Part III

Microbiology as Applied to
Infectious Diseases

CHAPTER 24 (A)
GASTROINTESTINAL
INFECTIONS

Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Phone: 040-2766 5446/5447
Email: info@universitiespress.com
marketing@universitiespress.co
 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

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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

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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

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 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)
INFECTION Dysentery: Inflammation of the large intestine,
S OF THE accompanied by fever and abdominal cramps
associated with blood and mucus (pus) in stool
GIT (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)
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 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
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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

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Table 24.1 Pathogenic mechanism of gastroenteritis

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 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
PATHOGENE microscopy

SIS 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

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 ETIOLOGY
Table 24.2 Etiology of infective
gastroenteritis

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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

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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

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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

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LABORATOR
Y
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
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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

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LABORATORY DIAGNOSIS OF GI INFECTIONS
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

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 LABORATORY DIAGNOSIS OF GI INFECTIONS
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

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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)

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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

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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

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 Part III
Microbiology as Applied to
Infectious Diseases

CHAPTER 24 (B)
GASTROINTESTINAL
INFECTIONS

Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Phone: 040-2766 5446/5447
Email: info@universitiespress.com
marketing@universitiespress.co
 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

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BACTERIAL CAUSES
OF
GASTROINTESTINAL
INFECTIONS

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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

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 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)

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

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 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

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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

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LABORATORY DIAGNOSIS
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

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 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

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 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)

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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.)

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ANTIGENIC STRUCTURE AND VIRULENCE
FACTORS
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

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ANTIGENIC STRUCTURE AND
VIRULENCE FACTORS
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)

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ANTIGENIC STRUCTURE AND VIRULENCE
FACTORS
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

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Table 24.3 Methods for detecting ETEC-
labile (LT) and ETEC stable (ST)
enterotoxins
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

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CLINICA Diarrhea

L Septicemia, neonatal sepsis and neonatal

meningitis (Chapter 20 and 23)
FEATUR Urinary tract infection (Chapter 27)

ES

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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

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DIARRHEA IS CAUSED BY SIX TYPES OF
E. COLI
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

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DIARRHEA IS CAUSED BY SIX TYPES OF E.
COLI
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

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DIARRHEA IS CAUSED BY SIX TYPES OF E.
COLI
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

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DIARRHEA IS CAUSED BY SIX TYPES OF E.
COLI
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

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DIARRHEA IS CAUSED BY SIX TYPES OF E.
COLI
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

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LABORATO Table 24.4 Characteristics of diarrheagenic E. coli and methods
to detect them
RY
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

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PREVENTI Antibiotic treatment is not indicated for E. coli
ON AND diarrhea
Personal hygiene and food safety for
TREATME prevention
No vaccines available
NT

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VIBRIO CHOLERAE
Slender, gram-negative, curved bacilli
Causes cholera

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

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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)
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VIBRIO CHOLERAE
The non-O-1 vibrios (the non-
agglutinating vibrios) have been
classified up to 139 serogroups; O-139
causes epidemics of cholera Table 24.5 O serotypes of cholera
vibrios
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

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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

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VIBRIO CHOLERAE
 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 Fig. 24.6 Attachment of subunit B to GM1 ganglioside on
 IgG, IgM and IgA epithelial cells and entry of subunit A of the cholera toxin
into the intestinal epithelial cells, leading to hypersecretion
 Natural infection confers immunity, for 6–12 of sodium chloride and water (Source: Jessica Brochu, CC
BY-SA 4.0, via Wikimedia Commons)
months

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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

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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

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LABORATORY DIAGNOSIS
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

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LABORATORY DIAGNOSIS

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

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LABORATORY
DIAGNOSIS
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 Fig. 24.7 Yellow colonies on TCBS
centre and a turbid halo (Source: Department of
Microbiology, Pondicherry Institute
of Medical Sciences, Puducherry)

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 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
Fig. 24.8 String test used to differentiate
Vibrio spp. From Aeromonas spp. and
cholera O subgroup
Plesiomonas

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 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

LABORATO Incubated at 37°C for 6–8 hours

RY Enriched a second time before it is plated on

cholera-specific selective media

DIAGNOSI ii) Filtration technique:

S
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

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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)

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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

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

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HALOPHILIC VIBRIOS
Vibrios that have a high requirement of sodium chloride

Their natural habitats are seawater and marine life

Halophilic vibrios known to cause human disease

• V. parahaemolyticus
• V. alginolyticus
• V. vulnificus

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

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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

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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

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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

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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

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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

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 PATHOGENICIT
Y
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:

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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

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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

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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

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LABORATORY DIAGNOSIS
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

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 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
Fig. 24.9 Red colonies of Shigella sonnei on XLD Improving personal and environmental
agar (Source: CDC, PHIL, Image ID 17191) sanitation

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 Part III
Microbiology as Applied to
Infectious Diseases

CHAPTER 24 (C)
GASTROINTESTINAL
INFECTIONS

Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Phone: 040-2766 5446/5447
Email: info@universitiespress.com
marketing@universitiespress.co
 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

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BACTERIAL CAUSES
OF
GASTROINTESTINAL
INFECTIONS

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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

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This Photo by Unknown Author is licensed under CC BY-SA
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

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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

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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

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LABORATORY DIAGNOSIS
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

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 TREATMENT
Fluid and electrolyte replacement
When needed, erythromycin is the best
antibiotic

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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.

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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

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 PATHOGENICIT
Y
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
Fig. 24.10 Helicobacter pylori interact with site of colonisation
gastric mucosa and colonise (Source:
https://openstax.org/books/
microbiology)
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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

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 LABORATORY DIAGNOSIS
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: Fig. 24.11
Helicobacter pylori
IgM and IgG ELISA may be used for seroepidemiological
gastritis—silver stain
studies in the community

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LABORATORY DIAGNOSIS
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

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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)

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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

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 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

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This Photo by Unknown Author is licensed under CC BY-NC-ND
 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)

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LABORATORY DIAGNOSIS
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

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 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

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 AGENTS
ASSOCIATE
D WITH
FOOD
POISONING

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This Photo by Unknown Author is licensed under CC BY-NC-ND
 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
This Photo by Unknown Author is licensed under CC BY-SA-NC carrier

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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

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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

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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

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LABORATORY DIAGNOSIS
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

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

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

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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

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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

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LABORATORY DIAGNOSIS TREATMENT
 Special selective media are
useful in isolating B. cereus from Both types of the illness are mild and self-limiting, requiring no
feces and food sources specific treatment
 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

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Table 24.6 Summary of bacterial
infections of the GI tract

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

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 Part III
Microbiology as Applied to
Infectious Diseases

CHAPTER 24 (D)
GASTROINTESTINAL
INFECTIONS

Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Phone: 040-2766 5446/5447
Email: info@universitiespress.com
marketing@universitiespress.co
 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

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FUNGAL AGENTS
ASSOCIATED WITH
FOOD
POISONING

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This Photo by Unknown Author is licensed under CC BY-NC-ND
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

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 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

Mycotoxico Mycotoxins are natural products produced by

fungi and found in some articles of food
ses 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

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Table 24.7 Important mycotoxins and their sources

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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

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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

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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

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VIRAL AGENTS
ASSOCIATED
WITH
GASTROENTERITI
S

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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

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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

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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

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

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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

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LABORATORY DIAGNOSIS
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

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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

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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

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 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
NORWALK Epidemics of diarrhea associated with the
VIRUS consumption of raw oysters
Virus demonstrated in feces by electron
microscopy
Antibodies to the virus can be detected by
immune electron microscopy and
radioimmunoassay

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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

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

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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

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PARASITES CAUSING
INFECTIONS OF
GASTROINTESTINAL
TRACT

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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.

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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

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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

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 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

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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

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LABORATORY DIAGNOSIS
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

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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

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COMMENS Found in the caecum as harmless commensals
AL Are not known to cause any disease in humans
FLAGELLAT Chilomastix mesnili

ES OF THE Retortamonas intestinalis

Enteromonas hominis
INTESTINE

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 Commensal

Known to cause intermittent diarrhea, flatulence

DIENTAMO and abdominal cramps in some people
EBA
FRAGILIS Majority of cases are asymptomatic

Exists as small (5–12 µm) trophozoites with 1–2

nuclei; it does not have a cystic stage

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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

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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

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

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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

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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

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

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 Cystoisospora belli was formerly known as
Isospora belli

LIFE CYCLE
Cystoisospora require a single host for their life
CYSTOISOS cycle
PORA 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

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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

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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

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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

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 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
LIFE Humans (definitive hosts) gets infected when they consume

CYCLE 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

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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

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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

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  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
LABORATORY  Modified acid-fast staining to visualise oocysts
DIAGNOSIS OF  Auramine, safranin and lactophenol cotton blue stains to
DIARRHEA visualise cysts
SUSPECTED  Autofluorescence under UV light for Cyclospora and
TO BE CAUSED Cystoisospora but is not useful for visualising
BY INTESTINAL Cryptosporidium
 Direct fluorescent antibody staining can be used to detect
SPOROZOA 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

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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

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Table 24.8 Microscopic characteristics of oocysts of intestinal sporozoa

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 Table 24.9 Amoeba causing disease in humans

Entamoeba histolytica and Balantidium

coli are the most prominent causes of
PARASITES CAUSING parasitic dysentery
DYSENTERY Are motile with the help of pseudopodia

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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

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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.

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LIFE CYCLE
AND
PATHOGEN
ESIS
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

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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

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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

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 Table 24.10
Differentiatio
n between
bacillary and
amoebic
dysentery

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 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
LABORATO spp. include modified Boeck and Drbohlav medium and egg
RY diphasic medium
Isoenzyme analysis
DIAGNOSIS
Serology: Detection of antibodies by ELISA
Fecal antigen detection assays
Molecular diagnostics: PCR or DNA probes

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 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

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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

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Table 24.11 Amoebae causing disease in humans

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 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
Fig. 24.18 Cyst and trophozoite of Balantidium cysts are passed in feces

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LABORATORY DIAGNOSIS
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

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 Part III
Microbiology as Applied to
Infectious Diseases

CHAPTER 24 (E)
GASTROINTESTINAL
INFECTIONS

Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Phone: 040-2766 5446/5447
Email: info@universitiespress.com
marketing@universitiespress.co
 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

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PARASITES CAUSING
INFECTIONS OF
GASTROINTESTINAL
TRACT

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 Intestinal
Nematode
Infections
MOST COMMON INFECTIONS
WORLDWIDE

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 Largest nematode that resides in the small
intestine. Infection more common in children
Morphology
Adult, larva (four stages) and egg stages
Egg:
ASCARIS The fertilised egg (infectious form) is round or
LUMBRICOI oval and around 90 × 45 µm in size
DES It is surrounded by a thick, albuminous coat
containing a large, unsegmented ovum of granular
(ROUNDW mass. It floats in the saturated salt solution
ORM) 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

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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

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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

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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

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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

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 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
Fig. 24.20 Egg and larva of
hookworm There is clear space between the shell
and the ovum

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Table 24.12 Differences between Necator americanus and Ancylostoma duodenale

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 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

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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

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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

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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

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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

Fig. 24.22 Morphology and life cycle of

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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

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LABORATORY DIAGNOSIS
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.

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 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
This Photo by Unknown Author is licensed under CC BY-SA
solution

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 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

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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

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 Majority of cases are seen in Southeast Asia, South America
and Africa
Exists in the free-living state as well as a parasite

STRONGYLOIDES Female worm lives in the duodenum and the upper part of
the jejunum
STERCORALIS Male worms are never found in humans
Reproduction by parthenogenesis—a natural form of
asexual reproduction, in which fertilisation by males is not
necessary

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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

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 LIFE
 CYCLE
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

Fig. 24.24 Morphology and life cycle of

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Strongyloides
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

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LABORATORY DIAGNOSIS
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

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

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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

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 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
TOXOCARA 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

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LABORATORY DIAGNOSIS
ELISA is used for the detection of antibodies to Toxocara

TREATMENT
The drug of choice is albendazole for five days

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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

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 Adult cestodes residing in the intestine
are
INTESTINA
Taenia saginata
L CESTODE
Taenia solium
INFECTION
S Hymenolepis nana and H. dimunita
Diphyllobothrium

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

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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

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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

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 Eggs are ingested by cattle and subsequently

LIFE
hatch into oncospheres.
The oncosphere penetrates the intestinal wall and

CYCLE IN reaches skeletal muscles where it changes into a

bladderlike sac filled with larvae

CATTLE This is known as cysticercus bovis

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 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
LIFE CYCLE 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

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 Fig.
24.25
Morpholog
y and life
cycle of
Taenia

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 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
TAENIA may be the only sign of infestation

Clinical features of cysticercosis

The presentation depends on the site of the
lesion

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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

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LABORATORY DIAGNOSIS
Stool examination: To detect eggs

• 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

Antigen detection: ELISA

Species-specific diagnosis can be made using PCR

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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
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 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

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 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
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LABORATORY DIAGNOSIS
Wet mount of stool sample: Characteristic H. nana eggs

TREATMENT
Praziquantel is the drug of choice and is given as a single oral
dose

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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

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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

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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

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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

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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

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FASCIOLOP
SIS 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

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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

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Fig. 24.30 Life cycle of
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

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OTHER UNCOMMON
INTESTINAL Table 24.14 Rare intestinal trematodes

TREMATODES
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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

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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

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

E
INFECTIONS

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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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