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DTMH Block 3 > Intestinal diseases > Flashcards

Intestinal diseases Flashcards

1
Q

What is the leading cause of morbidity and mortality worldwide?

A

Gastroenteritis

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2
Q

Where are infectious intestinal diseases usually contracted in the UK?

A

Home

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3
Q

Compare paediatric diarrhoea in developed vs developing countries

A

Developed
- <1 episode/y
- winter
- rare dehydration, nutrition-sequelae, assoc with measles, epidemics
- polymicrobial unusual

Developing
- 3-10 episod/y
- any season
- frequent dehydration, common nutrition-sequelae, 15-65% measles assoc, frequent epidemics
- >20% polymicrobial

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4
Q

What are common viruses that cause intestinal disease?

A

Rota
Noro
Astro
Adeno 40/41
Calci
Corona

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5
Q

What are common bacteria that cause intestinal disease?

A

E.coli (EPEC, ETEC, EAggEC, EIEC)
Salmonella
Shigella
Yesenia enterocolitica/pseudotubercolosis
Campylobacter
Vibrio

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6
Q

What are common protozoa that cause intestinal disease?

A

Microsporidia
C. parvum
Isospora belli
Entamoeba histolytica
G. lamblia

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7
Q

What are common trematodes that cause intestinal disease?

A

Fasciolopsis buski
Heterophyes heterophyes
Fasciola hepatica
Clonorchis sinensis

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8
Q

What are common cestodes that cause intestinal disease?

A

Taenia saginata

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9
Q

What are common helminths that cause intestinal disease?

A

Pinworms
Whipworms
Threadworms
Hookworms

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10
Q

Which bacteria causing IID are NOT zoonotic?

A

S. typhi
Shigella

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11
Q

What are the host factors that influence IID?

A

Species, age
Hygiene
Intestinal motility
Specific immunity (phagocytic, humoral, cell-mediated)
Non-specific
Intestinal receptors
Underlying diseases

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12
Q

What are the environmental factors that influence IID?

A

Sanitation
Hygiene
Education
Overcrowding
Climate
Hospitals

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13
Q

What are the microbe factors that influence IID?

A

Transmission mode
Infectious dose
Virulence factors
Toxins

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14
Q

Which bacteria produces mucinase?

A

V. cholera

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15
Q

What are the modes of transmission of IIDs?

A

Predominantly fecal-oral
Person-to-person
Aerosolisation (norovirus after vomiting)

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16
Q

What is the latin name for the common house fly?

A

Musca domestica

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17
Q

How are common house flies related to transmission of IIDs?

A

Transfer focal matter via
- feces on hairy limbs
- stomach contents regurgitation onto food
- defecation onto food

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18
Q

What is it called when a domestic house fly regurgitates its stomach contents?

A

Vomit drop

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19
Q

What are the 3 types of diarrhoea?

A

Acute, chronic, persistent
OR
Non-inflammatory, inflammatory and penetrating

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20
Q

Define acute diarrhoea

A

Loose/watery stools >3x in 24h

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21
Q

Define chronic diarrhoea

A

Diarrhoea lasting >4 weeks

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22
Q

Define persistent diarrhoea

A

Diarrhoea lasting >2 weeks

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23
Q

What is the difference in the epidemic pattern of waterborne vs foodborne diarrhoea?

A

Waterborne - explosive
Foodborne - localised

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24
Q

Discuss the mechanisms of non-inflammatory diarrhoea

A

Adherence and sequelae
- villus tip disruption
- brush border disruption
- enterotoxin production

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25
Q

Name examples of causative organisms of non-inflammatory diarrhoea

A

ETECT
EAEC
V. cholerae
C. perfringens
B. cereus
G. lamblia
Rotavirus
Norovirus
C. parvum

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26
Q

Discuss the mechanisms of inflammatory diarrhoea

A

Invasion
Cytotoxins

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27
Q

Name examples of causative organisms of inflammatory diarrhoea

A

EIEC
S. enteritidis
Shigella
V. parahemolyticus
C. difficile
C. jejune
Entamoeba histolytica

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28
Q

What is significant about penetrating diarrhoea?

A

Does not primarily present as diarrhoea

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29
Q

Name examples of causative organisms of penetrating diarrhoea

A

S. type
Yersinia enterocolitica
Campylobacter fetus

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30
Q

Name the 5 e.coli types

A

Enteropathogenic (EPEC)
Enterotoxigenic (ETEC)
Enteroaggregrative (EAggEC)
Enteroinvasive (EIEC)
Enterohemorrhagic (EHEC)

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31
Q

What is the major cause of infantile diarrhoea (<6m) in developing countries?

A

EPEC

Breastmilk is protective (lipids and immunoglobulins limit adherence)

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32
Q

Discuss the features of EPEC

A

Transmission: person-to-person
Reservoir: humans
Site: small intestine
Treatment: primarily supportive but antibiotics can be used in severe cases to shorten duration
Vaccine: none

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33
Q

Discuss the pathophysiology of EPEC

A

Attachment and effacement of enterocytes
1. Intimin (adhesin) allows binding to host intestinal cells
2. Adherence -> actin rearrangement and host cell deformation
3. Moderate invasion of host cells -> inflammation -> loss of microvillus surface area and loosening of tight junctions -> direct fluid secretion

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34
Q

Discuss the clinical presentation of EPEC

A

Severe acute watery diarrhoea
Vomiting
Fever
Can be persistent

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35
Q

Discuss the properties of stool in EPEC

A

Copious
Watery
RBCs absent
WBCs scanty (moderate inflammation)

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36
Q

What is the major cause of childhood diarrhoea in developing countries?

A

ETEC

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37
Q

What is the number 1 cause of traveller’s diarrhoea?

A

ETEC

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38
Q

Discuss the features of ETEC

A

Transmission: fecal-oral
Reservoir: humans, animals, aquatic sources
Site: small intestine
Treatment: primarily supportive, anti-motility agents, fluroquinolones
Vaccine: no specific, commercially available

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39
Q

Discuss the pathophysiology of ETEC

A

Enterotoxins!
1. Attachment via fimbrial adhesions and colonisation factor antigens
2. No invasion!!!
3. Expression of
- heat labile toxin (LT)
- heat stable toxin (ST)

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40
Q

Discuss the pathophysiology of LT and ST

A

LT
- active adenylate cyclase -> incr cAMP -> incr fluid secretion
ST
- incr cGMP

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41
Q

ETEC’s heat labile toxin is similar to which other toxin?

A

Cholera toxin (similar structure and function)

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42
Q

Discuss the clinical presentation of ETEC

A

Severe acute diarrhoea
Abdominal cramping
Occasional vomiting

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43
Q

Discuss the properties of stool in ETEC

A

Copious
Watery
RBCs absent (no invasion)
WBCs absent (minimal inflammation)

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44
Q

Which e.coli strain is associated with emerging infection in childhood, traveller and persistent diarrhoea?

A

Enteroaggregative e.coli (EAEC)

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45
Q

Discuss the features of EAEC

A

Transmission: fecal-oral
Reservoir: asymptomatic humans
Site: small intestine
Treatment: primarily supportive, fluoroquinolones for traveller’s
Vaccine: none

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46
Q

Discuss the pathophysiology of EAEC

A
  1. Adherence via bundle-forming pili -> loss of microvillus surface -> decreased absorption
  2. Mucus biofilm formation
  3. Enterotoxins
    Plasmid encoded toxin (PET) -> crypt dilation, cell damage, fluid and electrolyte secretion
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47
Q

What is the suggested reason for persistence with EAEC?

A

Mucus biofilm

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48
Q

Which enterotoxins are involved in EAEC pathophysiology?

A
  1. Plasmid encoded toxin (PET) -> crypt dilation, cell damage, fluid and electrolyte secretion
  2. Enteroaggregative heat stable (EAST) -> fluid and electrolyte secretion
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49
Q

Discuss the clinical presentation of EAEC

A

Severe acute or persistent chronic mucoid diarrhoea
Low grade fever

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50
Q

Discuss the properties of stool in EAEC

A

Watery, mucoid
Occasional RBCs

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51
Q

Which e.coli is the cause of dysenteric-like syndrome?

A

Enteroinvasive e.coli (EIEC)

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52
Q

Discuss the features of EIEC

A

Transmission: fecal-oral and person-to-person
Reservoir: humans
Site: LARGE intestine
Treatment: primarily supportive
Vaccine: none

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53
Q

Discuss the pathophysiology of EIEC

A
  1. Attachment -< invasion w/ intracellular motility -> spread -> inflammation and ulceration of colonic wall
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54
Q

Discuss the clinical presentation of EIEC

A

Enterocolitis
Fever
Cramping
Watery -> dysentery
Tenesmus

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55
Q

Discuss the properties of stool in EIEC

A

Scant
Mucopurulent
RBCs common
WBCs prominent!

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56
Q

What is the most common e.coli serotype?

A

O157:H7 (EHEC)

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57
Q

Which diseases can EHEC cause

A

Hemorrhagic colitis
Hemolytic uremic syndrome

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58
Q

Discuss the features of EHEC

A

Transmission: fecal-oral, person-t-person
Reservoir: humans, animals, environment
Site: LARGE intestine
Treatment: entirely supportive, AVOID antibiotics
Vaccine: none

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59
Q

In which e.coli species should antibiotics be avoided and why?

A

EHEC -> induce expression and release of Shiga toxins which is associated with increased HUS in extremes of age

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60
Q

Discuss the clinical presentation of EHEC

A

NO fever!
Watery -> dysentery
Cramping
HUS

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61
Q

Discuss the properties of stool in EHEC

A

Copious
Bloody
Prominent RBCs
Few-absent WBCs

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62
Q

What is the primary pathogenic mechanism of ETEC?

A

Enterotoxin LT/ST

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63
Q

What is the primary pathogenic mechanism of EIEC?

A

Enterocyte invasion

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64
Q

What is the primary pathogenic mechanism of EHEC?

A

Shiga-like cytotoxin

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65
Q

What is the primary pathogenic mechanism of EPEC?

A

Adherence to enterocytes

66
Q

What is the primary site of ETEC?

A

Small intestine

67
Q

What is the primary site of EIEC?

A

Large intestine

68
Q

What is the primary site of EHEC?

A

Large intestine

69
Q

What is the primary site of EPEC?

A

Small intestine

70
Q

What is the mucosal pathology of ETEC?

A

Intact hyperaemia

71
Q

What is the mucosal pathology of EIEC?

A

Necrosis, ulceration and inflammation

72
Q

What is the mucosal pathology of EHEC?

A

Microvilli destruction
Cell death

73
Q

What is the mucosal pathology of EPEC?

A

Microvilli destruction

74
Q

In which e.coli strains is fever absent and in which stains is fever common?

A

Absent
- ETEC
- EHEC

Common
- EIEC
- EPEC

75
Q

When does rotavirus infection peak?

76
Q

Which family does rotavirus belong to? What kind of virus is it?

A

Reoviridae
dsRNA wheel-shaped virus

77
Q

What is the difference in seasonality of rotavirus in developed vs developing countries?

A

Developed - winter
Developing - year round

78
Q

Discuss the features of rotavirus

A

Transmission: fecal-oral
Reservoirs: humans
Treatment: fluids

79
Q

Discuss the clinical presentation of rotavirus

A

Profuse, watery diarrhoea
Low grade fever
Vomiting
Abdominal cramps

80
Q

How long does rotavirus shed?

81
Q

How is rotavirus diagnosed?

A

ELISA
Rotastrip (antigen)
Electron microscopy

82
Q

Which viruses are non-enveloped and what is important about their IPC?

A

Rota, adeno, entero
Inactivated by alcohol NOT common disinfectants (chlorhexidine, etc)

83
Q

What is the rotavirus vaccine?

A

Live attenuated vaccine
2 oral doses at 6w and 14w

84
Q

How protective is the rotavirus vaccine?

A

98% protective

85
Q

Which family does norovirus belong to?

A

Calciviridae

86
Q

What is the seasonality of norovirus?

A

Year round transmission
Increases in winter in temperate climates

87
Q

Discuss the features of norovirus

A

Transmission: fecal-oral, person-to-person, aerosolisation
Treatment: fluids
Vaccine: none

88
Q

Is norovirus highly infectious?

A

Yes, as few as 18 particles required

89
Q

Discuss the clinical presentation of norovirus

A

Nausea
Projectile vomiting
Cramps
Low grade fever
Myalgia
Moderate diarrhoea
Lasts 24-72h

90
Q

What is the incubation period of norovirus?

91
Q

How long does norovirus shed?

92
Q

Why is it possible to be infected with norovirus multiple times?

A

Many genotypes

93
Q

How is norovirus diagnosed?

A

PCR (stool, vomitus)
ELISA (poor sensitivity)

94
Q

How is norovirus prevented?

A

Hand washing
Surface decontamination
Food screening (clam/oyster PCR)

95
Q

Which disinfectant inactivates norovirus?

A

Chlorine NOT alcohol

96
Q

How long can norovirus survive in the environment?

A

7-12d on surfaces
Months in still water

97
Q

How is non-typhoidal salmonella classified?

A

Genus plus serotype

98
Q

How many species of non-typhoidal salmonella are there?

A

> 1500 antigenically different species

99
Q

Discuss the features of non-typhoidal salmonella

A

Broad host range (zoonotic)
High infectious dose
Fecal-oral

100
Q

Discuss the presentation of non-typhoidal salmonella

A

Fever
Vomiting
Diarrhoea > enterocolitis
Bacteremia

101
Q

What is the pathogenesis of non-typhoidal salmonella infection?

A

Invasion
Inflammation

102
Q

Discuss the treatment of non-typhoidal salmonella

A

Rehydration
Antibiotics for bacteraemia or patient at risk

103
Q

What is the prototype of enteric fever syndrome?

A

Salmonella typhi

104
Q

Discuss the features of salmonella typhi

A

Reservoirs: only humans
Endemic in SA
HIV assoc w/ increased severity
10% excrete bacteria for weeks
4% become carriers (excrete up to 1 year)

105
Q

What is enteric fever syndrome?

A

Sustained fever that increases over the first week
Headache
Abdominal pain
Diarrhoea -> constipation -> diarrhoea
Bacteremia
Rash
Splenomegaly
Bradycardia
Cough
Arthritis
Meningism

106
Q

What is the pathogenesis of salmonella typhi?

A
  1. Faecal-oral ingestion with 15d incubation
  2. Gut mucosa penetration -> uptake by macrophages -> carried via lymphatics to mesenteric lymph nodes -> blood stream via thoracic duct -> RES and other organs -> biliary infection reseeds the intestine
107
Q

What causes the inflammatory response in salmonella typhi?

A

LPS endotoxin

108
Q

Name complications of salmonella typhi

A

Abdo
- GIT haemorrhage > perforation
- Cholecystitis
Lung
- Pneumonia
- Empyema
CVS
- Thrombophlebitis
- Pericarditis
- Myocarditis
- Sepsis
CNS
- Meningitis
- Polyneuritis
- Toxic psychosis

109
Q

When will blood and bone marrow be positive for salmonella typhi?

110
Q

When will stool be positive for salmonella typhi?

111
Q

When will urine be positive for salmonella typhi?

A

Week 3-4
Transient
25% of patients

112
Q

What are FBC findings in salmonella typhi?

A

Decreased WCC with lymphocytosis

113
Q

Discuss the treatment of salmonella typhi

A

IV fluids
Fluoroquinolones
Ceftriaxone
Azithromycin

114
Q

Which patient populations often experience relapsing salmonella typhi infection?

A

Carriers
HIV
Schistosomiasis

115
Q

Discuss prevention of salmonella typhi

A

Hygiene
Vaccine (Ty21a Vi polysaccharide)

116
Q

Name 4 species of shigella

A

S. flexneri
S. sonnei
S. boydi
S. dysenteriae

117
Q

Discuss the features of shigella

A

Transmission: fecal-oral, person-to-person
Reservoir: humans
Low infectious dose

118
Q

Discuss the pathogenesis of shigella

A

Invasion
Verocytotoxin (shiga toxin)

119
Q

Discuss the clinical presentation of shigella

A

Dysentery
HUS
Systemic (immunocompromised)

120
Q

Discuss the treatment of shigella

A

Fluids
Antibiotics (CTX, fluoroquinolone)
AVOID anti-motility!!!

121
Q

Name bacterial causes of dysenteric syndrome

A

Shigella
Campylobacter
EIEC

122
Q

What is dysenteric syndrome?

A

An inflammatory, invasive, hemorrhagic process involving the colon and occasionally distal small intestine

123
Q

Discuss the clinical presentation of dysenteric syndrome

A

Fever
Vomiting
Diarrhoea
Tenesmus

124
Q

Name parasitic causes of dysenteric syndrome

A

Entamoeba histolytica

125
Q

How many stages does entamoeba histolytica have?

A

2 - trophozoite and cyst

126
Q

How does vibrio cholera appear on microscopy?

A

Gram negative
Comma shaped
Single polar flagella

127
Q

What is the nomenclature for classifying vibrio cholera?

A

Genus, species, serogroup, biotype, serotype

Eg vibrio cholerae O1 El Tor

128
Q

What are the 2 main biotypes of v. cholera?

A

O1 classical and El Tor

129
Q

What are the 2 main serotypes of v.cholerae?

A

Ogawa
Inaba

130
Q

What is the host of v.cholerae?

A

Humans are the ONLY host

131
Q

Discuss the features of v.cholerae

A

Faecal-oral transmission (person-to-person rare)
High infectious dose

132
Q

Which strains are the main cause of epidemic cholera?

A

Toxigenic strains

133
Q

Which biotype has more asymptomatic infections than the other?

134
Q

What are the interepidemic reservoirs of v.cholerae?

A

Copepods
Plankton
Crustaceans

135
Q

Which cholera pandemic are we in now?

A

7th great pandemic

136
Q

What is the theory regarding the re-emergence of El Tor biotype?

A

Global warming with El Niño -> warmer seawater -> phytoplankton expansion -> zooplankton copepods which carry v.cholerae on the surface and gut -> widespread dissemination

137
Q

Discuss the virulence factors of v.cholerae

A

Motility
Adherence
Enterotoxin (cholera toxin)

138
Q

Discuss the pathogenesis of cholera toxin

A
  1. B subunits attach to GMI ganglioside receptors
  2. A subunits enter intestinal epithelial cells -> activate adenylate cyclase -> increased cAMP which acts on small intestine epithelial cells w/ direct secretory effect on crypt cells and anti-absorption effect on villus cells
139
Q

Discuss the clinical presentation of cholera

A

No fever
Vomiting
Rice water diarrhoea

140
Q

Discuss the management of cholera

A

Rehydration
Antimicrobials to decrease diarrhoea
Monitor urine and stool output
Mass prophylaxis discourage
Vaccines

141
Q

What is the ‘bengal’ v.cholerae biotype?

142
Q

How does campylobacter appear on microscopy?

A

Gram negative spiral
“Seagull wing”

143
Q

Which campylobacter spp cause human infection?

A

> 10 spp
Most common: jejuni, coli

144
Q

Discuss the features of c.jejuni infection

A

Inflammatory diarrhoea (invasion, cytotoxin)
Distal small intestine and colonic dysentery

145
Q

What is the treatment of c.jejuni?

A

Azithromycin

146
Q

Name complications of c.jejuni

A

Guillain Barre Syndrome
HUS

147
Q

Discuss the features of campylobacter fetus

A

Cattle/sheep abortion
Cause thrombophlebitis and bacteria in humans with dissemination to other organs

148
Q

What is the treatment of choice for campylobacter foetus?

A

Gentamicin
Ceftriaxone (CNS)

149
Q

Which bacteria cause traveller’s diarrhoea?

A

ETEC
EAEC
Shigella
Salmonella
Campylobacter
Cholera

150
Q

Which viruses cause traveller’s diarrhoea?

A

Rotavirus
Calcivirus
Astrovirus
SRS (small round structured)
Hepatitis A

151
Q

Which protozoa cause traveller’s diarrhoea?

A

G. lamblia
Crypto parvum

152
Q

Which bacteria cause infantile diarrhoea?

A

Diarrhoeagenic e.coli
Shigella
Salmonella
Yersinia enterocolitica

153
Q

Which protozoa cause infantile diarrhoea?

A

G. lamblia

154
Q

Which viruses cause infantile diarrhoea?

A

Rotavirus
Adenovirus (41, 42, 44)
Echovirus

155
Q

Which pathogens commonly cause weaning diarrhoea in developing vs developed countries?

A

Developing - bacterial
Developed - rotavirus

156
Q

Discuss the new strain of c.difficile

A

B1/NAP1/O27
Produces more toxins
Increased fluoroquinolone resistance
Also community acquired

157
Q

What is the pathogenesis of c.diff?

A
  1. Disruption of colonic membrane -> colonisation
  2. Toxin A/B release
  3. Mucosal injury and inflammation
158
Q

What are the two toxins released by c.diff?

A

A - enterotoxin
B - cytotoxin

159
Q

What are complications of acute infectious diarrhoea illness?

A

Chronic diarrhoea
IBS
Reiter’s syndrome
HUS

160
Q

Which organisms are most likely to cause Reiter’s syndrome?

A

Shigella
Salmonella
Campylobacter

DTMH Block 3 (18 decks)

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