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4.1 Medical Microbiology > Gastrointestinal Tract Infections - Campylobacter, Salmonella, Shigella > Flashcards

Gastrointestinal Tract Infections - Campylobacter, Salmonella, Shigella Flashcards

1
Q

There is a broad range of organisms that cause gastroenteritis but not all cause fevers, what does a fever indicate?

A

Fever suggests a more invasive organism such as shigella or salmonella

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2
Q

The incubation period for gastroenteritis pathogens varies greeatly, why is this?

A

If the damage and symptoms are caused by a toxin and not the actual pathogen itself there may be a longer incubation time e.g. shiga toxin in shigella with an incubation period of2-3 days

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3
Q

Give a general note on the epidemiology of gastroenteritis

A

Sporadic cases
Often a single source that ends up affecting many people - outbreaks, epidemics etc
Community or hospital acquired
Cases are reported to the HPSC but are greatly under reported
Outbreak investigation and infection control

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4
Q

Why is it thought that gastroenteritis is so under reported?

A

This is because many of these infections are self limiting with most people just recovering at home
- nobody is going to bring a sample into their GP

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5
Q

What cases have increased in the last few years and why?

A

Shigella case notifications have been increasing

This is because the case definition has changed

PCR is now accepted for shigella ID

Shigella is also now considered an STI in MSMs and not just a foodborn illness

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6
Q

How does gastroenteritis spread?

A

Faeces from human/animals containgin pathogens/toxins

Spread to food, water/milk, contaminated hands

Ingestion of organism and/or toxins

Spread to gut

Organisms either multiply locally and produce toxins to cause diarrhoea or they invade and their toxins are absorbed and disseminated to bring about systemic infection i.e. fever

Pathogens are then excreted in faeces

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7
Q

What host mechanisms are in place to defend against gastroenteritis

A

Gastric acidity
Intestinal peristalsis
Mucous secretions from globlet cells in mucosal epithelium
Physical barrier of epithelial layer
Endogenous intestinal micorbiome
Phagocytic cells
Humoral factos
Cellular factors

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8
Q

What host defences in the mouth prevent gastroenteritis?

A

Flow of liquids
Saliva
Lysozyne
Normal microflora

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9
Q

What host defences in the oesophagus prevent gastroenteritis?

A

Flow of liquids
Peristalsis

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10
Q

What host defences in the stomach prevent gastroenteritis?

A

acid pH

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11
Q

What host defences in the small intestine prevent gastroenteritis?

A

Flow of gut contents
Peristalsis mucus:
- bile
- sIgA
- lymphoid tissue sheddin and replacement of epithelium
Normal microflora

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12
Q

What host defences in the large intestine prevent gastroenteritis?

A

Normal microflora
Peristalsis
Mucus shedding and replication of epithelium

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13
Q

How do pathogens get arounf the acidic pH of the stomach, give some examples?

A

Salmonella and Shiga-toxin producing E coli are really good at persisting in low pH environments

C. difficile is spore forming - spores make its way down to the gut

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14
Q

What is direct culture not the gold standard for enterics anymore?

A

It required a high index of clinical suspicion to choose the appropriate diagnostic test - huge problem when all cause diarrheal like disease

Very specific selective plates needed often with poor sensivity - but usually very specific

Enrichment and subculture often needed

Very time consuming and burdensum all for usually a self limiting infection

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15
Q

What are the main cons of using molecular methods for enteric diagnostics?

A

Asymptomatic carriage is often a problem

Need reflex culture -> think of what we did in the Mater whereby positive camps, salmonellas and shigellas were cultured -> often sent to reference lab aswell

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16
Q

What is the first step in enteric processing?

A

Macroscopic observation and description:
- formed/loose/liquid

Samples should “take the shape of the container” to qualify for testing, very few exceptions to this

The presence of blood, mucus or parasites should be noted

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17
Q

What are the hospital acquired GIT pathogens?

A

Salmonella species
Campylobacter species
Shigella species
E. Coli VTEC O157
Cryptosporidium
C. difficule
Norovirus
OVA cysts and parasites
Giardia

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18
Q

What are the community acquired GIT pathogens?

A

Salmonella species
Campylobacter species
Shigella species
E. Coli VTEC O157
Cryptosporidium (increasingly common CAI with travel)
C. difficile (increasingly common CAI)
Ova cysts and parasites (travel)
Giardia (travel)

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19
Q

What additional GIT pathogens are found in children?

A

Rotavirus
Adenovirus
Norovirus
Astrovirus
Sapovirus

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20
Q

Give a general description of campylobacter caused gastroenteritis

A

Camp is the most common cause of bacterial gastroenteritis in Ireland and Europe
C. jejuni causes 90% of these
C. ureolyticus seems to be an emerging pathogen
It is a notifiable disease in Ireland

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21
Q

What incubation is preferred by campylobacter?

A

Camp is microaerophilic
It likes to grow at 42 degrees

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22
Q

What are the complications of Camp?

A

Complications are rare but:
- Haemolytic Uraemic sydnrome (HUS)
- 1/1000 cases lead to Guillain-Barre Syndrome (a neurological disorder)

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23
Q

Incidence of campylobacter in Ireland, in Europe, resistance

A

There has been a steady year-on year increase of camp, 3737 in 2023
Only 13% of campylobacter is speciated in Ireland
9 million cases per year in Europe
Antimicrobial resistance is increasing

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24
Q

How many cases of camp were there in Ireland in 2023, compare this to how many cases in Europe

A

There was 3737 cases in 2023
There is about 9 million cases a year throughout Europe

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25
Q

Resistance in Camp is increasing, why is this happening?

A

This is driven from the food industry whereby animals are being given antimicrobials
Resistance spreads through the food chain

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26
Q

Only 13% of camp are speciated, why are we concenred wih this, what are we doing to get around this?

A

Only 13% speciated means we only have AST or 13% of Camp cases

Cherry Orchard is now acting as a reference lab where they will speciate any camps found

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27
Q

Compare Camp incidence in Ireland over the years t european average

A

Up until 2020 Ireland was below the EU average
We are now above the average for all age categories other than 5-14yr olds
IE incidence: 71/100,000
EU incidence: 46/100,000

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28
Q

Source and transmission of C. jejuni, how does it spread

A

Source = untreaed water, association with amoeba
Camp is ingested by the chicken or cow
Camp resides ontop of epithelium in intestine (colonises)
Human injests campylobacter by eating undercooked chicken or unpasteurised milk
In humans camp invades epithelial layer to cause gastroenteritis

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29
Q

Why do we incubate camp at 42 degrees?

A

Chicken intestine is at @42 degrees, this is its preferred growing temperature, hence why we incubate at this temp

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30
Q

What foods are associated with camp

A

Undercooked poultry -> often causing cross contamination of other foods -> fresh poultry has a higher contamination rate than frozen

Raw/unpasteurised milk - major outbreak in US

Unchlorinated water - outbreaks in UK, NewZealand, Scandanavia etc

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31
Q

What are the three most common Camp species

A

C. jejuni
C. Coli
C. lari

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32
Q

Talk about Camp infection (in healthy person), what is the pathophysiology

A

Infectious dose about 200 viable cells
Incubation period between 1 and 7 days (average of 3)
Clinical symptoms similar to salmonellosis (diarrhear, vomiting etc)

Causes ulceration, inflammed bleeding of mucosal surfaces (not a halmark as with STEC) in the jejunum, ileum and colon, invasion etc

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33
Q

What are the camp virulence factors?

A

Enterotoxin
Cytotoxin
Flagellar adhesins

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34
Q

What camp strains are more associated with systemic disease

A

Camp rarely causes systemic disease but:
C. fetus, C. cinaedi and C. lari are known to cause systemic infections in the immunocompromised (HIV)

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35
Q

What are some sequelae of camp?

A

Reactive arthritis in 1% of patients (1-2 weeks after)
Bursitis
Endocarditis
Neonatal spesis

1/1000 cases result in peripheral polyneuopathy known as Guillain-Barre syndrome -> it can cuse paralysis related to nerve demyelination

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36
Q

What camp serotype is most associated with Guillain-Barre syndrome?

A

O.19

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37
Q

Why is Camp lab ID so difficult?

A

Fastidious - microaerophilic

Biochemical inertness

Complex taxonomy

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38
Q

What are the three ways of IDing Camp in the lab

A

Conventional culture
MALDI ID and additional sub culture on supplemental agar
Molecular screening

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39
Q

Talk about antibiotic resistance in camp

A

Macrolides and fluoroquinolones are the agents of choice
No international AST criteria for Camp spp
Increased resistance to these antibiotics

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40
Q

Talk about antibiotic resistance in camp

A

Macrolides and fluoroquinolones are the agents of choice
No international AST criteria for Camp spp
Increased resistance to these antibiotics

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41
Q

Why is there no AST criteria for camp?

A

Camp kind of swarms on agar so an MIC is hard to interpret accurately

42
Q

Why is there no AST criteria for camp?

A

Camp kind of swarms on agar so an MIC is hard to interpret accurately

43
Q

What are the methods of resistance in Camp

A

Target gene mutations
Active efflux pumps
- not class specific - will pump out all antimicrobials - instils mutli-drug resistance

44
Q

What are the 6 ways camp can become resistant?

A

Through the bacterial ribosome

Point mutations in 23S rRNA

Outer membrane protein MOMP

Thr-86-Ile substitution in DNA gyrase

CmeABC multi-drug efflux pump

Aminoglycoside modifying enzymes (AME)

45
Q

How does the bacterial chromosome confer resistance in camp

A

Binding of the TetO protein prevents tetracycline from occupying that site but sill allows access of the amioacyl tRNA so that protein synthesis continues

46
Q

How does mutations in rRNA confer resistance in camp?

A

Point mutations in 23 rRNA decrease hte binding affinity for macrolides and lead to resistance

47
Q

How does MOMP confer resistance in camp

A

MOMP = Major outer membrane protein

It limits the entry of most antibiotics that are negatively charged or with a molecular weight larger than 360 kDA

48
Q

How does DNA gyrase mutations confer resistance in Camp?

A

Thr-86-Ile substitution in DNA gyrase confers fluoroquinolone resistance

49
Q

How does CmEBC confer resistance in Camp?

A

CmeABC is a multi-drug efflux pump which contributes to resistance against fluoroquinolones, macrolides, B-lactams and tetracylcines

50
Q

How does AME confer resistance in Camp?

A

AME = aminoglycoside modifying enzymes

aminoglycoside phosphotransferases

51
Q

Why are so few camp ASTs recorded?

A

Only 13% of Camp is cultured -> a large proportion that we dont know if they are resistant or not etc

The infection is often self limiting so there is rarely a need for antimicrobials

52
Q

Tall about resistance in Camp in Ireland in 2018

A

Out of 46 isolates, 32 were resistant -> very high proportion

53
Q

Talk about Salmonella

A

There about 2500 serovars of zoonotic Salmonella based on O H and Vi antigens

We are mostly concerned with salmonella enteric subspecies enterica

Out of this subspecies we are most concerned with serotype Typhimurium and Enteritidis (salmonella enterica subsp. enterica serotype Enteritidis)

54
Q

Why is the VI capsular antigen important in serotyping?

A

VI capsular antigen is only found in S. typhi and paratyphi i.e. in typhoid and paratyphoid fever

55
Q

Talk about the incidence of Salmonella in Ireland

A

406 cases in 2023, drop during covid years
a 10th of the cases compared to camp

No super obvious trend, decreasing since 2017

56
Q

Talk about salmonella outbreaks in ireland

A

17 outbreaks in 2022 (5 were general outbreaks, 12 were family outbreaks)
3 general outbreaks investigated as national outbreaks
There was 1 smaller outbreak comrpising 5 cases where the source was not identified
2 general outbreaks were investigated as regional outbreaks

57
Q

Talk about Salmonella in chocolate outbreak

A

A multi-country outbreak

16 laboratory-confirmed cases of Monophasic S. typhimurium

Linked to consumption of chocolate products

58
Q

Talk about Salmonella in chocolate outbreak

A

A multi-country outbreak

16 laboratory-confirmed cases of Monophasic S. typhimurium

Linked to consumption of chocolate products

59
Q

How does the incidence of salmonella in ireland compare to the EU?

A

Lower than the EU average

60
Q

How does the incidence of salmonella in ireland compare to the EU?

A

Lower than the EU average

61
Q

Which salmonella strains are notifiable diseases in Ireland

A

Typhoidal and paratyphoid salmonella

62
Q

Talk about the trends in typhoidal and paratyphoid salmonella notifications

A

Number of Typhoid increasing year on year, at its higherst in 2022
Paratyphoid numbers remaining the same over the years
Drop in both in covid years

63
Q

How many Typhoid and paratyphoid notifications were there in 2022

A

31 cases of S. typhi
7 cases of S. paratyphi

64
Q

What is our main concern with S. typhi ID in the lab

A

Concern with MDR and XDR in S, typhi

65
Q

When we ID S. typhi in the lab who is it always associated with?

A

In people whove travelled or someone with a close contact
S. typhi can be carried for a really long time afterwards
-> hence why vaccination prior to travel to endemic regions is suggested

66
Q

Where is S. typhi endemic

A

Pakistan
Afghanistan

67
Q

What foods are associated with Salmonella

A

Infected food animals such as poultru, pork, beef
Fresh foods and ready to eat food such as vegetables, fruits and nuts

68
Q

What was the most major recent outbreak in Ireland

A

In May 2017 there was 79 cases of Salmonella linked to a north dublin pub
- a communion function
- one woman died

Salmonella Brandenburg

69
Q

What was the most recent multi-country Salmonella outbreak

A

S. Newport Watermelon outbreak
Germany, UK, Wales, Scotland and Ireland affected

70
Q

How our outbreaks traced for Salmonella

A

Serum Protein Electrophoresis on Salmonella DNA -> similar DNA shown throughout an outbreak

71
Q

What are the three kinds of Salmonella infections

A

Enteric fevers
Septicemias
Enterocolitis

72
Q

Talk about Salmonella enteric fever

A

7-20 days incubation period
Insidious onset
Gradual fever with high plateau with “typhoidal” state
Lasts several weels
Often early constipation followed by bloody diarrhea
Blood culture positive in first to second week of disease
Stool culture positive from second week on

73
Q

Talk about salmonella enterocolitis

A

8-48 hours incubation
abrupt onset
Usually low grade fever
2-5 days duration of disease
Causes nausea, vomiting and diarrhea
Blood culture negative
Positive stool culture soon after onset

74
Q

How does non typhoid salmonella infect a person

A

In the small intestine salmonella replicate in the lumen
They then pass through single layer intestinal epithelium into the lamina propria (deep mucosa)
Incurs an inflammatory response
Activation of dendritic cells
Bacterial cells taken up by macrophages - limited disemination so infection is not likely to spread

75
Q

How does infection by non gastro salmonella differ from gastro type

A

Same up until uptake by macrophages

Non gastro salmonella has the ability to change what happens when inside the macrophages

The result is intra-macrophage replication and no massive inflammatory response

From this the bacteria can make its way into the bloodstream and then to the glabladder where it tends to colonise

Bacteria will seed from the gallbladder into the gut from here

76
Q

How do Salmonella get to the GIT

A

They have high acid tolerance meaning they can survive pH as low as 1.5

77
Q

How does Salmonella typhi affect the small intestine?

A

Salmonella typhi target Peyers patches of small intestine

S. typhi has specialised fimbirae that attache to epithelium over Peyer Patches where the organism may be phagocytosed

78
Q

How does S. typhi infiltrae macrophages?

A

Bacterially mediated endocytosis (BME)

79
Q

How does Salmonella undergo bacterially mediated endocytosis
(4)

A

SPI-1 contains genes for a type III secretion system

This system includes macromolecular channels that bacteria insert into eukaryotic cells and intracellula membrane to inject virulence proteins into the epithelial cell

These proteins disrupt the normal brush border of intestine and force cells to form membrane ruffles which engulf bacilli and create vesicles

These carry the bacteria across the epithelial cell cytoplasm and the basolateral membrane where they are presented to macrophages

80
Q

What is an SPI

A

Salmonella pathogenicity island-1

81
Q

How does S. typhi evade immune recognition

A

VI capsular polysaccharide prevents recognition of pathogen specific molecular patterns (PAMPs) by toll-like receptors and other surveillance mechanisms

S. typhi is also undetected by the immune system when travelling inside a macrophage

82
Q

How does Salmonella typhi resist digestion

A

SPI-2 codes for virulence factors that prevent or alter function of the macrophage vacuole with othe nitracellular compartments and may prevent the implantation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and nitric oxide synthase into the vacuole membrane

83
Q

How does S. typhi reproduce inside the macrophage

A

SPI-2 encods for a type III secretion system that inserts pores into vacuole membrane to deliver bacterial effectors sseG, SseF and SifA

These rearrange the macrophage cytoskeleton to carry S typhi in its vacuole to the Golgi apparatus here it multiplies

SPI-2 also codes for a type II system that iserts pores into vacuole membrane to deliver bacterial effectors Ssed, SseF and SifA

These reearange the macophage cytoskeleton to carry S typhi in its vacuole to the Golgi apparaus where it multiples

84
Q

Talk about Typhoid fever, incubation, source etc

A

Enteric or typhoid fever occurs whn the bacteria leave the intestine and multiply within cells of the reticuolendethelial system

The bacteria then re-enter the intestine, causing GI symptoms

Typhoid fever has a 10-14 day inubation period and may last for several weeks

S. Typhi is the most common cause of tuphoid fever

Human reservoir: carrier state common for S. typhi

Contaminated food: water supply

Poor sanitary conditions

85
Q

When is Salmonella culture positive?

A

Blood and faeces positive in 85-90% positive after week 1 of onset
20-30% positive later in disease course

86
Q

When should you take Salmonella blood cultures?

A

Temperature spike occurs on day 7
Blood cultures should be taken in relation to this spike in temperature

87
Q

Talk about resistance in Salmonella

A

Resistance has been increasing in both humans and farm animalas - resistance driven by antimicrobials in animals
Determinants located on integrons, transposons or plasmids

88
Q

What is the most known resistant salmonella strain

A

serovar typhimurium definitive type

104 (DT104) -> MDR

89
Q

Talk about 104 (DT104) antibiotic resistance

A

ACSSuT resistance
Ampicillin, chloramphenicol, streptomycin, sulfonamides, tetracycline

Due to Salmonella genomic island 1 (SGI1)
- this one island confers all of this resistance

90
Q

Talk about the S. Heidelberg outbreak

A

Outbreak in USA 2013
Associated with consumption of Foster Farms brand chicken
At least 362 people affected in 21 states
38% of these were hospitilised
Seven outbreak strains
Resistant to combinations of antimicrobials

91
Q

Where is the salmonella reference lab

A

UHG Galway

92
Q

Talk about Salmonella resistance in Ireland

A

53% of salmonella were susceptible to all antimicrobia agents tested
21% MDR to 3 or more antimicrobials
1/3 were ASuT resistant (ampicillin, sulphonamide and tetracycline) and were mainly monophasic S. Typhimurium
1 ESBL was noted

93
Q

What work is done on Salonella in the reference lab

A

They detect genes and use this to predict the resistance profile of the bacteria

94
Q

What are the most common species of Shigella

A

Most common: S. dysentriae serogroup A

Most serious: S. flexneri (B), S. boydii (C)

Severe disease: S. sonnei serogroup D

95
Q

Talk about Shigella. how is it spread, how is it transmitted?

A

Confined to humans some higher primates
Spread via faecal-oral route through faeces, food, fingers, flies, fomites etc
Fragile in human faeces but can survive for months in food, water, fomites
Not affected by acidity of stomach
Toxico infection: shiga toxin (AB toxin)
Low infectious dose

96
Q

What is the infectious dose of shigella

A

Less than 200 viable cells, as little as 10 cells

97
Q

Comment on the fragility of shigella

A

Prone to drying in human faeces

98
Q

Talk about the incidence of shigella

A

Incidence increasing

Large increase since 2018
- definition of shigella changed in 2018
- molecular detection allowed from 2018

99
Q

What are the most common shigella species identified by the reference lab?

A

S. flexneri = 64% of cases
S sonnei = 35% of cases
S.boydii = 2 cases
S. dysenteriae = 1 case

100
Q

Talk about the distribution in Shigella cases in Ireland , comparing males vs females

A

Highest rates of shigella in three groups:
- children under 9 yrs old
- males between 35 and 54 (women between 44 and 54)
- majority in males 25-34

101
Q

Talk about shigella in MSMs

A

In recent times shigella has become less associated with food and more as an STD in MSMs

Research is limited but in one study the likelihood for shigella was more than twice as high in MSMs vs non-MSMs

102
Q

How does Ireland compare to the rest of Europe in terms of Shigella?

A

Ireland used to be below the average but snce 2015 weve been above the EU average
- thought to be due to improvements in molecular detection and change in ID definition

EU average = 1.47/100,000 people

4.1 Medical Microbiology (30 decks)

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