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Phase 2a - ICS > Gram negative bacteria > Flashcards

Gram negative bacteria Flashcards

1
Q

Where is LPS found?

A

Endotoxin forms the outer leaflet of the outer membrane of Gram negatives.

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2
Q

What does LPS comprise of?

A

Lipid A - toxic portion

Core (C) antigen (core oligosaccharide) - short chain of sugars, some are unique to LPS

Somatic (O) antigen (O-polysaccharide) - a highly antigenic repeating chain of oligosaccharides.

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3
Q

Virulence factors:

A

Any product or strategy that contributes to pathogenicity.

Colonisation factors: adhesins, invasins, nutrient acquisition.

Toxins: usually secreted proteins (cause damage and subversion).

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4
Q

Gram negative rod bacteria

A

Coliforms: Escherichia; Klebsiella, Salmonella, Shigella, Cirobacter, Proteus, Yersinia

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5
Q

Describe coliforms:

A
  • Enterobacteria
  • Rod shaped
  • Motile (peritrichous flagella)
  • Facultative anaerobic
  • Colonise the intestinal tract
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6
Q

What metabolic process helps distinguish between pathogenic Enterobacteria?

A

Lactose fermentation - differentiate between E. coli and Klebsiella sp.

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7
Q

MacConkey-lactose agar

A

Lactose fermenters – red (pink)
Acid produced by fermentation turns neutral red dye in plate red.

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8
Q

Xylose Lysine Deoxycholate (XLD)

A

Lactose fermenters turn phenol red in media yellow
Isolates Salmonella and Shigella.

Shigella cannot ferment lactose remains red.

Salmonella cannot ferment lactose but reduce thiosulphate to produce hydrogen sulphide (black).

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9
Q

Further discriminate between species by…

A

Serology

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10
Q

Cell surface antigens of Gram -ve bacteria

A

Amino acid or carbohydrate variation in cell surface structures gives rise to antigenic variation among species AND between isolates (strains) of the same species.

Capsula - polysaccharide
LPS - polysaccharide
Flagellum - protein

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11
Q

Serovars examples

A

E. coli O157:H7 - Enterohaemorrhagic E. coli (EHEC).

E. coli O45:K1:H7 - Neonatal meningitis-associated E. coli NMEC

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12
Q

E. coli

A

Commensals
Most abundant facultative anaerobe (107-108/g faeces)

Gastroenteritis
Travellers’ diarrhoea
Bacteraemia (potentially sepsis syndrome)
Meningitis (infants) – rare in UK

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13
Q

Principal infections caused by pathogenic E. coli

A
  • Wound infections (surgical)
  • UTIs (Cystitis 75-80% of female UTIs –faecal source or sexual activity
    Catheterisation – most common type of nosocomial infection)
  • Gastroenteritis
  • Travellers’ diarrhoea

Bacteraemia (? sepsis syndrome)

Meningitis in infants

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14
Q

ETEC

A

Stimulates CFTR (Chlorine ion transporter) in intestinal lumen to release ions and water through toxins (heat-labile toxin and heat stable toxin) – leads to watery diarrhoea.

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15
Q

EPEC

A

Invades cells in small intestine.

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16
Q

EIEC

A

Enteroinvasive Escherichia coli
Bacteria

Invades cells in large intestine.

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17
Q

Why pathogenic?

A

Acquisition of pathogenicity genes ‘en bloc’ by ‘lateral gene transfer’.

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18
Q

What are the four species of Shigella?

A

S. dysenteriae
S. flexneri
S. boydii
S. sonnei

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19
Q

Shigellosis

A

Shigellosis: severe bloody diarrhoea (bacillary dysentery)
S. dysenteriae causes most severe form
S. sonnei most prevalent in developed world

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20
Q

Symptoms of shigellosis

A

Frequent passage of stools (>30/day)
Small volume, pus and blood, prostrating cramps, pain in straining and fever.

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21
Q

Pathogenesis of Shigella infection

A
  • Acid tolerant with a low infective dose
  • Person to person, or contaminated water and food (fresh raw vegetables used in salad)
  • Entry through colonic M cells (antigen sampling cells, overlie lymphoid follicles and deliver AGs to underlying immune cells.
  • Induced uptake
  • Shiga toxin inhibits protein synthesis -> cell death.
  • Systemic absorption of Shiga toxin - targets kidneys - haemolytic uraemic syndrome / microvascular thrombosis in kidneys - kidney failure.
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22
Q

What are the three forms of salmonellosis caused by S. enterica?

A
  1. Gastroenteritis/enterocolitis (serovars Enteritidis and Typhimurium)
    Frequent cause of food poisoning (milk, poultry meat & eggs)
    Second highest no. of food-related hospitalisations/deaths (UK)
    6-36 hr incubation period, resolves (~7 days)
    Localised infection, only occasionally systemic
  2. Enteric fever - typhoid/paratyphoid fever (serovars Typhi and Paratyphi)
    Poor quality drinking water/poor sanitation
    Systemic disease
    ~20 million cases, ~200,000 deaths/year (globally)
  3. Bacteraemia (serovars Cholerasuis and Dublin)
    Uncommon
23
Q

Pathogenesis of slamonellosis

A

Ingestion of contaminated food/water - high I.D.
- invasion of gut epithelium
- transcytosed to basolateral membrane
- enters submucosal macrophages
- intracellular survival/replication

24
Q

Serovars Enteritidis and Typhimurium

A

Localised intestinal secretory and inflammatory response.

Do not produce toxins.

25
Q

Serovar Typhi

A

Systemic infection due to dissemination within macrophages.

Produces typhoid toxin (DNA-ase activity = genotoxin).

26
Q

Proteus mirabilis (pathogenic enterobacteria)

A

Can differentiate into an elongated hyperflagellated form = surface motility (‘swarming’)

Causes catheter-associated UTIs (~30% cases)  pyelonephritis

Produces urease (causes urine pH increase) - calcium phosphate precipitation - formation of bladder/kidney stones, catheter blockage.

27
Q

Klebsiella pneumoniae (pathogenic enterobacteria)

A

Environmental.

Opportunistic, nosocomial infections (neonates, elderly, compromised)

Colonisation of gastrointestinal tract (normal) and oropharynx (less frequently) is benign but can lead to:
-UTI
-pneumonia (aspiration from oropharynx)
-surgical wound infections
-bacteraemia = sepsis (high mortality)

Multi-drug resistant (resistant to carbapenems)

28
Q

Pseudomonas aeruginosa

A

Ubiquitous, free-living
Motile (single polar flagellum)
Rod-shaped

Opportunistic (serious cause of nosocomial infections)

Resistant to multiple antibiotics (& disinfectants) - very difficult to treat

Acute infections (due to multiple toxins):
Localised
Burn/surgical wounds, UTI, Keratitis

Systemic (bacteraemic = sepsis)
neutropenic patients (leukaemia, chemotherapy, AIDS)
ICU patients (ventilator acquired pneumonia)
leading cause of nosocomial pneumonia
Chronic infections:
Cystic fibrosis (CF) patients

Common denominator to all infections - compromised host defences.

29
Q

P. aeruginosa and CF

A

CF, most common inherited lethal disorder among Caucasians.

Defective CFTR = thick mucus produced in lungs.

Lungs prone to microbial infection.

P. aeruginosa most problematic.
P. aeruginosa ‘wild-type’ (non-mucoid).
P. aeruginosa ‘CF’ phenotype (mucoid)
Isolates that secrete a thick coating of exopolysaccharide: provides additional protection against host defences in the lung

Chronic inflammation leading to progressive lung damage and deterioration of lung function
Occurs following infection of the CF lung by P. aeruginosa
Mainly due to host immune system trying to clear the infection.

30
Q

Vibrio cholerae

A

Facultative anaerobe
Saline environments: commensal to planktonic crustaceans such as copepods
Ingestion by shellfish
Contamination of drinking water due to flooding of coastal areas or poor sanitation (faecal contamination).

31
Q

Cholera

A

Most severe diarrhoeal disease
Characterised by pandemics (7 recorded since 1817)

1P-6P, Indian subcontinent

7P began in Sulawesi (1961)  SE Asia (1963)  Africa (1970)  Latin America (1991)  Caribbean (2010)

O1 serotype  epidemics (and occasionally O139 variant)

1.4-4.0 million cases/year, 20,000-140,000 associated deaths

32
Q

Pathogenesis of V. cholerae

A

Faecal-oral route (not person-to-person) - high infective dose required
Faecal contaminated water (poor sanitation)
Undercooked shellfish from risk areas)

Incubation, few hours to 5 days (V.c. multiplies in small intestine)

Voluminous watery stools (‘secretory’ diarrhoea)

Can lose 20 litres fluid/day plus electrolytes
Dehydration/death (hypovolaemic shock)
 50-60% mortality if untreated

No blood, pus or fever (i.e. not dysenteric)
i.e. no invasion or damage to mucosa
Release of cholera toxin causes pathogenesis

Most cases can be treated with ORT

33
Q

Campylobacter

A

C. jejuni
C. coli

Spiral rods
Unipolar (monotrichous) or bipolar (amphitrichous) flagella

Most common cause of food poisoning in UK & US
Undercooked poultry
Cattle (unpasteurised milk)

I.D. 500-800 (low)

Mild to severe diarrhoea, often with blood
Usually self-limiting (≤ 1 week)

Campylobacter shed in faeces for ~3 weeks

34
Q

Helicobacter pylori

A

Spiral shaped
Tuft of polar flagella

Discovered in gastric mucus, 1982 (stomach previously thought to be sterile)

Present in ~50% global population, but only a fraction develop disease

Major role in gastritis and peptic ulcer disease (80-90% of ulcers)

Implicated in ~10% cases of gastric adenocarcinoma & mucosa-associated lymphoid tissue lymphoma (linked to production of VacA and CagA toxins)

Barry Marshall ingested H. pylori → gastritis → Nobel prize 2005

35
Q

Haemophilus influenzae

A

Exclusively human reservoir
Nasopharyngeal carriage in 25-80% population (non-capsulate strains)
Transient carriage of capsulate strains occurs in 5-10%

36
Q

What are the opportunistic infections caused by H. influenzae?

A

Opportunistic infections seen mainly in young children and adult smokers:

  • Meningitis* (age <5 yrs), 5-10% of adult cases
  • Bronchopneumonia
  • Epiglottitis*, sinusitis, otitis media
  • Bacteraemia* (often associated with pharyngitis)
  • Pneumonia in CF, COPD, HIV patients
    *infections caused by capsulate strains (invasive) – uncommon in healthy adults
37
Q

Diagnostics for H. influenzae

A

Fastidious
Requires ‘factor X’ (haem) and ‘factor Y’ (NAD)
Cultured on chocolate agar

Non-motile.

38
Q

What are the virulence determinants of H. influenzae?

A

Capsule - invasive strains are capsulate (‘encapsulated’)

Can penetrate nasopharyngeal epithelium

Resistance to phagocytosis and complement system

6 different capsule serotypes (a-f)

Hi b strains are the main cause of meningitis
‘Hib’ vaccine has reduced the incidence

Commensals and upper respiratory tract pathogens are non-capsulate (‘unencapsulated’) referred to as ‘non-typeable’ H. influenzae (NTHi)
Incidence increasing

LPS (‘endotoxin’)
Inflammation
Complement resistance

39
Q

Bordetella pertussis

A

Short (sometimes oval) rods (‘coccobacilli’)
Fastidious
Humans - only known reservoir (obligate human pathogen)

Pertussis (whooping cough)
B. parapertussis causes mild pharyngitis

Highly contagious (low I.D.) - aerosol transmission
Non-specific flu-like symptoms (~7 d), followed by paroxysmal coughing
https://www.youtube.com/watch?v=l5SHtdczSBc

Non-invasive
Produces two toxins
Pertussis toxin
CyaA
Hypersynthesis of cAMP  suppresses innate immune function particularly macrophage phagocytosis

40
Q

Legionella pneumophila

A

Discovered 1976
Legionnaires’ disease - severe inflammatory pneumonia (1-3% of all pneumonias)
Immunocompromised (elderly, alcoholics, smokers)

Severe (15-20% mortality)
Infection from man-made aquatic environments
air-conditioning cooling towers, shower heads, nebulisers, humidifiers…

Replicate within freshwater protozoa - intracellular parasite of amoeba

Can survive and replicate within alveolar macrophages
Upregulates pro-inflammatory genes in alveolar macrophages
Excessive influx of neutrophils into lungs → inflammation.

41
Q

Bacteroides

A

Non-motile rods
Strict (obligate) anaerobes

Commensal flora (large intestine) - most abundant (30-40% of the total)
>1010/g faeces (outnumbers E. coli 20:1)

Opportunistic - tissue injury (surgery, perforated appendix or ulcer)
Predominantly peritoneal cavity infections (peritonitis, intraabdominal abscesses are most common) can lead to bacteraemia

Most frequent cause of anaerobic infections, usually B. fragilis (although it is only 0.5-1.0% of total commensal Bacteroides)

Often present in polymicrobial infections with enterobacteria
Presence of facultative anaerobes depletes O2, allowing anaerobes such as Bacteroides to proliferate

Treatment requires specific anti-anaerobe antibiotics e.g. metronidazole

42
Q

Neisseria (growing as single cells)

A

Non-flagellated diplococci

Fastidious

Two species of medical importance:
N. meningitidis
N. gonorrhoeae

Humans are the only known reservoir.

43
Q

Neisseria meningitidis

A

Meningococcus

Nasopharyngeal carriage in 5-10% population (asymptomatic)
Rises to 20-90% during outbreaks
Person-to-person (aerosol) transmission (universities, barracks, Haj)

Pathogenesis:
Crosses nasopharyngeal epithelium and enters bloodstream
Low level bacteraemia (asymptomatic) or septicaemia (sepsis)
Meningitis: invasion of the meninges - bacteria enter CSF of subarachnoid space
second most frequent cause of meningitis in young children

Very high mortality from septicaemia if not treated
Requires rapid diagnosis!

Virulence determinants of N. meningitidis
Capsule is major virulence determinant (serogroup B - 90% cases in UK)
Anti-phagocytic
Noncapsulated N.m. only found in nasopharynx - not pathogenic
LPS (membrane ‘blebs’)
Cytokine cascade
Sepsis

44
Q

N. gonorrhoeae

A

Gonococcus
Gonorrhoea - second most common STD worldwide
82.4 million (2020)
Cases doubled in the UK last year

Person-to-person only
Infection can be asymptomatic (~10% men, ~50% women)
Usually characterised by urethritis with additional infection of female genitalia
Serious complications in women - can lead to salpingitis and/or PID if infection ascends.

Proctitis, gingivitis, pharyngitis depending on sexual preference

Multi-drug resistance arising

Note: gonococci are non-capsulated (unlike pathogenic N. meningitidis)

45
Q

What bacteria grow as single cells and belong to spirochaetes?

A

Leptospira
Treponema
Borrelia

46
Q

Spirochaetes

A

Long, slender, helical, highly flexible
Most are free-living and non-pathogenic
Pathogenic varieties difficult to culture

Modified outer membrane (“outer sheath”)
Treponema and Borrelia lack LPS, replaced by a different glycolipid

Endoflagella (‘axial filaments’ = periplasmic flagella)
Located between peptidoglycan and outer membrane
Fixed at each end of the bacterium and confers shape

Overlap in the centre of the bacterium.

Propels bacterium in a corkscrew motion
Swim faster in high viscosity medium
“Hides” antigenic flagellum

Three medically important genera

47
Q

Borrelia burgdorferi

A

Lyme disease (zoonosis) (~300 cases in UK)
B.b. infects small mammals (rodents)
B.b. acquired by tick larvae feeding on infected animal

Transmitted to humans by tick nymphs (adults easier to spot!)
bull’s eye rash, flu-like symptoms (fever, fatigue, headache)

Dissemination via lymphatics/blood to other organs
neurological problems in 10-15% patients, joints → arthritis

Most symptoms arise due to immune response

48
Q

Leptospira interrogans

A

Leptospirosis (zoonosis)
Rare in UK

Common infection of rats
Systemic infection of the rat, excreted in faeces and urine
Proximity of rats to water often means water sources are colonised
Rivers, streams country parks, lakes

Contact of infected animal urine with mucous membrane or abraded skin
Flu-like symptoms
Severe form (Weil’s disease*) in 10-15% infected individuals
2-4 week incubation period, clinical multi-organ infection occurs
Liver infection leads to cell destruction and jaundice
Acute renal and hepatic failure
Pulmonary distress
Haemorrhage

49
Q

Treponema pallidum

A

Syphilis (STD)
2,800 cases in UK – increasing again

Primary stage
Localised genital infection (ulcer (“chancre”))
Days-weeks post-infection
Highly transmissible phase

Secondary stage (~50% cases)
Systemic
Skin (rash), swollen lymph nodes, joint pains, muscle aches, headache, fever
1-3 months post-infection
Still highly transmissible

Tertiary stage (~30% cases)
‘Gummas’ (granulomas) in bone and soft tissue
Cardiovascular syphilis (aorta)
Neurosyphilis (brain and spinal cord)
Occurs several years post-infection
Non-infectious form

All stages are treatable with ABx but treatment is longer for tertiary stage syphilis and tertiary damage cannot be reverted.

50
Q

Obligate intracellular bacteria

A

Rickettsia
Chlamydia
Coxiella

51
Q

Chlamydia

A

Very small, non-motile

Obligate intracellular parasites

Many species within this group live asymptomatically as endosymbionts in amoebae, invertebrates and vertebrates

Cannot culture in bacteriological media - detect by serum Abs or PCR
Detects presence of anti-Chlamydia antibodies in serum
May be the result of a previous infection
Test must not be used to detect a current infection without an alternative confirmatory test

Also referred to as NAA (nucleic acid amplification) or NAAT (nucleic acid amplification test)

52
Q

Life cycle of Chlamydia

A

Unique growth cycle: 2 developmental stages:
Elementary bodies (EBs)
Rigid, extracellular form, ~0.3 μm, dormant
Infectious
Enter cell through endocytosis
Prevent phagosome-lysosome fusion

	↓ differentiates into...

Reticulate bodies (RBs)
Fragile, intracellular form, ~1.0 μm, metabolically active
Replicative
Non-infectious
Acquire nutrients from host cell

53
Q

Medically important members of Chalmydia

A

C. trachomatis (3 biovars):
Trachoma biovar (serotypes A-C) → trachoma → blindness
Eye-to-eye transmission via hands, fomites or flies

Genital tract biovar (serotypes D-K)
most common STD - infects epithelial cells of mucous membranes of urethra (both sexes) and vagina
can ascend to uterus and ovaries (PID, infertility)
usually asymptomatic (i.e. 70-80% cases in women)

conjunctivitis (STD), hand-to-eye transmission

Lympho granuloma venereum (LGV) biovar (serotypes L1-L3)
causes LGV (an STD) - invasive urogenital or anorectal infection
endemic to the tropics, cases rising in Europe/N. America

C. pneumoniae
Respiratory tract (mild or “walking” pneumonia)
~10% community acquired pneumonias

C. psittaci
Mainly birds
Psittacosis (zoonotic infection), severe pneumonia

Phase 2a - ICS (43 decks)

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