GI Infections Flashcards

1
Q

What groups are most vulnerable to GI infections

A

Infants

Elderly

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2
Q

What are the reportable GI infections of note

A
Campylobacter
Salmonella 
Shigella 
E.coli O157
Listeria 
Norovirus
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3
Q

No fever or low grade fever

No white blood cells in stool sample

A

Secondary diarrhoea

E.g. vibrio cholerae, ETEC, EAggEC, EPEC, EHEC

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4
Q

Fever

White blood cells in the stool sample (neutrophilia)

A

Inflammatory diarrhoea

E.g. campylobacter jejuni, shigella spp, non-typhoid salmonella serotypes, EIEC

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5
Q

Fever

White blood cells in stool sample (mononuclear cells)

A

Enteric fever
E.g. typhoidal salmonella serotypes
Enteropathogenic yersinia spp
Brucella spp

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6
Q

Incubation period for campylobacter

A

1-10 days

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7
Q

Disease duration of campylobacter

A

2-20 days

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8
Q

Most common source of campylobacter

A

Poultry

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9
Q

Incubation period for E.coli O157

A

1-5 days

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10
Q

Disease duration of e.coli O157

A

1-4 days

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11
Q

Incubation period of shigella

A

12-96 hours

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12
Q

Disease duration of shigella

A

5-7 days

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13
Q

Incubation period of salmonella

A

8-48 hours

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14
Q

Disease duration of salmonella

A

4-7 days

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15
Q

Incubation period of vibrio parahaemolyticus

A

24-72 hours

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16
Q

Disease duration of vibrio parahaemolyticus

A

2-10 days

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17
Q

Most common source of vibrio parahaemolyticus

A

Shellfish

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18
Q

Mechanism of disease of cholera toxins

A

It is a secretory diarrhoea toxin production
cAMP: opens Cl channel at the apical membrane of enterocytes
Efflux of Cl to lumen: loss of H2O and electrolytes

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19
Q

Mechanism of disease of superantigens

A

They are secretory diarrhoea-toxin production
Superantigens bind directly to T cell receptors and MHC class II molecules OUTSIDE the peptide binding site.
This leads to a massive cytokine production by CD4 cells (i.e. systemic toxicity and suppression of adaptive responses)

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20
Q

Host responses in enteric fever

A

Intestinal inflammation –> bacteraemia (in an immunocompromised patient) –> weak stimulation of acute phase responses (monocytes) –> no septic shock and no neutrophilia

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21
Q

Host responses in inflammatory (exudative) diarrhoea

A

Exudative inflammation –> bacteraemia (immunocompromised patient) –> detection of LPS by monocytes expressing TLR4 –> TNFa, IFNg, IL1B –> neutrophilia and septic shock

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22
Q

Features of staphylococcus aureus food poisoning

A

1/3 population chronic carriers, 1/3 transient
Spread by skin lesions on food handlers
Catalase, coagulase positive Gram positive coccus
Appears in tetrads, clusters on Gram stain
Yellow colonies on blood agar
Produces enterotoxin, an exotoxin that can act as a superantigen in the GI tract, releasing IL1 and IL2, causing prominent vomiting and watery, non bloody diarrhoea
Don’t treat, self limited

23
Q

Bacillus cereus

A

Causes food poisoning
Gram positive rod: spore forming
Spores germinate in reheated fried rice (e.g. chinease fried rice)
Heat stable emetic toxin - not destroyed by reheating
Heat labile diarrhoeal toxin - food is not cooked to a high enough temperature

Causes: water non-bloody diarrhoea which is self-limited
Rare cause of bacteraemia in vulnerable population
Can cause cerebral abscesses

24
Q

Clostridium botulinum

A

Gram positive anaerobe
Causes botulism
Source : canned or vacuum packed food (honey / infants)
Ingestion of preformed toxin (inactivated by cooking)
Blocks Ach release from peripheral nerve synapses
Treatment with antitoxin

25
Q

Clostridium pefringens infection

A

Gram positive anaerobe
Causes food poisoning
Source : reheated food (meat)
Normal flora of colon but not small bowel, where the enterotoxin acts (superantigen)
Incubation 8-16hrs
Watery diarrhoea, cramps,little vomiting lasting 24hrs

26
Q

Clostridium difficile

A

Causes pseudomembranous colitis
Occurs in 3% general population, 30% of hospitalised patients
Antibiotic related colitis (any can cause it, but mainly cephalosporins, ciprofloxacin and clindamycin)
Avoidance involved infection control
Treatment: metronidazole, vancomycin, and stop the causative antibiotics where possible

27
Q

Listeria monocytogenes infection

A

Outbreaks of febrile gastroenteritis
Beta haemolytic, aesculin positive with tumbling motility
Source : refrigerated food (“cold enhancement”),i.e. unpasteurised dairy, vegetables
Grows at 4 ºC GI watery diarrhoea, cramps, headache, fever, little vomiting
Perinatal infection, immunocompromised patients
Treatment : ampicillin

28
Q

Enterobacteriacae infection

A

Facultative anaerobes, glucose/lactose fermenters (LF),

oxidase negative

29
Q

Escherichia coli infection

A

Enterobacteriacae
Causes traveller’s diarrhoea
Source: food/water contaminated with human faeces

Enterotoxins:
Heat labile stimulates adenyl cyclase and cAMP
Heat stable stimulates guanylate cyclase
Act on the jejeunum, ileum not on colon

ETEC; toxigenic, main cause of traveller’s diarrhoea
EPEC; pathogenic, infantile diarrhoea
EIEC; invasive, dysentery
EHEC; haemorrhagic O157:H7 EHEC: shiga- like verocytotoxin causes HUS
Avoid antibiotics

30
Q

Salmonella infection

A

Non lactose fermenters,
H2S producers,
TSI agar,
XLD agar, selenite F broth

Antigens:
cell wall O (groups A-I)
flagellar H
capsular Vi (virulence, antiphagocytic)

Three species:
S. typhi (and paratyphi)
S.enteritidis
S.cholerasuis

31
Q

S. enteritidis salmonella infection

A

Causes enterocolitis
Transmitted from poultry, eggs, meat
Invasion of epi- and sub-epithelial, tissue of small and large bowel
Bacteraemia infrequent
Self limited non bloody diarrhoea ,usually no treatment
Stool positivity

32
Q

S.typhi salmonella infection

A
Causes typhoid (enteric) fever 
Transmitted only by humans
Multiplies in Payer’s patches,
Spreads ERS 
Bacteraemia, 3% carriers
Slow onset, fever and constipation,
Splenomegaly,rose spots, 
anaemia, leucopaenia,
Bradycardia, haemorrhage and
Perforation
Blood culture  positive           
Treatment : ceftriaxone
33
Q

Shigellae infection

A

Non lactose fermenters, non H2S producers, non motile
Antigens:
cell wall O antigens
Polysaccharide (groups A-D) : S.sonnei, S.dysenteriae, S.flexneri (MSM)

The most effective enteric pathogen (low ID 50)
No animal reservoir
No carrier state
Dysentery: invading cells of mucosa of distal ileum and colon
Producing enterotoxin (Shiga toxin)
Avoid antibiotics (ciprofloxacin if required)

34
Q

Vibrios infection

A

Curved, comma shaped, late lactose fermenters, oxidase positive.
Subtypes: cholera, parahaemolyticus, vulnificus

35
Q

Vibrios cholera infection

A

O1 group: epidemics, biotypes El Tor, Cholerae and serotypes Ogawa, Inaba, Hikojima
Non O1 group: sporadic or non pathogens
Transmitted by contamination of water and food from human faeces ( shellfish, oysters, shrimp)
Colonisation of small bowel and secretion of enterotoxin with A and B subunit, causing persistent stimulation of adenylate cyclase
Causes massive diarrhoea (rice water stool) without inflammatory cells
Treat the losses

36
Q

Vibrio parahaemolytiocus infection

A

Ingestion of raw or undercooked seafood (ie oysters),
Major cause of diarrhoea in Japan..or when cruising in the Carribean.. ,
Self limited for 3 days
Cholerae : grows in salty 8.5% NaCl..

37
Q

Vibrio vulnificus infection

A

Cellulitis in shellfish handlers
Fatal septicaemia with D&V in HIV patients
Treat with doxycycline

38
Q

Campylobacter infection

A

Curved, comma or S shaped
Microaerophilic
C.jejuni at 42 ºC
oxidase pos ,motile
Self limiting but symptoms can last for weeks (20 days)
Only treat if immunocompromised (macrolide)
Transmitted via contaminated food and water with animal faeces (poultry, meat,unpast. milk)
? Enterotoxin (watery diarrhoea) ? Invasion (+/- blood)
Watery, foul smelling diarrhoea, bloody stool, fever and severe abdo pain
Treat with erythromycin or cipro if in the first 4-5days
Associated with GBS syndrome, reactive arthritis, Reiter’s ..

39
Q

Yersinina enterocolitis infection

A

-Non lactose fermenter, prefers 4ºC “cold enrichment”
Transmitted via food contaminated with domestic animals excreta
Enterocolitis
Mesenteric adenitis
Associated with reactive arthritis , Reiter’s

40
Q

Mycobacteria infection (M. tuberculosis, M, avium, intracellulare)

A

Will appear as gram variable

Always think of TB

41
Q

Entamoeba histolytica infection

A
Protozoa
Motile trophozoite in diarrhoea
Non motile cyst in nondiarrhoeal illness
Killed by boiling, removed by water filters
4 nuclei
No animal reservoir
Ingestion of cysts -->trophos in
ileum -->colonize cecum, colon -->“flask shaped” ulcer 

Dysentery,flatulence,
tenesmus
Chronic : wt loss,+/- diarrhoea
Liver abscess

Diagnosis: stool micro (wet mount, iodine and trichrome), serology in invasive disease

Treat : metronidazole + paromomycin in luminal disease

42
Q

Giardia lamblia infection

A
Protozoa 
Trophozoite “pear shaped” 
2 nuclei
4 flagellas and a suction disk
Ingestion of cyst from fecally contaminated water,food

Excystation at duodenum
tropho attaches
no invasion
malabsorption of protein and fat

Travellers, hikers,
day care, mental hospitals,
MSM

Foul smelling non
bloody diarrhoea, cramps
flatulence, no fever

Diagnosis : stool micro, ELISA, “string test”

Treatment: metronidazole

43
Q

Cryptosporidium parvum infection

A

Protozoa infection
Infects the jejunum
Severe diarrhoea in the immunocomromised
Oocysts seen in stool by modified Kinyoun acid fast stain

Treatment : reconstitution of immune system

44
Q

Norovirus unfection

A
Causes outbreaks
Low ID (18-1000 viral particles)
Environmental resilience (0-60 ºC)
No long term immunity
GII.4 currently predominant strain
45
Q

Rotavirus infection

A

dsRNA “wheel like”
Replicates in mucosa of small intestine
Secretory diarrhoea, no inflammation
Watery diarrhoea ? by stimulation of enteric nervous system
By age 6 most children worldwide have antibodies to at least one type
Exposure to natural infection twice confers lifelong immunity
Huge economic burden worldwide

46
Q

Adenovirus infection

A

Types 40, 41 cause non bloody diarrhoea <2yrs of age
Can affect any type in immunocompromised
Diagnosis : stool EM, antigen detection, PCR
Types: Poliovirus, Enteroviruses (coxsackie, ECHO), Hepatitis A

47
Q

Best prevention tactics for GI infections

A
Breastfeeding, improved weaning practice
Clean water for drinking
Safe disposal of stools of young children
Precautions when travelling
Food handling
Public health notification
Good handwashing
Good handwashing
Good handwashing
48
Q

What vaccines are available against GI infections

A

Cholera
Campylobacter
ETEC
Salmonella typhi

49
Q

Cholera vaccine

A

Serogroups O1(Inaba , Ogawa, biotypes El Tor and classical), O139

Inactivated, whole cell, contains all above + B subunit of toxin (PO)

Live attenuated (PO) not recommended

50
Q

Campylobacter vaccine

A

Military, infants,traveller, candidate vaccines exist..

51
Q

ETEC vaccine

A

Inactivated and live vaccines in trails

52
Q

Salmonella typhi vaccine

A

Vi capsular PS (IM) and (PO)live

53
Q

Rotavirus vaccines

A

Rotarix: live attenuated human strain monovalent, 2(PO) doses
Rotateq: pentavalent, 3 (PO) doses, one bovine and four human strains
Rotashield and intussusception (8-20 weeks)
Age of vaccine is 6-12 weeks.

54
Q

What are the public health implications in GI infections

A

Notifiable disease
Each trust to notify to local Health Protection Unit
Notifiable diseases: Campylobacter, Clostridium sp, Listeria monocytogenes, Vibrio, Yersinia
Identify outbreaks in areas
Environmental Health Officers to inspect premises and take samples from environment and food