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Human Microbial Diseases > Bacteria + Protozoa > Flashcards

Bacteria + Protozoa Flashcards

1
Q

what are pros to intracellular survival

A

-survive or die
-gain access to a protected/nutritious environment
-some protection from immune response
hostile takeover

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2
Q

what are the cons to intracellular survival

A

-must overcome host barriers
-modulate innate immunity
-modulate cell mediated immunity
-overcome normally bactericidal stress

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3
Q

examples of facultative intracellular pathogens

A

-salmonella
-legionella
-shigella
-yersinia

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4
Q

examples of obligate intracellular pathogens

A

-mycobacterium
-chlamydia

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5
Q

examples of pathogens that survive and grow in phagocytic cells after phagocytosis

A

-salmonella
-listeria monocytogenes
-mycobacterium
-legionella pneumophila

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6
Q

examples of pathogens that survive and grow in non-phagocytic cells

A

-salmonella
-shigella
-listeria

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7
Q

what’s the morphology of macrophages

A

large, mononuclear with granular cytoplasm

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8
Q

what’s the morphology of neutrophils

A

small with multilobed nucleus and granular cytoplasm

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9
Q

location of kupffer cells

A

liver

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10
Q

location of alveolar macrophage

A

lung

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11
Q

location of osteoclasts

A

bone

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12
Q

location of microglia

A

brain`

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13
Q

location of neutrophils

A

found in blood-require recruitment to site of infection

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14
Q

killing ability of macrophages

A

require activation by IFNg

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15
Q

killing ability of neutrophils

A

activated during recruitment

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16
Q

after killing what happens to macrophages

A

migrate to local lymph nodes

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17
Q

after killing what happens to neutrophils

A

die at site by apoptosis

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18
Q

do macrophages present antigens

A

yes

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19
Q

do neutrophils present antigens

A

not normally

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20
Q

mechanism of phagocytosis

A

-internalization of pathogen into phagosome
-acidification of phagosome
-fusion of phagosome with lysosomes/ granules containing anti-microbial compounds=phagolysosome
-oxygen and nitrogen species generated

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21
Q

what is the role of toll-like receptors

A

recognise pathogen-associated molecular patterns resulting in cytokine production and cellular activation

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22
Q

what is the receptor- ligand interaction utilised during phagocytosis dependent upon

A

bacterial species and macrophage phenotype

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23
Q

do macrophages and neutrophils have phagosome acidification

A

yes

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24
Q

do macrophages and neutrophils have primary granules

A

only neutrophils

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25
Q

do macrophages and neutrophils have secondary granules

A

only neutrophils

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26
Q

do macrophages and neutrophils have lysosomes

A

only macrophages

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27
Q

do macrophages and neutrophils have oxygen dependent and independent mechanisms

A

yes

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28
Q

do macrophages and neutrophils have nitrogen dependent mechanisms

A

yes

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29
Q

what are the different strategies for intracellular survival in phagocytes

A

-avoid/prevent phagocytosis
-able to proliferate in vacuole
-escape vacuole and survive in cytoplasm

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30
Q

mechanisms for resisting bactericidal activities during phagocytosis

A

-detoxification of killing agents
-prevention of access to killing agents
-prevention of iNOS activity

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31
Q

salmonella as an intracellular pathogen

A

-survives in and modifies phagosome
-resists bactericidal activities
-invades non-phagocytic cells

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32
Q

shigella as an intracellular pathogen

A

-escapes phagosome
-kills macrophages
-invades non-phagocytic cells
-intracellular motility

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33
Q

first phase of typhoid fever

A

slow fever, rose spots, mild, bacteraemia

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34
Q

second phase of typhoid fever

A

organism reaches gall bladder, re-invasion of intestine, ulcer, haemorrhage, death (20%)

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35
Q

what’s enteric fever

A

similar to typhoid fever nut less severe and rarer. S. paratyphi

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36
Q

how long is incubation period of salmonella

A

12-36 hours
- chills/fever, nausea/vomiting, abdominal pain, diarrhoea (1-7days)

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37
Q

salmonella and toll-like receptors

A

TLR stimulation by salmonella PAMPs trigger burst of ROI and RNIss

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38
Q

salmonella and ROIs

A

SPI-2 and PhoPQ involved in evasion of ROIs as is the salmonella containing vacuole

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39
Q

salmonella and RNIs

A

salmonella induces arginase II which limits substrate for iNOS activity. arginase is also recruited into the salmonella containing vacuole

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40
Q

salmonella and P-L fusion

A

salmonella actively avoids salmonella containing vacuole fusion with lysosomes

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41
Q

salmonella and metal ions

A

macrophages try to establish balance to starve bacteria

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42
Q

salmonella and cell death

A

salmonella effectors modify cell death pathways, e.g activation of PKR kinase leads to phosphorylation of eIF2a, hampering protein synthesis

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43
Q

define endotoxin

A

the lipid A portions of lipopolysaccharides that are part of the outer membrane of the cell wall of gram-negative bacteria with the exception of listeria, liberated when bacteria die and cell wall breaks

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44
Q

define exotoxin

A

proteins produced inside pathogenic bacteria, most commonly gram+ but can be gram-negative, exotoxin secreted into surrounding medium during log phase

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45
Q

what is the toxicity of exotoxin

A

high, specific activity targeting specific sites

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46
Q

what is the toxicity of endotoxin

A

moderate, non-specific

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47
Q

what’s the antigenicity of exotoxin

A

highly antigenic

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48
Q

what’s the antigenicity of endotoxin

A

poorly antigenic

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49
Q

heat stability of exotoxin

A

heat liable

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50
Q

heat stability of endotoxin

A

heat stable

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51
Q

how does endotoxin trigger gram-negative bacterial sepsis

A

induces systemic inflammatory response characterized by pro-inflammatory cytokines, nitric oxide, fever, hypotension, intravascular coagulation, organ failure, and culminating in septic shock

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52
Q

what are the direct mechanisms of bacterial exotoxins

A

-facilitate spread of bacteria through tissue (hyaluronidase)
-damage cell membranes/body structures (collagenase)
-immunomodulatory (IgA protease)
-inhibit protein synthesis (diphtheria, shigatoxin)
-inhibit release of neurotransmitters (botulinum)

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53
Q

cytokine induction by endotoxin

A

-endotoxins mainly activate antigen-presenting cells to produce cytokines

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54
Q

cytokine induction by exotoxin

A

super-antigens affect antigen-presenting cells and t-cells and induce macrophage and t-lymphocyte cytokines leading to cytokine storm

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55
Q

what are type I exotoxins

A

bind to surface receptors, are not translocated into the host cell and stimulate transmembrane signals

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56
Q

what are type II exotoxins

A

act directly on cell membranes

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57
Q

what are type III exotoxins

A

A-B toxins which translocate an active enzymatic component into target cell which modifies an intracellular target molecule

58
Q

what are the features of A-B (type III) toxins

A

-A part = active component
-B part = binding component
-A attacks host structure or function and B binds to host cell receptor
-toxin enters cell
-vacuole becomes acidified and membrane breaks down
-A + B dissociate from one another, A enters cytoplasm to inflict its activity and everything else removed via exocytosis

59
Q

structure of AB toxin

A

-product of a single gene
-single protein with A + B domains
-A linked to B by disulphide bond

60
Q

structure of AB5 toxin

A

-product of several genes
-separate subunits covalently linked
-could be 5 different B’s so multiple host cell receptors

61
Q

ADP-ribosylation

A

enzyme that catalyses removal of an ADP-ribose moiety from NAD+ and subsequent transfer to a specific target molecule in host cells resulting in activation or inactivation of cell functions modulated by these proteins

62
Q

what is the target and effect of cholera toxin

A

Gs protein, constitutive adenylate cyclase activation

63
Q

what is the target and effect of E.coli LT toxin

A

Gs protein, constitutive adenylate cyclase activation

64
Q

what is the target and effect of Pertussis toxin

A

Gi protein, prevent adenylate cyclase deactivation

65
Q

what is the target and effect of Diphtheria toxin and Pseudomonas exotoxin A

A

elongation factor 2, stops protein synthesis

66
Q

what is the causative agent in cholera

A

Vibrio cholerae

67
Q

what is death by cholera due to

A

-hypovolemic shock (due to abnormally low volume of circulating fluid)
-metabolic acidosis (loss of bicarbonate and thus buffering capacity)

68
Q

how is cholera treated

A

rehydration therapy, antibiotics may make it worse

69
Q

mechanisms of cholera

A

-attaches to intestinal epithelial cells and release of CTX
-B binds to specific ganglioside
-A subunit transferred into cell
-A protein adds an ADP-ribose molecule to the G-protein making it permanently active
-adenyl cyclase converts ATP to cAMP
-normal transport of sodium from lumen blocked and Cl- and Na+ enter intestinal lumen
-water flows by osmosis from blood stream due to loss of ions

70
Q

what’s the structure of the cholera toxin

A

-A-B type
- A unit is enzymatic
-B unit binds to host GM1 ganglioside
produced in inactive form but nicked by bacterial endopeptidase during processing in body to produce active form

71
Q

how is chxA. another virulence factor for V.cholerae

A

1/3 of non 01 and non-0139 V.cholerae encode this PE like toxin ChxA
-ADP-ribosylation of EF2, inhibits translation and kills cells, potential cancer treatment

72
Q

what is the causative agent of whooping cough

A

Bordetella pertussis

73
Q

what’s the catarrhal stage of whooping cough

A

-1-2 weeks
-fever
-malaise with mild cough

74
Q

what’s the paroxysmal stage of whooping cough

A

-1-6 weeks
-5-20 forceful coughs with no time to breath
-whoop when air rushes back into lungs
-vomiting and exhaustion

75
Q

mechanism of B.pertussis virulence

A

-inhalation of aerosols containing B.pertussis
-adherence to ciliated epithelial cells + colonisation of upper respiratory tract
-toxin produced
-damage to mucosal cells or action on neurons

76
Q

describe the pertussis toxin

A

-5 different subunits (A-5B)
-A (S1) is a ribosyl transferase
-S1 activated by calmodulin
-increases cAMP production + disrupts cell function
-S2 (B) binds to lactosylceramide
-S3 binds to macrophages

77
Q

what’s the causative agent of diphtheria

A

Corynebacterium diphtheriae

78
Q

describe diphtheria

A

-2-6 days incubation
-fever, malaise, sore throat, formation of pseudomembrane. damage to mucosal cells, damage to organs by toxin, breatrhing obstruction, death

79
Q

what’s the mechanism of C.diphtheriae virulence

A

-inhaled
-adherence to throat epithelial cells + colonisation
-elaboration of toxin and organ damage
-formation of pseudomembrane

80
Q

what’s the mode of action diphtheria toxin

A

-binds to heparin-binding epidermal growth factor precursor
-complex taken up by endocytosis
-acidification changes conformation of T-domain allowing it to insert into the membrane
- A is translocated into cytoplasm activating it

81
Q

describe toxins as a therapy

A

-bacterial protein toxins utilized as vaccine antigens
-vehicles for taking in heterologous proteins into cell
-immunotoxins enable targeting of diseased cells
-botox used in treatment of neurological disorder

82
Q

what’s a type III secretion system

A

a multi-protein complex that’s formed between inner + outer membrane of bacteria delivering bacterial proteins directly to host cell

83
Q

what are the functional attributes of the T3SS components

A

-translocon interacts with host cell
-tip complex caps needle filament to stop it growing larger
-base body holds apparatus in place
-export apparatus is a gated pore that controls export of effectors

84
Q

what are the 7 main families of T3SSs

A

-Ysc
-Inv-Mxi-spa
-Esc-Ssa
-Hrp1
-Hrp2
-chlamydia
-Rhizobiales

85
Q

what is the function of the Ysc T3SS family

A

dampen host immune responses- indicative of an extracellular pathogen

86
Q

what is the function of the Inv-Mxi-Spa T3SS family

A

trigger bacterial uptake by non-phagocytic- indicative of an invasive pathogen

87
Q

what is the function of the Ssa-Esc T3SS family

A

promotes adherence to epithelial cells or allows survival inside host cells

88
Q

what is the function of the chlamydiales T3SS family

A

alters host membrane structure to allow uptake into a membrane-bound vacuole

89
Q

what is the function of the Hrc-Hrp1 and Hrc-Hrp2 T3SS family

A

manipulate host cell signalling, nutrient accessibility

90
Q

what is the function of the Rhizobiales T3SS family

A

form symbiotic relationships with plants causing formation of nodules on roots of leguminous plants

91
Q

describe the process of T3SS assembly

A

-outer membrane (OM) secreting ring joins inner membrane (IM) protein at same time, inner ring assembles on IM
-OM ring and IM complex join together
-integration of the 2 assemblies into one complex allows recruitment of cytoplasmic components

92
Q

what’s the role of the LEE-encoded Map effector

A

induces transient filopodia formation
-causes mitochondrial dysfunction
-affects fluid secretion
-disrupts tight junctions
-causing loss of epithelial barrier

93
Q

what’s the role of the LEE-encoded EsgG effector

A

-disrupts microtubules, tight junctions and paracellular permeability, also Golgi function and protein secretion

94
Q

what’s the role of the LEE-encoded EspH effector

A

disrupts focal adhesion proteins
-remodels brush border
-promotes actin nucleation and pedestal elongation

95
Q

what’s the role of the LEE-encoded EspF effector

A

-disrupts mitochondrial function, nucleolus, tight junctions and intermediate filaments
-inhibits phagocytosis
-induces apoptosis

96
Q

what’s the role of the LEE-encoded EspZ effector

A

-inhibits apoptosis and cytotoxicity
-regulates type III secretion via translocation stop activity

97
Q

what’s the role of the LEE-encoded EspZ effector

A

-inhibits apoptosis and cytotoxicity
-regulates type III secretion via translocation stop activity

98
Q

describe the tubercle bacillus

A

-unicellular rods
-gram positive
-complex cell walls- sugars, proteins and lots of lipid

99
Q

what are the clinical manifestations of TB

A

-fever, weight loss, weakness, cachexia
-disease is pneumonia, impairment of the lung tissue itself
-can spread anywhere in body

100
Q

mechanism of TB

A

-aerosols travel to alveoli of lungs
-M. tuberculosis engulfed by alveolar macrophages
-if inactivated, bacteria survive and replicate in macrophages attracting more cells, damage tissue and form granulomatous tubercle

101
Q

M.tb survival in macrophages

A

-enter via receptors that avoid stimulation of oxidative burst
-detoxifies reactive oxygen by producing superoxide dismutase and catalase
-induces an efficient stress response to resist effects of damaged proteins

102
Q

describe phagosome maturation

A

-uptake
-small GTPase Rab5 recruited to phagosome membrane
-rab5 directs stimulation of PI3K, enzyme that generates PI3P
-Rab5 recruits Rab7
Rab 5 + EEA1 lost
-Rab 7 important for fusion of late endosome to lysosomes forming the phagolysosome

103
Q

what does M.tb inducing macrophage necrosis ESX-1 dependent contribute to

A

-dissemination-infection of new cells
-inflammation, attracting new immature phagocytes
-formation of cellular architecture of the granuloma
-caseation in granuloma centre
-transmission

104
Q

what is the treatment regimen for TB

A

-first line of oral anti-TB drugs

105
Q

what are the signs and symptoms of meningococcal meningitis

A

-vomiting
-intense headache
-skin rash, confusion, sensitivity to light
-neck stiffening
-convulsions
-if untreated fluid build-up in ventricles of the brain resulting in unconsciousness or death

106
Q

describe meningococcal sepsis

A

-N.meningitidis invade blood stream
-meningococcaemiacan rapidly progress toward a septic shock leading to a purpura fulminans, an acute systemic inflammatory response associated with intravascular coagulation and tissue necrosis
-40% mortality

107
Q

what’s the Labatory diagnosis of meningococcal disease

A

-CSF and blood samples
- microscopy
-culture
-PCR
-detection of soluble bacterial polysaccharides in CSF by latex agglutination

108
Q

what’s the Labatory diagnosis of gonococcal disease

A

-direct examination of exudates in GUM clinics
-endocervical, cervical, anal and eye swabs and urines
-nucleic amplification tests
-QRT PCR

109
Q

describe the infection with Neisseria meningitidis

A

-natural habitat is in human nasopharynx, transmitted by aerosol droplets or direct contact with contaminated fluid
-grows on top of mucus-producing epithelial cells surrounded by complex microbiota
-formation of micro-colonies that extend overtime to fill micro vessels

110
Q

describe the interactions between N. meningitidis and human host

A

-meningococci survive by expressing capsule, LOS, the MtrCDE efflux pump, and factors that capture nutrients
-express 2 families of polymorphic toxins; MafB and CdiA
-meningococci cross epithelial layer into bloodstream where they adhere to vascular wall
-adhesive bacteria proliferate + induce an active signalling leading to better adhesion and opening of vascular barrier, vessel leakage and massive thrombosis

111
Q

capsule of N. meningitidis

A

-can be encapsulated or not
-N. gonorrhoea lacks capsule
-serogroup B not antigenic
-serogroups associated with disease are A, B, C, W, Y, and X
-capsule switching can occur- vaccines based on capsular type causes problem

112
Q

how does Neisseria use adhesion

A

-pili traverse the capsule + act as adhesins
-integral outer membrane adhesins mediate interactions with specific host cell receptors
-lipoolygosaccharide may interfere with adhesion functions of OM proteins, can also contribute to cellular interactions by interacting with cellular receptors

113
Q

how does meningococci survive in serum

A

-uptake nutrients + iron from extracellular environment
-avoid complement killing by antigenic variation and complement resistance

114
Q

treatment of meningococcal disease

A

-IV antibiotics
maintenance therapy for shock
-vasoactive treatments IV adrenaline
-steroids
-experimental therapies, such as anti-cytokine + anti-endotoxin

115
Q

describe the Bexsero B vaccine

A

-developed by reverse vaccinology
-possible protection against serogroup W and cross-protection against neisseria gonorrhoeae infection

116
Q

what are the symptoms of pelvic inflammatory disease

A

-abnormal vaginal discharge
-bleeding between periods
-pain in lower part of abdomen
-uncomfortable/painful sex
-pain or difficulty when urinating fever

117
Q

describe Neisseria gonorrhoeae infection

A

-adherence to urogenital epithelium
-colonisation and invasion of epithelium
-release of peptidoglycan, LOS + OMVs
-cytokine, chemokine + inflammatory transcription factor activation
-peptidoglycan, LOS + OMVs cause NOD + TLR activation on epithelial cells, macrophages + DCs; HBP causes activation of TIFA-dependent innate immunity in epithelial cells and macrophages
-influx of neutrophils; adherence and phagocytosis of N. gonorrhoeae
-neutrophil rich purulent exudate facilitates transmission

118
Q

how does N. gonorrhoeae modulate the immune system

A

-prevents complement activation, opsonization and bacterial killing
-modulates activities of macrophages, DCs and neutrophils
-modulates T cell function + varies its surface components to avoid adaptive immune system

119
Q

what is LpxC

A

a zinc metalloamidase that catalyses the second step of critical lipid A biosynthesis

120
Q

what natural protection exists against malaria

A

-sickle cell anaemia
-thalassemia
-lack of duffy factor
-glucose-6-dehydrogenase deficiency

121
Q

what are the 3 main antigen groups present on malaria infected RBC

A

-P.falciparum erythrocyte membrane protein (PfEMP1)
-repetitive interspersed families of polypeptides (RIFINs)
-subtelomeric variant open reading frame (STEVOR)

122
Q

what’s the life cycle of Cryptosporidiosis

A

-penetrate intestinal wall
-mature in extra-cytoplasmic vacuoles
-develop into 8 merozoites
-second round infection- some cells develop into gametocytes
-further multiplication and release with faeces

123
Q

what’s toxoplasmosis

A

-toxoplasma gondii
-toxon= bow, plasma= cell
-apicomplexan- obligate intracellular parasite

124
Q

describe toxoplasmosis in neonates

A

-infection during 1st and 2nd trimesters is most serious
-possible outcomes; ocular abnormalities, brain damage, foetal damage
-infection in 3rd trimester has milder symptoms

125
Q

identification of alpha streptococcus

A

-partially break down blood agar, produces large amounts of polysaccharide capsule, gram positive

126
Q

identification of beta streptococcus

A

complete breakdown of haemoglobin

127
Q

what’s necrotising fasciitis

A

-post pharyngitis or direct inoculation
-rampant unfettered tissue damage, vascular dissemination + systemic disease
-high morbidity and mortality

128
Q

what’s acute rheumatic fever

A

-potential sequelae to pharyngitis
-4-8 weeks post infection; inflammation of heart + joints
-can reoccur + cause permanent damage to heart valves

129
Q

what’s acute glomerulonephritis

A

-post pharyngitis or skin infection
-few weeks post infection; haematuria, proteinuria, hypertension, impaired renal function
-risk factor for chronic kidney disease + end stage renal failure

130
Q

describe the colonisation and carriage of GAS

A

-assymptomatic carriage low in healthy adults, higher in kids
-in nasopharyngeal mucosa, skin and vaginal tract
-saliva important reservoir of GAS
-saliva is carbohydrate limited environment
-reliant on amylase to degrade starch

131
Q

give some examples of non-invasive GAS infections

A

-pharyngitis
-scarlet fever,
-impetigo
-otitis media

132
Q

give some examples of severe invasive GAS infections

A

-meningitis
-puerperal fever
-septicaemia
-necrotizing fasciitis
-TSS

133
Q

describe the adherence of GAS

A

-LTA establishes weak attachment between bacteria + host
-long surface attachment mediated by longer pili like surface structures + other surface fibronectin binding proteins + the M protein
-allows higher affinity attachment by numerous protein adhesins that permit bacterial interactions with multiple host components= GAS colonise diverse tissue sites

134
Q

how is the M protein in S. pyogenes a major virulence factor

A

-enables GAS to resist complement-mediated killing by polymorphonuclear leukocytes + macrophages
- required for attachment of GAS to keratinocytes
-causes GAS to aggregate when they attach to tonsillar epithelial cells

135
Q

how does GAS resist phagocytosis

A

-M protein- thwarts complement binding
-capsule- shields bacteria by molecular mimicry, blocks antibody access, inhibits complement deposition, enhances survival in NETs
-secreted proteases-inhibit phagocyte recruitment
-Mac1/2 blocks phagocytosis
-SpyCEP, ScpA- degrades cytokine

136
Q

describe super antigens

A

-potent immuno-stimulatory molecules
-produced by variety of microorganisms
-bind TCR irrespective of its antigenic specificity

137
Q

what infections are caused by S.pneumoniae

A

-meningitis
-occult bacteraemia
-sepsis with haemorrhagic shock
-pneumonia
-arthritis
-peritonitis

138
Q

transmission of S. pneumoniae

A

-colonizes mucosa of URT
-carriers can shed S.pneumoniae in nasal secretions
-dissemination by aspiration, bacteraemia or local spread

139
Q

what are risk factors for S.pneumoniae infection

A

-no spleen
-viral infection
-heart disease
-very young/ elderly
-diabetes
-alcoholism
-HIV infections
-smoking

140
Q

describe the identification of S.pneumoniae

A

-alpha haemolytic streptococcus
-very mucoid colonies due to production of large amounts of capsule
-production of hydrogen peroxide causes greening around colonies (haemoglobin broken down into methaemoglobin)

141
Q

how does pneumococcus compete

A

-produce pneumocins which target other membranes of same species
-commit fratricide (kill and lyse non-competent sister cells and members of closely related species)

Human Microbial Diseases (1 decks)

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