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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
Resistance in Camp is increasing, why is this happening?
This is driven from the food industry whereby animals are being given antimicrobials Resistance spreads through the food chain
26
Only 13% of camp are speciated, why are we concenred wih this, what are we doing to get around this?
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
27
Compare Camp incidence in Ireland over the years t european average
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
28
Source and transmission of C. jejuni, how does it spread
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
29
Why do we incubate camp at 42 degrees?
Chicken intestine is at @42 degrees, this is its preferred growing temperature, hence why we incubate at this temp
30
What foods are associated with camp
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
31
What are the three most common Camp species
C. jejuni C. Coli C. lari
32
Talk about Camp infection (in healthy person), what is the pathophysiology
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
33
What are the camp virulence factors?
Enterotoxin Cytotoxin Flagellar adhesins
34
What camp strains are more associated with systemic disease
Camp rarely causes systemic disease but: C. fetus, C. cinaedi and C. lari are known to cause systemic infections in the immunocompromised (HIV)
35
What are some sequelae of camp?
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
36
What camp serotype is most associated with Guillain-Barre syndrome?
O.19
37
Why is Camp lab ID so difficult?
Fastidious - microaerophilic Biochemical inertness Complex taxonomy
38
What are the three ways of IDing Camp in the lab
Conventional culture MALDI ID and additional sub culture on supplemental agar Molecular screening
39
Talk about antibiotic resistance in camp
Macrolides and fluoroquinolones are the agents of choice No international AST criteria for Camp spp Increased resistance to these antibiotics
40
Talk about antibiotic resistance in camp
Macrolides and fluoroquinolones are the agents of choice No international AST criteria for Camp spp Increased resistance to these antibiotics
41
Why is there no AST criteria for camp?
Camp kind of swarms on agar so an MIC is hard to interpret accurately
42
Why is there no AST criteria for camp?
Camp kind of swarms on agar so an MIC is hard to interpret accurately
43
What are the methods of resistance in Camp
Target gene mutations Active efflux pumps - not class specific - will pump out all antimicrobials - instils mutli-drug resistance
44
What are the 6 ways camp can become resistant?
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
How does the bacterial chromosome confer resistance in camp
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
How does mutations in rRNA confer resistance in camp?
Point mutations in 23 rRNA decrease hte binding affinity for macrolides and lead to resistance
47
How does MOMP confer resistance in camp
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
How does DNA gyrase mutations confer resistance in Camp?
Thr-86-Ile substitution in DNA gyrase confers fluoroquinolone resistance
49
How does CmEBC confer resistance in Camp?
CmeABC is a multi-drug efflux pump which contributes to resistance against fluoroquinolones, macrolides, B-lactams and tetracylcines
50
How does AME confer resistance in Camp?
AME = aminoglycoside modifying enzymes aminoglycoside phosphotransferases
51
Why are so few camp ASTs recorded?
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
Tall about resistance in Camp in Ireland in 2018
Out of 46 isolates, 32 were resistant -> very high proportion
53
Talk about Salmonella
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
Why is the VI capsular antigen important in serotyping?
VI capsular antigen is only found in S. typhi and paratyphi i.e. in typhoid and paratyphoid fever
55
Talk about the incidence of Salmonella in Ireland
406 cases in 2023, drop during covid years a 10th of the cases compared to camp No super obvious trend, decreasing since 2017
56
Talk about salmonella outbreaks in ireland
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
Talk about Salmonella in chocolate outbreak
A multi-country outbreak 16 laboratory-confirmed cases of Monophasic S. typhimurium Linked to consumption of chocolate products
58
Talk about Salmonella in chocolate outbreak
A multi-country outbreak 16 laboratory-confirmed cases of Monophasic S. typhimurium Linked to consumption of chocolate products
59
How does the incidence of salmonella in ireland compare to the EU?
Lower than the EU average
60
How does the incidence of salmonella in ireland compare to the EU?
Lower than the EU average
61
Which salmonella strains are notifiable diseases in Ireland
Typhoidal and paratyphoid salmonella
62
Talk about the trends in typhoidal and paratyphoid salmonella notifications
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
How many Typhoid and paratyphoid notifications were there in 2022
31 cases of S. typhi 7 cases of S. paratyphi
64
What is our main concern with S. typhi ID in the lab
Concern with MDR and XDR in S, typhi
65
When we ID S. typhi in the lab who is it always associated with?
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
Where is S. typhi endemic
Pakistan Afghanistan
67
What foods are associated with Salmonella
Infected food animals such as poultru, pork, beef Fresh foods and ready to eat food such as vegetables, fruits and nuts
68
What was the most major recent outbreak in Ireland
In May 2017 there was 79 cases of Salmonella linked to a north dublin pub - a communion function - one woman died Salmonella Brandenburg
69
What was the most recent multi-country Salmonella outbreak
S. Newport Watermelon outbreak Germany, UK, Wales, Scotland and Ireland affected
70
How our outbreaks traced for Salmonella
Serum Protein Electrophoresis on Salmonella DNA -> similar DNA shown throughout an outbreak
71
What are the three kinds of Salmonella infections
Enteric fevers Septicemias Enterocolitis
72
Talk about Salmonella enteric fever
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
Talk about salmonella enterocolitis
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
How does non typhoid salmonella infect a person
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
How does infection by non gastro salmonella differ from gastro type
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
How do Salmonella get to the GIT
They have high acid tolerance meaning they can survive pH as low as 1.5
77
How does Salmonella typhi affect the small intestine?
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
How does S. typhi infiltrae macrophages?
Bacterially mediated endocytosis (BME)
79
How does Salmonella undergo bacterially mediated endocytosis (4)
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
What is an SPI
Salmonella pathogenicity island-1
81
How does S. typhi evade immune recognition
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
How does Salmonella typhi resist digestion
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
How does S. typhi reproduce inside the macrophage
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
Talk about Typhoid fever, incubation, source etc
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
When is Salmonella culture positive?
Blood and faeces positive in 85-90% positive after week 1 of onset 20-30% positive later in disease course
86
When should you take Salmonella blood cultures?
Temperature spike occurs on day 7 Blood cultures should be taken in relation to this spike in temperature
87
Talk about resistance in Salmonella
Resistance has been increasing in both humans and farm animalas - resistance driven by antimicrobials in animals Determinants located on integrons, transposons or plasmids
88
What is the most known resistant salmonella strain
serovar typhimurium definitive type 104 (DT104) -> MDR
89
Talk about 104 (DT104) antibiotic resistance
ACSSuT resistance Ampicillin, chloramphenicol, streptomycin, sulfonamides, tetracycline Due to Salmonella genomic island 1 (SGI1) - this one island confers all of this resistance
90
Talk about the S. Heidelberg outbreak
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
Where is the salmonella reference lab
UHG Galway
92
Talk about Salmonella resistance in Ireland
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
What work is done on Salonella in the reference lab
They detect genes and use this to predict the resistance profile of the bacteria
94
What are the most common species of Shigella
Most common: S. dysentriae serogroup A Most serious: S. flexneri (B), S. boydii (C) Severe disease: S. sonnei serogroup D
95
Talk about Shigella. how is it spread, how is it transmitted?
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
What is the infectious dose of shigella
Less than 200 viable cells, as little as 10 cells
97
Comment on the fragility of shigella
Prone to drying in human faeces
98
Talk about the incidence of shigella
Incidence increasing Large increase since 2018 - definition of shigella changed in 2018 - molecular detection allowed from 2018
99
What are the most common shigella species identified by the reference lab?
S. flexneri = 64% of cases S sonnei = 35% of cases S.boydii = 2 cases S. dysenteriae = 1 case
100
Talk about the distribution in Shigella cases in Ireland , comparing males vs females
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
Talk about shigella in MSMs
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
How does Ireland compare to the rest of Europe in terms of Shigella?
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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