Egg: The eggs are large about
130 µm in length
Elliptical and yellowish-
brown with a clear thin shell
They are operculated at the
top and unembryonated
Fig. 24.29 Morphology of Fasciolopsis
buski: (a) egg and (b) adult

LIFE CYCLE
Humans are infected by
consuming uncooked aquatic
plants such as water chestnuts,
lotus stem or seeds that may be
infested with encysted
metacercaria
Fig. 24.30 Life cycle of Fasciolopsis

CLINICAL FEATURES
Infection is light: No symptoms
Heavy parasitemia: Abdominal pain, diarrhea or intestinal obstruction
Complications: Ascites, anemia and general edema are common
Chronic heavy infections may cause chronic diarrhea leading to malabsorption or
vitamin B12 deficiency

OTHER UNCOMMON
INTESTINAL TREMATODES
Table 24.14 Rare intestinal trematodes

INTESTINAL SCHISTOSOMIASIS
Schistosoma mansoni and S. japonicum deposit eggs in the intestinal mucosa
Diarrhea and dysentery are the presenting complaints
Colorectal and liver carcinoma have been reported with S. japonicum
S haematobium is associated with cancer of bladder

DIAGNOSIS OF INFECTIONS DUE TO INTESTINAL
TREMATODES
Microscopy of stool may demonstrate eggs
Eggs are operculated and do not float in a saturated salt solution
The eggs of S. haematobium can be detected in urine or bladder biopsy
The eggs of Schistosoma infecting intestines can be detected in stool samples and
intestinal biopsy
All eggs except those of Schistosoma haematobium are acid-fast

TREATMENT OF
INTESTINAL
TREMATODE
INFECTIONS
Praziquantel is the drug of choice to treat all trematode
infections
Niclosamide may be used as an alternative therapy

CONTROL OF INTESTINAL PARASITIC INFECTIONS
Health education, improved sanitation and avoidance of the use of human feces as
fertiliser
Mass treatment in highly endemic areas
Improved personal hygiene among people who handle food
Water vegetables should be adequately washed, preferably in hot water
Preventing contamination of ponds and other waters with pig or human excreta
Night soil should be sterilised before it is used as a fertiliser
Mollusc and snail populations should be controlled (chlorination of water)

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