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Gastrointestinal Infections Flashcards

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1
Q

What are the two methods in which bacterial GI infection agents can cause illness?

A

Infection - bacterial pathogens develop in the gut after ingestion of contaminated food
Intoxication (poisoning) - bacterial pathogens grow in foods and produce toxins

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2
Q

Give some examples of pathogens that grow in the gut after the ingestion of contaminated food (Infection).

A

Salmonella
Campylobacter
Pathogenic E.Coli

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3
Q

Give some examples of pathogens that grow in foods and produce toxins to make us ill (intoxication).

A

Bacillus cereus

Staphylococcus aureus

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4
Q

Describe the clinical syndrome of diarrhoea.

A

Abnormal frequency and/or fluid stool
Usually indicates small bowel disease
Causes fluid and electrolyte loss
Severity varies from mild and self limiting to fatal
- balance between virulence of the organism and the degree of compromise of the host

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5
Q

Describe the symptoms associated with gastroenteritis.

A

Nausea, vomiting, diarrhoea and abdominal discomfort

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6
Q

What is the clinical definition of dysentery?

A

Inflammatory bowel disorder of the large bowel
Causes blood and pus in the faeces
Symptoms include pain, fever and abdominal cramps

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7
Q

What is enterocolitis?

A

Inflammatory process affecting the small and large bowel

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8
Q

What are the two places in which a GI infection can manifest?

A

Within the GI tract

Outwith the GI tacit

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9
Q

How do pathogens cause disease when they manifest within the GI tract?

A 
Toxin effects (e.g. Cholera) 
Cause inflammation de to microbial invasion
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10
Q

How do pathogens cause disease when they manifest outwith the GI tract?

A

Systemic effect of toxins (e.g. STEC - toxins get into the bloodstream)
- Shigatella toxin from E.Coli
They cause invasive infection of the GI tract with wilder dissemination (e.g. metastatic salmonella infection)

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11
Q

List the barriers to GI infection.

A

Mouth - lysozyme
Stomach - acid pH
Small intestine
Large intestine

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12
Q

Describe how the small and large intestine protect the body against GI infections.

A 
Small intestine
- mucous
- bile (antibacterial)
- secretory IgA
- lymphoid tissue (Peyer's patches)
- epithelial turnover - removes adherent bacteria 
- normal flora - competition 
Large intestine 
- epithelial turnover
- normal flora
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13
Q

Name some sources of GI infection.

A

Zoonotic
- symptomatic animals
- asymptomatic shedders - e.g. Reptiles and salmonella carriage
Human carriers
- Typhoid - enteric fever
Environmental sources
- contamination of soil and produce (e.g. Listeria, E.Coli)

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14
Q

Name the four Fs of person-to-person transmission

A

Faecal-oral - when infectious organisms from human/animal faeces can gain access to the GIT of susceptible host
Food - contamination and cross-contamination
Fluids - water and contaminated juices
Fingers - washing hands
- after the toilets and before preparing or consuming foo and drink

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15
Q

Describe enrichment broth in a laboratory diagnosis of GI infection.

A

Contains nutrients that promote preferential growth of the pathogen

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16
Q

Describe the selective media in laboratory diagnosis of a GI infection?

A

Suppress growth of background flora while allowing growth of the pathogen.

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17
Q

Describe differential media in the laboratory diagnosis of a GI infection.

A

Distinguishes mixed micro organisms on the same plate. Uses biochemical characteristics of micro organisms growing in presence of specific nutrients combined with an indicator that changes colour
- examples include Salmonella and Shigella species which are non-lactose fermenters

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18
Q

What colour does Shigella turn MacConkey’s agar?

A

It doesn’t change colour - because Shigella is non-lactose fermenting

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19
Q

What colour does E.Coli turn MacConkey’s agar?

A

Pink - because it is lactose fermenting

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20
Q

With a basic, low-level infection. What is the general treatment?

A

Given that most mild bacterial infections resolves spontaneously, antibiotics are not given.
Hydration is maintained and can be lifesaving - most important aspect of treatment anyway

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21
Q

When and why is it not appropriate to give antibiotics for treatment of a bacterial infection?

A

Antibiotic treatment is reserved for severe/prolonged symptoms
This is because the therapy itself
- may prolong symptom duration
- may exacerbate symptoms
- promotes resistance
- may actually be harmful (STEC infection)

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22
Q

How are GI infections controlled?

A

By breaking the chain of infection

  • adequate public health measures (clean drinking water, proper sewage disposal)
  • education in hygienic food preparation (avoid cross-contamination, cook food properly and hand hygiene)
  • pasteurisation of milk and dairy products
  • sensible travel food precautions (wash it, peel it, cook it or forget it)
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23
Q

Describe the microbiology of campylobacter.

A

These are curved, gram negative bacilli.
They are microaerophilic and thermophilic (42C)
They are cultured on Campylobacter selective agar
C.jejuni are the most important species

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24
Q

Describe the epidemiology of Campylobacter.

A

Most common food borne infection in the UK
- large animal reservoir (POULTRY, cattle, sheep, rodents and wild birds)
- infection transmitted via contaminated food, milk or water
- 70% of raw retail fresh chicken is infected (becomes safe if cooked properly)
Seasonal peaks of infection in May and September
Person to person spread is rare
Large point source outbreaks are uncommon because once in food, it doesn’t multiply

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25
Q

What is the pathogenesis of Campylobacter?

A

Bacterial invasion causes inflammation, ulceration and bleeding in the small and large bowel
Can cause bacteraemia (immunocompromised or extremes of age)
Can cause post-infectious demyelination syndrome (Guillain-Barre)
- characterised by ascending paralysis, can cause respiratory paralysis
- can take weeks/months

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26
Q

What are the clinical signs of a campylobacter infection?

A

Incubation tales 2-5 days
Causes bloody diarrhoea, fever (inflammation of the gut wall) and severe abdominal cramps
Vomiting rarely occurs
Duration is between 2-10 days.

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27
Q

How is Campylobacter treated?

A

Fluid replacement is sufficient in most cases.
For more severe/persistent disease, Clarithromycin is used
For invasive disease
- Quinolone (ciprofloxacin) or gentamicin is used

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28
Q

What are the best ways to control spread of Campylobacter bacteria?

A

Reduction in the contamination of raw, retail poultry meat

- followed by adequate cooking

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29
Q

Describe the microbiology of Salmonella bacteria.

A

It is a gram negative bacilli
It is a member of the Enterobacteriaceae group
Nomenclature confusing
Non-lactose fermenters
XLD plates are most commonly used in clinical labs

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30
Q

How is Salmonella nomenclature confusing?

A

Most human infections are caused by Salmonella Enterica
However there are over 2000 serotypes defined on a basis of lipopolysaccharide O antigens of the cell wall and flagellar province H antigens

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31
Q

Describe the epidemiology of Salmonella.

A

Found in cold and warm blooded animals
- acquired from contaminated food (especially pork, poultry and other meat and milk/dairy products)
- waterborne is less common
- large food borne outbreaks can occurs because it can multiply in foodstuffs
Low infectious dose
Secondary spread may be person-to-person
Seasonal peaks in Summer and Autumn

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32
Q

Which salmonella types don’t have an animal reservoir?

A

S.Typhi and S.Paratyphi

  • the causative organisms of enteric fever
  • person to person transmission
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33
Q

What is the pathogenesis of Salmonella?

A

Invasion of the epithelial cells in the distal small intestine causing subsequent inflammation and diarrhoea
Bacteraemia can occur

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34
Q

Can Salmonella have a systemic/distant effect?

A

Yes, it can metastasise to different organs and cause inflammatory problems there

  • joints - septic arthritis
  • bones - osteomyelitis
  • brain - meningitis
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35
Q

What are the clinical symptoms of Salmonella infections?

A 
Incubation takes 12-72 hours
Watery diarrhoea 
Vomiting is common
Fever can occur - associated with more invasive disease
Duration is for 2-7 days
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36
Q

What is the treatment for a Salmonella infection?

A

Fluid replacement is normally sufficient
Antibiotics are used for severe cases and bacteraemia
- Beta-lactams, quinolone so or aminoglycosides
Antibiotics, however, prolong the excretion of Salmonella into the faeces

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37
Q

How can the spread of Salmonella be controlled?

A

There was an introduction of immunisation of poultry flocks which reduced S.Enteritdis in the UK

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38
Q

Describe the microbiology of the Shigella bacteria.

A

Gram-negative bacilli
Member of the Enterobacteriaceae family - biochemically similar to E.Coli
Non-lactose fermenters
XLD plates are most commonly used in clinical labs

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39
Q

What are the most common subtypes of Shigella bacteria?

A

S.Sonnei - milder infections
S.Boydii and S.Flexerni - more severe disease
S.Dysteneriae - most severe disease

40
Q

Describe the epidemiology of Shigella infections.

A

Associated with diarrhoeal disease in children
Human only reservoir - doesnt persist in the environment
Faecal-oral transmission

41
Q

What is the pathogenesis of a general Shigella infection.

A

Organisms attach to and colonise mucosal epithelium of the terminal ileum and colon
- no systemic invasion

42
Q

Describe the pathogenesis of an S.Dystenteriae infection.

A

This produces a potent exotoxin (Shiga) which damaged the intestinal epithelium and the glomerular endothelium causing renal failure (part of haemolytic uraemic syndrome - HUS)

43
Q

What are the clinical features of a Shigella infection?

A

Dystentery
Incubation for 1-3 days
Watery diarrhoea followed by bloody diarrhoea
Marked, cramping abdominal pain
Fever reflects invasive nature of disease
Duration of 2-7 days

44
Q

What is the treatment for a Shigella infection?

A

Usually self-limiting - fluid replacement is sufficient

Some cases of S.Dystenteriae infection will require renal failure treatment

45
Q

Describe the microbiology of a V.Cholera bacteria.

A

Comma shaped gram negative bacilli
Serotypes are defined on the basis of O antigens
Sucrose-fermenter
- Thiosulphate-bile sucrose selective/differential medium
- changes from green to yellow

46
Q

What are the important serotypes of V.Cholerae?

A

Serotype O1
- classical
- EI Tor (less severe)
Serotype O139

47
Q

Describe the epidemiology of V.Cholerae infections.

A

These can live in fresh water and only infect humans
- spread via contaminated food or water
Can cause epidemics and pandemics in parts of SE Asia, Africa and South America

48
Q

What is the pathogenesis of a V.Cholerae infection?

A

Flagellae and mucinase enzyme facilitate penetration of intestinal mucous
- attach to mucosa via specific receptors
Diarrhoea occurs due to production of a potent protein exotoxin

49
Q

What are the clinical signs of a V.Cholerae infection?

A 
Severe, profuse, non-bloody, watery diarrhoea (rice water)
Profound fluid loss and dehydration
- hypokalaemia
- metabolic acidosis 
- hypovolaemic shock 
- cardiac failure
Untreated - 30% mortality
50
Q

What is the treatment for a V.Cholerae infection?

A

Oral and IV rehydration is most important

Tetracycline antibiotics may shorten the duration of shedding

51
Q

Describe the general microbiology of E.Coli.

A

Gram-negtive bacteria
Members of the Enterobacteriaceae family
Six different groups are capable of causing diarrhoea
- different serotypes are described on the basis of O and H antigens

52
Q

What is the pathogenesis of Enteropathogenic E.Coli?

A

There is initial adherence via pili, followed by formation of a characteristic ‘attaching and effacing’ lesion
- this is mediated by intimin protein on the gut wall and Tir (translocated intimin receptor on the E.Coli)
This infiltrates and destroys the intestinal microvilli

53
Q

What are the clinical signs of an Enteropathogenic E.Coli infection?

A 
Incubation is 1-2 days
Watery diarrhoea
Abdominal pain
Vomiting 
Fever
Duration 1-several weeks
54
Q

What is the major cause of travelers diarrhoea?

A

Enterotoxigenic E.Coli (ETEC)

55
Q

What is the pathogensis of an Enterotoxigenic E.Coli infection?

A

Diarrhoea due to the action of 1 or 2 plasmid encoding toxins

  • heat labile - structural and functional analogue of cholera toxin
  • heart stable - produced in addition to or instead of LT
56
Q

What are the clinical features of an ETEC infection?

A 
Incubation for 1-7 days
Watery diarrhoea
Abdominal pain
Vomiting
No associated fever
Duration 2-6 days
57
Q

Describe the microbiology of Enterohaemorrhagic E.Coli (EHEC).

A

More than 100 serotypes
E.Coli O157:H7 is the best known one
- it’s a non-sorbitol fermenter (colonies remain colourless)

58
Q

What is the epidemiology of EHEC?

A

Animal reservoirs
Persistent in the environment
Consumption of contaminated food, water and dairy products and direct environment contact with animal faeces
Secondary person to person

59
Q

What is the pathogenesis of EHEC?

A

Attaching and effacing lesion (similar to EPEC)

Production of Shiga-like toxins (STEC - shiga toxin producing EC) or VTEC (verotxin-producing EC)

60
Q

What are the clinical signs and symptoms of EHEC?

A

Incubation 1-7 days
Bloody diarrhoea with abdominal pain
Vomiting (difference between campylobacter)
No fever
Haemolytic uraemic syndrome (5-10% of cases)
- most common cause of acute renal failure in children
Duration 5-10 days

61
Q

List the six types of E.Coli.

A 
Enteropathogenic E.Coli
Enterotoxigenic E.Coli
Enterohaemorrhagic E.Coli
Enteroinvasive E.Coli
Enteroaggregative E.Coli
Diffuse aggregative E.Coli
62
Q

What is the treatment for an E.Coli infection?

A

Adequate rehydration

Antibiotics and antimobility agents may increase risk of HUS risk in the case of EHEC

63
Q

Describe the microbiology of Yersinia entercolitica.

A

Gram-negative bacteria
Member of the Enterobacteriaceae
Not normally cultured - under diagnosed

64
Q

What is the pathogenesis of Yersinia entercolitica?

A

It invades the terminal ileum with inflammation of mesenteric lymph nodes causing abdominal pain

65
Q

What are the clinical symptoms of a Yersinia enterocolitica?

A

Diarrhoea which may be bloody
Abdominal cramps
Fever present
Mesenteric adenitis with fever may mimic acute appendicitis

66
Q

How is Yersinia entercolitica treated?

A

Generally self-limiting
Severe infections may require antibiotics
- quinolones
- aminoglycosides

67
Q

What is the microbiology of Staph aureus infections?

A

Gram-positive cocci
Grow well on routine media
Testing for enterotoxins is not routinely performed

68
Q

What is the pathogenesis of S.Aureus?

A

Bacteria multiply at room temperature and produce toxins.

Heat stable and acid-resistant protein toxins - not broken down by cooking or the acid in the stomach

69
Q

Describe the epidemiology of S.Aureus.

A

50% produce enterotoxins (types A-E)
Food is contaminated by human carriers
- cooked meats, cakes and pastries

70
Q

What are the clinical signs or an S.Aureus infection?

A 
Incubation 30 mins - 6 hours
Profuse vomiting
Abdominal cramps
No fever
No diarrhoea
Duration 12-24 hours
71
Q

What is the microbiology of a bacillus cereus bacteria?

A

Aerobic, spore-forming
Gram positive bacilli
Not routinely tested for

72
Q

What is the epidemiology of bacillus cereus infections?

A

Spore and vegatative cells contaminate foodstuffs

73
Q

What is the pathogenesis of a bacillus cereus infection?

A

Emetic disease
- spore survive boiling
- sporulates and produces a protein enterotoxin
- heat stable toxin
Diarrhoeal disease
- organisms multiply in food
- once ingested they produce a heat-labile toxin in the gut (acts like cholera toxin)

74
Q

What are the clinical features of a Bacillus Cereus infection?

A 
Emetic disease
- short incubation
- duration 12-24 hours
- profuse vomiting, watery diarrhoea with cramping abdominal pain
- no fever
Diarrhoeal
- incubation 8-12 hours
- duration 12-24 hours
- watery diarrhoea with cramping abdominal pain
- no vomiting or fever
75
Q

What is the microbiology of a Clostridium perfringens bacteria?

A

Anaerobic, spore forming gram-positive bacilli

Not routinely tested for

76
Q

What is the epidemiology of C.perfringens infections?

A

Spores and vegetative cells ubiquitous in soil and animal gut

  • contaminated foodstuff
  • multiply in cooling food
77
Q

What is the pathogensis for C.perfringens?

A

Organisms ingested and sporulate in large intestine with production of enterotoxin - toxin mediated disease

78
Q

What are the clinical signs of a C.Perfringen infection?

A

Incubation 6-24 hours
Profuse watery diarrhoea and sever abdominal cramps
No fever and no vomiting

79
Q

What is the microbiology of a C.Botulinum bacteria?

A

Anaerobic, spore forming gram-positive bacilli

Diagnosis based off toxin detection

80
Q

What is the epidemiology of a C.Botulinum infection?

A

Spore and vegetative cells are everywhere in the soil and animal GIT.
Improperly canned food

81
Q

What is the pathogenesis of a C.Botulinum infection?

A

Produces a powerful heat-labile protein neurotoxin (types A, B and E - human disease)
Absorbed toxins spread via the bloodstream and enter peripheral nerves where they cause neuromuscular blockade at the synapses

82
Q

What two ways can C.Botulinum enter the body, and what happens when a baby ingests it?

A

Foodborne botulism
- preformed toxin in food
Wound botulism
- organisms implanted in the wound produce toxins

Infant botulism
- organisms germinate in gut of babies fed honey that contain spores (floppy baby syndrome)

83
Q

What are the clinical signs of a C.Botulinum infection?

A

Neuromuscular blockade results in flaccid paralysis and decending progressive muscle weakness
- can affect the muscles of the chest wall and diaphragm

84
Q

What is the treatment for a C.Botulinum infection?

A

ICU support due to breathing and swallowing problems

Antitoxin - stops further effects

85
Q

What is the microbiology of a C.Difficile bacteria?

A

Anaerobic, spore-forming gram positive bacilli
Spores resistant to hear, drying, disinfectant and alcohol
Clinical features are due to toxin production (A and B)

86
Q

How is C.Diff transmitted, and who does it affect most?

A 
Person-to-person
- can have asymptomatic carriers
- 3-5% of adults community are carriers 
Mostly affects the elderly
Primary cause of healthcare associated infections
87
Q

What are the clinical signs of a C.Diff infection?

A

Mild to severe abdominal pain
Pseudomembranous colitis (severe inflammatory exudate due to toxin release)
Colonic dilation and perforation
Relapses are common and multiple

88
Q

What are the markers which suggest the C.Diff infection is mild?

A 
Colonic dilation (>6cm)
WCC (>15x baseline)
Creatinine (>1.5 x baseline)
Temperature (>38.5C)
Immunosuppression
89
Q

What is the treatment of a C.Diff infection?

A

Stop precipitating antibiotics
Oral metronidazole if mild
Oral vancomycin is severe or no improvement after 5 days on metronidazole
Refractory current diseases may need a faecal transplant

90
Q

Which antibiotics are known to specifically cause C.Diff?

A

Cephalosporins
Fluroquinolones
Clindamycin
Co-amoxyclav

91
Q

Why must people/items that have been in contact with C.Diff be cleaned with hypochlorite disinfectants?

A

Because C.Diff spores are resistant to normal cleaning agents

92
Q

Describe the microbiology of a Listeria monocytogene bacteria.

A

Gram positive coccobacilli

Can cause meningitis if it spreads through the bloodstream

93
Q

What is the epidemiology of Listeria?

A

Widespread among animals and the environment
Common in pregnant women, the elderly and the immunocompromised
Infection associated with contaminated foods
- unpasteurised milk, soft cheeses, pate, cooked meats, smoked fish and coleslaw
Can multiply at 4C

94
Q

Describe the pathogenesis of Listeria.

A

Invasive infection from the GI tract results in systemic spread via the bloodstream

95
Q

What are the clinical signs of a Listeria infection?

A

Incubation period 3 weeks
Initial flu-like symptoms
Can have diarrhoea
Most present with severe systemic infection if they don’t have diarrhoea - either septicaemia or meningitis

96
Q

What is the treatment for a Listeria infection?

A

IV antibiotics

  • Ampicillin
  • Synergistic gentamicin

Microbiology (21 decks)

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