Gastrointestinal Infections

Dra. Gloria Mayela Aguirre García

Internal Medicine – Infectious Diseases Physician
February 2022
Name the top 3 most common causes of disentery
Shigella is described as

a. Gram-negative, rod-shaped bacteria

b. Gram-positive, rod-shaped bacteria
c.  Gram-negative, rod-shaped protozoa
d. Gram-positive, rod-shaped protozoa
How is dysentery defined?

a. 3 stools or more in 10 hours

b. Large volume stools
c. Bloody and mucous stools
d. Watery diarrhea
What is the infective form of Entamoeba
histolytica?

 Trophoizoite
 Cyst
 Spores
 Spherules
Which species of Shigella has a type that produces
Shiga toxin?

a. S. boydii
b. S. flexneri
c. S. dysenteriae
d. S. sonnei
Inflammatory gastroenteritis - Dysentery

 Dysentery is bloody diarrhea caused by infection with certain bacteria

(Shigella spp) or parasites (Entamoeba histolytica)
 This form of intestinal infection affects the large intestine.
 Most of these organisms are invasive and cause the host to mount an
inflammatory response.
 Frequently the stool volume is small, contains mucus and white blood
cells, and if invasion is deep enough can be heme-positive.
 The patient usually has a fever, complains of abdominal pain, and of pain
while attempting to defecate (tenesmus).
Types of dysentery

Amoebic dysentery Bacillary dysentery

 Occurs in warm climates
 Spread through contaminated food and water
 Called Amoebiasis
 Caused by amoeba (single celled, can change
shape)
 Caused by bacterium (single celled organisms,
move in groups, cause diseases)
 Stronger form of shigellosis
 -Usually contracted in colder climates
 Caused by a type of Shigella bacteria
Shigella

 Shigella is classified in the family Enterobacteriaceae

 Shigella are nonmotile, facultatively anaerobic, gram-negative rods
 Infections can be caused by 4 subgroups: S. dysenteriae, S. flexneri, S. boydii, and/or S. sonnei that colonize
the GI tract. 
 The 4 species of Shigella and E. coli represent a single genomospecies
 Shigella dysenteriae type 1 produces a Shiga toxin
 Ingested bacteria pass into the small intestine where they multiply, large numbers of bacteria then pass into
the colon, where they enter the colonic cells
 Into a phagosome, they can
Shigella can invade escape and live in the
intestinal epithelial cells cytoplasm of the cell or
move to adjacent cells

Epithelium and structures Severe cases: ulceration of

may become ulcerated and the mucosa, dehydration,
cause loss of fluid and rectal bleeding
S. dysenteriae type 1 produce Shiga toxin

Shiga toxin targets the endothelial cells of small blood vessels in

small and large intestine

Shiga toxin binds to glycosphingolipid

Toxin targets the large ribosomal subunit affecting protein

synthesis

Hemorrhaging and lesions in the colon can result

Shigella

 It is transmitted by direct person to person spread and contaminated food and water
 The incubation period ranges from one to three days
 Typically presents high fever, abdominal cramps, bloody and mucoid diarrhea as well tenesmus is common
 All four serogroups cause dysentery, but S. dysenteriae serotype 1 has been associated with a particularly severe form
of illness thought to be related in part to its production of Shiga toxin.
 Complications: HUS, reactive arthritis.
Shigella Infection

A) MacConkey agar
B) Hektoen enteric agar
C) Xylose lysine doxycholate agar
Shigella

 Treatment
 Diagnosis  Self-limited
 Clinical suspicion  Hydration
 WBC and blood in fecal samples (70%)  Antibiotic therapy (immunocompromised, severe
 Immunoassays disease, whoever that have the potential to spread
the disease)
 Stool culture
 Fluoroquinolone
 Molecular testing – PCR  3 gen cephalosporin
 Macrolides

*Beware with resistance

Shigella
Enteroinvasive E. coli

Similar to V. cholerae

Produces Shiga-like toxin

Similar a Shigellosis
Enteroinvasive E. coli

 E. coli is a common member of the normal microbiota of the colon

 Vast majority of strains are helpful commensal bacteria
 Some can be pathogenic
 E. coli ferments lactose
Enteroinvasive E. coli

 E. coli  attaches to the intestinal mucosa, and toxins interrupt normal intestinal cell secretion and absorption
(secretory toxins) or damage the intestinal cell (cytotoxins)
 Pathogenic mechanism similar to that of Shigella
 EIEC invades the intestinal cell, multiplies intracellularly, and extends into the adjacent intestinal cells
 These adherence factors and toxins are encoded on accessory genetic elements in E. coli, such as plasmids,
transposons, and bacteriophages
 May be differentiated from Shigella principally by the fact that EIEC strains ferment glucose and xylose. 
Enteroinvasive E.coli

 Incubation period have a median incubation of three days , with a range of 1-10 days
 It begins as watery diarrhea that can or cannot progress to dysentery.
 Infection can result in severe disease
Enteroinvasive E.coli

 Diagnosis
 Clinical suspicion
 Treatment
 Selective culture
 Hydration
 Sorbitol-MacConkey (E. coli O157:H7 don’t ferment
sorbitol)  Antimotility agents
 Molecular testing – NAATs  Non-steroidal anti-inflammatory
 Certain antibiotics can shorten the duration of
illness but are not always necessary.
Strain O157:H7 has been
responsible for several
outbreaks.
O and H are surface
antigens that contribute
to pathogenicity and
trigger host immune
response
O: O-side chain of the
lipopolysaccharide
H: flagella
Entamoeba hystolytica

 Intestinal amebiasis caused by the protozoan

Entamoeba histolytica
 Clinical manifestations include amebic dysentery and
extraintestinal disease like amebic liver abscess and
other manifestations such as pulmonary, cardiac and
brain involvement but some cases could be
asymptomatic
Cyst: responsible for person-to-
person transmission

Trophozoite: only form present in

the tissue
Entamoeba hystolytica

 The trophozoite is able to kill both epithelial cells and inflammatory cells, which is thought to
occur through a number of different mechanisms, including:
 Secretion of proteinases by the trophozoites
 Lysis of target cells via a contact-dependent mechanism
 Killing of mammalian cells by apoptosis (programmed cell death)
 Formation of amebapores, a family of small peptides that can form pores in lipid bilayers, resulting in
cytolysis of infected cells
 Changes in intestinal permeability, probably via disruption of tight-junction proteins
Entamoeba hystolytica

 Diagnosis
 Stool microscopy  Treatment
 Stool antigen detection  Metronidazole

 Stool PCR  Tinidazole

 Serology  Nitazoxanide

 Colonoscopy with histologic examination  Patients without symptoms or active disease

 Paromicyn
 Idoquinol
Yersinia spp.

 Pathogenic species:
 Y. pseudotuberculosis
 Y. enterocolitica
 Y. pestis

 These are zoonotic agents that cause disease in humans

 Gram negative non-spore-forming bacilli that exhibit bipolar staining
 Facultative anaerobes

 Pathogenic Yersinia species share a highly conserved virulence plasmid and a chromosomal high-pathogenicity island (HPI)
and show tropism for lymphoid tissue, there their ability to evade host innate immunity enables extracellular proliferation.
Yersinia enterocolitica

 Chromosomal virulence gene: yst, encoding a heat-stable toxin unique to enteropathogenic Yersinia, and
invA an epithelial cell adhesin gene.
 Invasin facilitates efficient binding to intestinal mucosal cells and translocation from the lumen to Peyer’s patches.
 Type 3 secretion system that forms a needle structure on the surfaces of pathogenic Yersinia, with a V
antigen at the tip, and interacts with target cells (macrophages, dendritic cells, granulocytes/neutrophils) to
enable inyection of Yops (Yersinia outer membrane proteins), which interfere with phagocytosis and other
innate host cell responses.¡, resulting in target cell apoptosis.
 Production of urease wich allows Yersinia to survive in the stomach and colonize the small intestine.
Yersinia enterocolitica

 Organisms are found in the GI tract of animal species, most commonly swine, rodents and dogs.
 Food products, unpasteurized milk and raw and undercooked meat.

 Trasmission: fecal-oral route

Clinical features

 Gastroenteritis associated with consumption of contaminated food or water.

 Severity of disease is related to the serotype and can range from self-limited gastroenteritis to terminal ileitis
and mesenteric lymphadenitis (often misdiagnosed as appendicitis)
 Young children: fever, watery diarrhea, occasionally bloody and severe, and abdominal pain
 Also accompanied by pharyngitis.
 Symptoms resolve within 7 days
 Uncommon complication: septicemia, reactive arthritis.
Diagnosis

 PCR
 Stool culture
Treatment

 The optimal treatment strategies are unclear

 Frequently produces beta lactamases
 Review susceptibility to aminoglycosides, tetracyclines, chloramphenicol, trimethoprim-sulfamethoxazole,
and fluoroquinolones 
Campylobacter

 24 species within the genus of Campylobacter.

 They are curved, S-shaped, spiral gram-negative rods

 Campylobacter spp are common commensals in the gastrointestinal tract of animals, especially poultry; thus,
animal-to-human transmission of infections occurs frequently. 
Pathogenesis

 The mechanism of pathogenesis

of Campylobacter jejuni comprises four
main stages:
 adhesion to intestinal cells
 colonization of the digestive tract,
 invasion of targeted cells
 toxin production. 
Clinical features

 The mean incubation period is three days (range one to seven days) 
 Early symptoms include abrupt onset of abdominal pain and diarrhea. 
  In about one-third of cases, a prodromal period characterized by high fever accompanied by rigors,
generalized aches, dizziness, and delirium is observed.
 The acute illness is characterized by cramping, periumbilical abdominal pain, and diarrhea. Patients
frequently report ten or more bowel movements per day
 Diarrhea is self-limited and lasts for a mean of seven days
Diagnosis

 Campylobacter enteritis should be suspected in the setting of severe abdominal pain with diarrhea. 
 The diagnosis is established by stool culture (or, in cases complicated by bacteremia, by blood culture) or
by culture-independent assays, such as molecular testing, on stool.
Treatment

 Given the self-limited nature of most Campylobacter infections and the limited efficacy of routine
antimicrobial therapy, treatment is warranted only for patients with severe disease or risk for severe
disease.

 Azythromycin
 Fluoroquinolones
 Carbapenems
Helicobacter pylori

 H. pylori is a spiral shaped, microaerophilic, gram negative bacterium

 The organism's urease, motility, and ability to adhere to gastric epithelium are factors that allow it to
survive and proliferate in the gastric milieu
 Bacterial urease hydrolyzes gastric luminal urea to form ammonia that helps neutralize gastric acid and form a
protective cloud around the organism, enabling it to penetrate the gastric mucus layer
 Its spiral shape, flagella, and the mucolytic enzymes which it produces facilitate its passage through the mucus
layer to the gastric surface epithelium 
 H. pylori then attaches to gastric epithelial cells by means of specific receptor-mediated adhesion
 H. pylori is the most common chronic bacterial infection in humans  
 Person-to-person transmission of H. pylori through either fecal/oral or oral/oral exposure seems most likely
Diagnosis

 Biopsy urease testing

 Histology
 Gastric biopsies can diagnose of H. pylori infection and associated lesions (eg, atrophic gastritis, intestinal metaplasia,
dysplasia, and MALT lymphoma). 
 Bacterial culture and sensitivity testing
 Noninvasive tests for the diagnosis of H. pylori include urea breath testing (UBT), stool antigen testing,
and serology. 
Clinical case

 A 25-year-old woman presented with 2 days of bloody diarrhea. She worked as a school teacher and had led
a school trip to a farm 4 days before her symptoms began. She had a history of mild asthma and used
occasional salbutamol inhalers as needed. She had no known allergies. She had not received any recent
steroids or antibiotics.
 On admission she was dehydrated. Her temperature was 36.8°C, and she was diffusely tender on abdominal
examination. She had a seizure shortly after admission and developed some motor weakness.
 Investigations:
 Creatinine clearance 42 mL/min
 Peripheral white cell count 14.0 ×109/L
 Hemoglobin 8.2 g/dL
 Platelet count 90,000/μL
 CT scan abdomen findings consistent with pseudomembranous colitis
 Supportive management with IV fluids was commenced
approach

 Lab tests and imaging

 Treatment
 A 47-year-old man presented with a fever and constipation for 5 days. He had been nonspecifically unwell
for 3 weeks. Two weeks before presentation, he had returned from a 6-month trip to India.On examination he
was systemically unwell with rigors and fever >38°C. He had palpable hepatosplenomegaly and generalized
abdominal tenderness.
 Investigations:
 Total white cell count 3.0 ×109/L
 Hemoglobin 10.2 g/dL
 Platelet count 150,000/μL
 Blood cultures negative at 24 hours
 He was commenced on intravenous ceftriaxone therapy.
What further investigation would have the
highest diagnostic yield?

a. Bone marrow culture

b. Computed tomography scan of the abdomen
c. Liver biopsy
d. Repeat blood cultures
e. Stool cultures