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3s2: Infection and Immunity > Week 7 > Flashcards

Week 7 Flashcards

1
Q

How do we view bacteria?

A

Brightfield - produces image on bright background (commonly used)
Darkfield - produces bright image on dark background no staining and use for live specimens
Phase contract - Refraction and interference caused by structutes in the specimen to create high resolution images without staining. Useful for live organisms and organelles
Differential interference contrast - Interference pattersn to enhance contrast between different features of a specimen to produce high contrat images of living organism with a 3d appearance

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2
Q

What examples of morphologies to classify bacteria?

A

Coccus - round
Bacillus - rod
Vibrio - Curved rod
Spirilliom - spiral

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3
Q

What examples of cell arangements to classify bacteria?

A

Coccus - single coccus
Diplo - pair of
Tetra - grouping of 4
Strepto - Chain of

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4
Q

What is a contrasting use of shape as a name?

A

Two rod-shaped (bacillus) bacteria:
Bacillus subtilis
Escherichia coli

Two spherical (coccoid) bacteria:
Streptococcus agalactiae
Neisseria gonorrhoeae

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5
Q

What is an overview of gram staining?

A

In 1884, Hans Cristian Gram first differentiated between two pathogens by testing different chemical stains
Crystal violet was retained by one, but not the other
Final step: Counterstaining added by Carl Weigert

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6
Q

What is an overview of gram staining method?

A

Step 1 - Crystal violet stains cell purple
Step 2 - Iodine makes dye less soluble so adheres to cell walls
Step 3 - Alcohol decolourises by washing stain away from gram-negative cell walls
Step 4 - Safranin counterstain allows dye to adhere to gram-negative cells

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7
Q

What is an overview of gram postive cell wall?

A

Gram-positive bacteria cell membrane are surrounded by many layers of peptidoglycan, which form a protective shell that is 30–100 nm thick.
The peptidoglycan layer are covalently modified with carbohydrate polymers including wall teichoic acids (WTAs) or functionally related anionic glycopolymers

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8
Q

What is an overview of gram negative cell wall?

A

A thin peptidoglycan layer is present (this is much thicker in gram-positive bacteria)
An outer membrane containing lipopolysaccharides (LPS, lipid A, core polysaccharide, and O antigen) in its outer leaflet and phospholipids in the inner leaflet

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9
Q

What is the difference between peptido-glycan cell wall between negative and positve cell wall?

A

Bacterial cell wall - Peptido-glycan (protein)-(sugar)
Gram-positive - stronger and thicker, pentapeptide intermediate links between tetrapeptides
Gram-negative - thinner and covered by outer membrane direct link between tetrapeptides so between NAGs and NAMs layers

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10
Q

What is an overview of the ways to distinguish bacterial isolates?

A

Gram-staining
Biochemical assays E.g. coagulase, hemolysis
Colony morphology
Sequence typing
Serological typing
Antimicrobial resistance (AMR) phenotypes

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11
Q

What is a description of the gram negative cell wall layers?

A

Inner membrane
Periplasmic space
Outermembrane with LPS and Porins (exchanging)

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12
Q

What are the main gram-negative burdening bacterial infections?

A

Escherichia Coli - ~950,000 deaths
Klebsiella pneumoniae - ~790,000 deaths
Pseudomonas aeruginosa - ~559,000 deaths
Acinetobacter baumanii - ~452,000 deaths

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13
Q

What is an overview of Escherichia Coli?

A

Gram negative enteric, motile, rod-shaped, coliform bacterium
Order: Enterobacterales
Family: Enterobacteriaceae
Two categories: Diarrhoeagenic / Extraintestinal E. coli
Commonly found: gastro-intestinal tract, lower intestine, urinary tract, surface-contamination with faecal material

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14
Q

What are the six distinct ‘pathovars’ of Escherichia coli?

A

Shiga-toxin producing Escherichia coli (STEC)
Enteropathogenic Escherichia coli (EPEC)
Enterohaemorrhagic Escherichia coli (EHEC)
Enterotoxigenic Escherichia coli (ETEC)
Enteroinvasive Escherichia coli (EIEC)
Enteroaggregative Escherichia coli (EAEC)

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15
Q

What are two extraintestinal pathogenic Escherichia coli?

A

Uropathogenic Escherichia coli (UPEC)
Neonatal meningitis Eschericia coli (NMEC)

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16
Q

How does attachment and invasion occur in Enteroaggregative Escherichia coli (EAEC)?

A

Forms biofilm on the surface of epithelial cells
Then secrete cytotoxins and enterotoxins, inclusing ShET1, Pic and PET

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17
Q

How does attachment and invasion occur in Enteropathogenic Escherichia coli (EPEC)?

A

Forms microcolony amogst the microvili of epithelial cell
Induces cell then forms a actin filiments as a pedistal for E.coli to live on where they can be internalised an cause damage through toxins, which causes diarrhea

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18
Q

What structures to Escherichia coli have to attach to cells

A

Fimbriae or pili - 5- 7 nm diameter
Curli - 2-5 nm diameter

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19
Q

What is an overview of the secretion systems in Escherichia coli?

A

Type 1 - Secretes Small molecules or antibiotics into environment
Type 2 - Secretes proteins into environment
Type 3 - Injects virulence effectors into host cell

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20
Q

How can E.coli get into gut eptithelial cell?

A

It can transcytose across M cell
It will be phagocytosed eg by macrophage
It can escape and live in cytoplasm where it can produce IPAB a proapoptopic molecule
Then penetrates epithelial cell and causes problems with virulence factors lie acrtin polymerisation

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21
Q

How does Uropathogenic Escherichia coli (UPEC) cause a reoccurant infection?

A

Uses pili which are recognised by bladder epithelial cells allowing entry
They reduce metabolic rate becoming dormany intracellular bacteria community, which are resisitant to antibiotics, and reescape causing new infection

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22
Q

How can Uropathogenic Escherichia coli (UPEC) make symptoms worse?

A

Shedding of epithelial cells with cystitis and inflammation
Attract polumorphic nuclear lymphocytes which in immune response damage more cells

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23
Q

What is an overview of LPS for immunity?

A

LPS (Lipopolysaccharide) and induces cytokine expression through TLR4
>180 types

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24
Q

What is an overview of flagellin for immunity?

A

Motility, induces cytokine expression through TLR5
>50 flagella subtypes

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25
Q

How do LPS and flagellin trigger severe immunity?

A

NFkB activation
pro-inflammatory cytokines TNF-a
Interleukin-1 (IL-1), IL-6, IL-8
Type-1 Interferon (IFN) responses
Hyper-inflammation leads to septic shock

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26
Q

What is an overview of Extraintestinal Escherichia coli?

A

Urinary tract infections (UTI) are one of the most common of all infectious diseases
50% of women, 10% of men will have an UTI in their lifetime
85-95% of all urinary tract infections are due to E. coli

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27
Q

What are the Stages of ascending UTI, Escherichia coli?

A

Bladder infection (cystitis) –(Mobilisation via ureters)–> Kidney infection (pyelonephritis) –(Access to blood supply)–> Bloodstream (bacteraemia)–(Spread to vital organs)–> Invasive disease (sepsis, meningitis)

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27
Q

What is an overview of Sequence-type 131 (ST131) E. coli?

A

Emerged in late 2008, globally disseminated, multidrug resistant (MDR) pathogen
The predominant strain of MDR E. coli in adults / children.
Extended-spectrum beta-lactamase (ESBL), resistant to most front-line antibiotics

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28
Q

What are the main causes of Escherichia coli deaths?

A

Mostly, bloodstream and intra-abdominal

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29
Q

What is an overview of Klbsiella pneumoniae?

A

Named after Edward Klebs, discovered bacteria were the cause of lung infections in late 1800s
Gram negative, non-motile, rod-shaped, encapsulated bacterium
Order: Enterobacterales
Family: Enterobacteriaceae

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30
Q

What is an overview of Klebsiella pneumoniae infection?

A

Aspiration pneumonia – breathing in contaminated material
Infection associated with alcohol addiction
Sputum appearance of currant jelly

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31
Q

What is an overview of Klebsiella pneumoniae growth?

A

Lives in a wide range of environments, grows aerobically or anaerobically
Coloniser of mouth, nasopharynx, gastrointestinal tract
Common nosocomial pathogen, opportunistic
Readily exchanges DNA with other bacteria

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32
Q

What are the two phenotypes of Klebsiella pneumoniae?

A

Classical Kp known to cause pneumonia and bladder infection
Hypervirulent Kp (hvKp) - soft tissue, liver and meningtitis

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33
Q

What is an overview of classical Klebsiella pneumoniae?

A

Multi-drug resistant
Encaplulated
Vulnerable to phagocytosis and opsonisation

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34
Q

What is an overview of hypervirulent Klebsiella pneumoniae?

A

Overproduces capsule
Inhibits phagocytosis and bacterial lysis
Membrane attack compelx cant breach outer membrane
Not typicaly asscociated with drug resistance

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35
Q

What is a problem with Klebsiella pneumoniae drug resistance?

A

Klebsiella pneumoniae is a key trafficker of drug resistance genes from environmental to clinically important bacteria
Occurs in all hosts

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36
Q

Why are Escherichia coli and Klebsiella pneumoniae considered an urgent threat?

A

Resistance to pencillins and cephalosporins
Emergence of carbapenem antibiotics (last-line of defence)
Also potential in the hypervirulent strains

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37
Q

What countries are most effected by Klebsiella pneumoniae?

A

China (most), Singapore, USA, UK and France

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38
Q

What is the cause of most Klebsiella pneumoniae deaths?

A

Mostly, Pneumonia, bloodstream and intra-dominal

39
Q

What is an overview of Pseudomonas aeruginosa?

A

Pseudomonas = ‘false germ’ ; aeruginosa = latin for ‘copper rust’
Gram negative, rod-shaped, facultative anerobic, encapsulated bacterium
Order: Pseudomonadales
Family: Pseudomonadaceae
Characteristic green colouration due to synthesis of pigments pyocyanin and pyoverdine

40
Q

What is an overview of Pseudomonas aeruginosa infections?

A

Pseudomonas aeruginosa is the predominant cause of death and morbidity in Cystic Fibrosis patients
Associated with hospital-acquired infection in patients using ventilators
Virulence factors include flagellum and Lipopolysaccharide which are immuno-stimulatory

41
Q

What is a problem with clearing Pseudomonas aeruginosa?

A

Biofilm formation is a major problem for Pseudomonas aeruginosa control
Sesile cells which resist external stresses and can then regrow and disperse

42
Q

Why is Pseudomonas aeruginosa hard to control long term?

A

Highly adaptable pathogen; can undergo hyper-mutation at a rate 1,000 times higher than ‘normal’

43
Q

How can Pseudomonas aeruginosa resist immunity and antibiotics?

A

Loss of immunogenic structure such as flagella
Produce toxins to inhibit immune cells
Prevention of LPS forming
Mutant antibiotic targets such as gyrase
Low membrane permeability

44
Q

How can Pseudomonas aeruginosa survive antibiotics?

A

Can enter a ’persister’ lifestyle to survive antibiotic treatment

45
Q

What is an overview of the persister lifestyle?

A

Remain dormant when exposed to antibiotics to wait it out
Or they can upregulate antibiotic reistance molecules

46
Q

What is an overview of Pseudomonas aeruginosa antibiotic resistance?

A

~60% of strains resistance across different penicillins
~42% of strains resistant to carbapenems

47
Q

What are the main causes of Pseudomonas aeruginosa deaths?

A

Heavily pneumonia (cycstic fibrosis link) and blood stream

48
Q

What is an overview of Acinetobacter baumannii?

A

Gram negative, short-rod shaped (coccobacillus) bacterium
Family: Moraxellaceae
Genus: Acinetobacter
Found almost exclusively in hospitals
Sometimes referred to as Carbapenem-resistant
Acinetobacter baumannii (CRAB)

49
Q

How do people get infected with Acinetobacter baumannii?

A

Ventilators
Central-line catheters (vein)
Surgery
Catheter-UTI

50
Q

How can Acinetobacter baumannii survive decontamination well?

A

Survives well on surfaces
Extreme resistance to desiccation (removal of water) (up to 100 days)
Resists disinfectants including hydrogen peroxide, chlorhexidine (hospital-grade antiseptic)

51
Q

What groups are most at risk from Acinetobacter baumannii?

A

Critically-ill patients
Immunocompromised

52
Q

How prevalent are Acinetobacter baumannii infections?

A

2-4% of all hospital acquired infections due to A. baumannii
Globally, 45% of all isolates are multidrug-resistant, up to 70% in some areas

53
Q

Where does Acinetobacter baumannii colonised?

A

Primarily the respiratory tract
Though can invade and infect the bloodstream

54
Q

How can Acinetobacter baumannii resist antibiotics and which mechansim goes to which antibiotic?

A

Reduction of memebrane permiabilty - betalactams
Antimicrobial expulsion - Beta-lactams, rifamycins and tetracyclins
Enzymatic modifications - Tetracyclines, Beta-lactams an rifamycins
Target site alterations - Tetracylines

55
Q

What is a key different to Acinetobacter baumannii cell surface?

A

Has a Lipooligosaccharide (LOS) rather than a Lipopolysaccharide (LPS)
LOS is truncated LPS, lacks the O antigen

56
Q

What is an overview of innate immune response to Acinetobacter?

A

Similar to E.coli with TLR4 recognition
Upregulation of NG-kamma beta which increase inflamatory cytokines such as TNF, IL-6 and IL-8 which increase immune response

57
Q

What is the relationship between Acinetobacter baumannii
and rare metal ions?

A

Availability of metal ions is central to antimicrobial action of innate immune cells
Neutrophils produce and export calprotectin which then bind and prevent infections from getting rare metal ions such as zinc and nickel
But Acinetobacter baumannii can produce enzymes to scavenge these metals at a higher affinity
Also Acinetibactin a siderophore

58
Q

What is metal intoxication?

A

After phagocytosis, immune cells like macrophages over concentrate these metals as they are reactive therefore toxic which kill bacteria cell
Though Acinetobacter baumannii can overcome this by expelling the metals

59
Q

Why is Acinetobacter baumannii an urget level threat?

A

Hospital-acquired infections
Urgent level threat to antimicrobial resistance
70% of Acinetobacter baumannii cases were people already in hosptial
17% mortality rate

60
Q

What are the main infection types of Acinetobacter baumannii?

A

30% Pneumonia
20% Pressure ulcer
12% UTI

61
Q

What is an overview of Zosurabalpin (ZAB)

A

Targets and blocks synthesis of LPS/LOS
Not as effective against E.coli or Staphylococcus aureus but effective against Acinetobacter baumannii

62
Q

What is an overview of Enterobacter?

A

Gram negative, facultatively anaerobic, rod shaped
Family: Enterobacteriaceae
Genus: Enterobacter
22 species of Enterobacter make up this group such as E. amnigenus, E. arachidis, E. asburiae, E. bugandensis
Associated with hospital (nosocomial) infections in susceptible patients

63
Q

What is an overview of Enterobacter taxonomy?

A

Similar taxonomy (relatedness) to other Enterobacteria such as E. coli and Klebsiella pneumoniae

64
Q

What is an overview of Enterbacter virulence?

A

Little is known about pathogenicity or virulence factors in Enterobacter spp due to lack of study
Flagella, endotoxins (Lipopolysaccharides), hemolysins, type-3 secretion systems all reported
Biofilm formation

65
Q

What is an overview of Enterobacter spp antibiotic resistance?

A

Often called XDR (Extensively drug-resistant)
Resistant to Carbapenem, Penicillin and Cephalosporins

66
Q

What is an overview of Salmonella?

A

Named after Daniel Salmon, discovered bacterium from pig intestine 1880’s
Gram negative enteric, motile, rod-shaped, intracellular bacterium
Family: Enterobacteriaceae
Genus: Salmonella

67
Q

What are the broad categories of salmonella?

A

Typhoidal, non-Typhoidal Salmonella
Pathogen of humans and animals
Food-borne illness, systemic infection, gastroenteritis

68
Q

What are the two species of Salmonella?

A

S. bongori - infects lizards, not normally in humans except young children
S. enterica - divided into Salmonella Typhi (typhoid fever) or Salmonella Typhimurium (Non-typhodial salmonella)

69
Q

What is a major symptom of salmonella?

A

Enteritis in humans
Diarrhoea, fever, abdominal (12 - 72h after infection)
Lasts 4-7 days.
Generally self-limiting

70
Q

What is an overview of salmonella epidemiology?

A

Second most common food poisoning pathogen - but most deadly!!!
41, 616 cases, 120 deaths/year in UK.
Salmonella isolated from 23% GB pigs at abattoir.

71
Q

How much does Salmonella Typhimurium cost NHS?

A

National cost estimated at £500 million p.a.

72
Q

How does Salmonella Typhimurium spread?

A

Pathogen distribution through global food distribution and international travel

73
Q

How was Salmonella Typhimurium controlled in UK?

A

Lion Quality code 1998
Compulsory vaccination
Best-before date stamped on eggs
On farm and packaging hygiene controls

74
Q

What is an overview of Defra abattoir survey of Salmonella in UK Salmonellaresoviors?

A

23% Pigs
5% Chickens
1% Cows
Salmonellosis increasingly linked to vegetables

75
Q

What is an overview of Salmonella Typhimurium infection?

A

Ingest > 105 bacteria
Bacteria invade mucosal cells
Na+ uptake inhibited
Cl- secretion increased
Loss of water by mucosal cells
Increase cAMP levels in mucosal cells

76
Q

What is an overview of the immune response to Salmonella Typhimurium?

A

Inflammatory response to bacteria in underlying tissue
Prostaglandin release by PMNs

77
Q

What is an overview of Salmonella Typhimurium infection?

A

Salmonella adheres to gut epithelium (Lamina Propria)
Salmonella invades epithelial cells
Host senses infection (LPS as signal?) Recruits phagocytes
Salmonella survives & multiplies inside vacuole (flagellin as signal)
Induction of pro-inflammatory response (NF-kB)

78
Q

How does inflammation worsen Salmonella Typhimurium infection?

A

Inflammation of gut mucosa
Epithelial cells undergo necrosis & detach
Inflammation accelerates & damages lamina propria
Fluid is released into gut lumen causing acute diarrhoea

79
Q

How does Salmonella Typhimurium infect cells?

A

Uses T3SS1 to invade epithelia
Uses a second T3SS2 to generate SCVs (Salmonella-containing vacuole)

80
Q

What is the function of SCVs?

A

Avoids innate immune defenses
Recruits inflammatory cells
Depletes resident microbiota via the previous recruitment
Colonises the lumen, expands via colonal expansion

81
Q

What is an overview of Salmonella Typhi disease?

A

Typhoid fever in humans – host restricted.
Oral infection - systemic spread to organs.
9 million cases/ year worldwide
110 000 deaths worldwide (2019)
Endemic in sub-Saharan Africa, Far East.

82
Q

What is an overview of Salmonella Typhi vaccines?

A

Single serotype: 2 conjugate vaccines available.

83
Q

Where is Salmonella Typhi most prolific?

A

India, Pakistan, Southeast Asia and subSaharen Africa

84
Q

What is an overview of Salmonelaa Typhic infection?

A

Exclusive human pathogen
Gram negative flagellated bacilli
Non-sporulating facultative anaerobe
Ferments glucose without producing gas
Reduces nitrate to nitrite
Synthesizes peritrichous flagella when motile

85
Q

Where can Salmonella Typhi infect and associated symptoms?

A

Neurology - Seizures
Respiratory - Dry Cough
Gastroindestinal - Diarrhoea and Jaundice
General - Fever
Cardiovascular - Myocarditis

86
Q

What is an overview of Typhoidal Salmonellosis: Enteric Fever?

A

Incubation: 7-14 days after ingestion
Duration: several days
Infective Dose = 105 organisms (100,000)

87
Q

What is an overview of Typhoidal Salmonellosis: Enteric Fever symptoms?

A

1st week: slowly increasing fever, headache, malaise, bronchitis
2nd week: Apathy, Anorexia, confusion, stupor
3rd week: rose spots (1-2 mm diameter on the skin): duration: 2-5 days, variable GI symptoms, such as abdominal tenderness (majority), abdominal pain (20-40% of cases) and diarrhea

88
Q

What are longterm symptoms to Enteric Fever?

A

Neuropsychiatric - delirium and mental confusion
Long term effects - arthritis

89
Q

What is an overview of Typhoidal Salmonellosis disease length?

A

Late stage complications include intestinal perforation and gastrointestinal hemorrhage
Immediate care such as increase antibacterial medications or surgical resection of bowel
Majority of bacteria gone from stool in 8 weeks; However, 1-5% become asymptomatic chronic carriers: gallbladder is the primary source of bacterium

90
Q

What is an overview of being a Typhoidal Salmonellosis carrier?

A

1-4% of untreated patients become chronic carriers (large environmental source of infection – shedding into environment).
Excrete for more than 1 year.

91
Q

What are the human health costs of being a Typhoidal Salmonellosis carrier?

A

Stool carriage is more frequent in people with preexisting biliary abnormalities and these people have a greater incidence of cholecystitis.
Greater risk for carcinoma of the gallbladder
6-fold increase in the risk of death due to hepatobiliary cancer.

92
Q

What is an overview of Typhoid Mary?

A

Infected some 50-120 people working as a cook as an asymptomatic carrier of Salmonella Typhi
Estimates of up to 50 people died
Typhoid Mary was quarantined for up to 30 years to prevent further infections

93
Q

How does being a Typhoidal Salmonellosis carrier increase gallbladder problems?

A

They form biofilms around Gallstones where they can burst out and through toxins and immune response damage gallbladder epithelium

94
Q

How is typhoid fever hard to control?

A

Long time between infection and symptoms
Also asymptomatic carriers

95
Q

What are other notable gram-negative pathogens?

A

Neisseria meningitidis and Neisseria gonorrhea
Chlamydia spp
Helicobacter pylori
Haemophilus influenza
Legionella pneumophila

96
Q
A

3s2: Infection and Immunity (12 decks)

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