Module 4 - Microbes as pathogens Flashcards
1
Q
Commensals
A
Pathogens performing an interaction with us where they are provided nutrients, growth factors, temp, and pH
Naturally either neutral or slightly beneficial (no harm caused) but may be opportunistic if needed
2
Q
Microbiota
A
Collection of pathogens in our body forming a mutualistic relationship
Most bacteria are in the GI tract
3
Q
Microbiota diversity on the skin, mouth, and oral cavity
A
Skin - restricted
Nasal cavity - restricted
Oral cavity - very high biodiversity
4
Q
Tooth colonisation
A
Bacteria bind to the salvia layer of teeth and the top community live anaerobically
5
Q
Pathogens in the stomach
A
The stomach has a pH of 2, and should be sterile but some pathogens live there and may cause gastric ulcers which can lead to gastric cancer
6
Q
Pathogens in the small intestine
A
pH - 4/5 (low biomass)
7
Q
Pathogens in the colon
A
pH - 7 (huge biomass)
8
Q
Gut microbiota in babies and their general effect
A
- Babies are typically sterile in the uterus but as the baby is released, colonisation occurs
- Microbiota in the gut allows us to break down oligosaccharides in breast milk
Stabilise our immune systems and help digest food
9
Q
Gut microbiota
A
Babies are typically sterile in the uterus but as the baby is released, colonisation occurs
Microbiota in the gut allows us to break down oligosaccharides in breast milk
10
Q
The four main types of pathogenesis
A
Commensals - normal microbial flora (harmless)
Mutualists - Both benefit from the relationship
Opportunistic - Take advantage of opportunities
Viralists - highly virulent pathogens
11
Q
Pathogenicity/virulence
A
The ability of a pathogen/virus to cause disease
12
Q
Opportunistic pathogens: what are some examples?
A
Severe burns, cystic fibrosis, and the skin are all places where opportunistic pathogens can exploit (in terms of living in, they are harmless)
13
Q
Catheters and biofilm generation: what does this mean and what issues arise from it?
A
Catheters are tubes inserted in the body and, given that there are likely pathogens on it, they will enter the body with the catheter and the plasma proteins will naturally form a conditioning film around it
S.epidermis may form a colony which forms an antibiotic-resistant biofilm
14
Q
Meningitis: what is it caused by and what are the symptoms?
A
It is caused by a commensal pathogen (N. meningitidis) which causes opportunistic pathogens to spread (incubation takes around 4 days)
Stiff neck, high fever, sensitivity to light, confusion, headaches, vomiting and, in extreme cases, brain damage and hearing loss
15
Q
Tuberculosis: how does it develop?
A
M.tuberculosis are virulent bacteria that incubate for years by forming granulomas in the lung after replicating in alveolar macrophages (forming a Ghon complex)
16
Q
The new dangers of tuberculosis
A
MDR-TB, XDR-TB and XXDR-TB are drug-resistant, against first-line, first-line and some second-line, and all first-line and second-line
17
Q
Syphilis: what pathogen causes it and what are the stages of the infection?
A
Flexible helical bacteria (Treponema Pallidum)
- Primary lesion (Chancre at the site of infection in 2 wks)
- Secondary stage (after 10 wks) - bacteria spread to eyes, joints, bones & skin rash (right)
- Latent phase (years) - 40% develop tertiary syphilis (insanity & death)
18
Q
Showing cause and effect relationship between pathogens and infections
A
1 - Organism found in lesions
2 - Grow organisms outside the body in the lab (sometimes impossible)
3 - Organisms must reproduce the disease in animals (ie sheep)
4 - Re-isolate from the test animal
19
Q
Issues with Koch’s postulates
A
1 - Most pathogens cannot be cultivated in the lab
20
Q
How is virulence measured?
A
By the time taken for the lethal dose to kill 50% of the species (LD₅₀)
Also used to quantify toxins
21
Q
What determines virulence?
A
Virulence is determined by the ability of the colony to defend against the immune system:
1 - Capsule of poly-D-glutamic acid (inhibits phagocytosis)
2 - Toxins (suppress immune cell responses in early infection and can cause toxic shock and death in the later stages of infection)
If either capsules or toxins are missing, then the virulence is severely diminished (attenuated)
22
Q
The two stages in the disease process
A
Infection stage and the disease stage
23
Q
Infection stage: the four steps in it?
A
Exposure, adherence, invasion, and multiplication
24
Q
The disease stage: what is the final effect and what leads to it?
A
Tissue or system damage
Toxicity (toxin effects) and invasiveness (pathogen spreading around the body)
25
Commensal adhesion: how does it work?
Composed of subunits carrying a tip adhesin (protein H) which specifically attaches to mannose receptors on the surface of epithelial cells
26
Pathogen adhesion: how many types are there?
Adhesion
27
Properties of toxins?
* Heat labile (60-80°C)
* Soluble simple proteins
* EXTRACELLULAR
* Often enzymes
* Many coded by bacteriophages and plasmids
* Rapidly transported in the body
28
Bacterial exotoxins?
Enterotoxins - A/B toxins that affect the GI system
Cytotoxins - Kill cells with an enzymic attack
Neurotoxins - affect neurons
29
Enterotoxins: what do they do and what examples are there (and what do these examples do)?
Interfere with the GI tract using A/B toxins which cause profuse fluid secretion
Vibrio cholerae (curved Gram-negative rod-shaped bacteria which is transmitted by food and water) causes diarrhoea and pain to occur (~15l can be lost per day) which is treated by balancing fluid loss with solutes
30
Cytotoxins: what do they do and what examples are there (and what do these examples do)?
Kill cells by enzymic attack
Membrane-disrupting cytotoxins bind to membrane cholesterol and forms pores in the host causing the internal parts of the cell to be released
Phospholipase enzymes remove charged hydrophilic phosphate head which destabilises the membrane and kills the cell
31
Neurotoxins: what do they do and what examples are there (and what do these examples do)?
Interfere with neuronal transmission
Botulinum toxins are comprised of a heavy and light chain linked by a disulphide bond. The heavy chain binds to a glycoprotein receptor in neurons and the light chain with zinc metalloproteinase prevents acetylcholine release and so flaccid paralysis occurs
32
The A/B model of toxin action
Subunit A - one molecule that is enzymatically active inside the cell and has no binding function
Subunit B - Five molecules which bind to a specific receptor
33
How exactly do cholerae toxins work?
In normal ion movement, Na⁺ from the lumen
to the blood (no net Cl⁻ movement)
1 - cholerae toxins bind to GM1 ganglioside by AB toxin and release A into the cell
2 - A subunit activates epithelial adenylate cyclase
3 - Na⁺ movement blocked and phosphorylation of CFTR by PKA causes net movement of Cl⁻ into the lumen
4 - Massive water movement to the lumen, cholera symptoms occur (profuse fluid loss)
34
Endotoxins: what can they do at high levels, what examples are there, and which type of bacteria exhibit endotoxin behaviour?
Toxic shock: fever, low blood pressure, intravascular coagulation, haemorrhage, shock, and possibly death
Salmonella, shigella, gonococci, meningococci
The lipid A molecule is only found in lipopolysaccharide (LPS) which is only found in bacteria with an outer cell wall (Gram-negative bacteria)
35
How do endotoxins exhibit their effects?
Once in the cell, lipid A activates monocytes which activate cytokines IL-1, IL-6, IL-8 and TNFₐ - initiating a fever
The complement cascade is then activated - triggering blood vessel permeabilization
Then the coagulation cascade is activated - causing vesicular coagulation
36
What determines lipid A toxicity
How many fatty acid chains there are in it (E.coli has 6xC14 chains and has high toxicity whereas H.pylori has 4xC16-18 chains and has low toxicity)
37
Lipopolysaccharide structure
Polysaccharide:
O-antigen - sticks out of the cell and consists of around 40 repeating units
Outer core
Inner core
Lipid:
Lipid A - a variable number of fatty acid tails
38
How can bacteria use endotoxins in an exotoxic way?
Vesicles containing endotoxins can 'blob' off and move around and cause damage elsewhere
This explains why antibiotic treatment can lead to toxic shock as the dying bacterial cells can release lipid A in abundance
39
Endotoxin vs exotoxin
Endotoxin - all use lipid A and have similar effects (toxic shock)
Exotoxins - varied types of toxins and have vastly different effects
40
Viruses
Intracellular parasites causing a variety of diseases
Only treatable by vaccination or a few licensed antiviral drugs
41
Types of virus
DNA viruses:
Herpes, Adeno, Pox, Popova
RNA viruses:
Retro, Orthomyxo, Rhedo, Paramyxo, Toga etc
Viruses can either be helical or icosahedral and can either be naked or membrane-bound
42
Viral transmission
Inhalation - respiratory tract (the most common method)
Ingestion - GI tract (mostly naked viruses)
Inoculation - often Iatrogenic (unintentional)
Congenital - Mother to foetus (ie Rubella)
43
Viral diagnosis
Aetiological (cause of disease) diagnosis:
Whole virus
Viral antigen - immunological tests
Viral nucleic acid - PCR
Specific antibody response - IgM/IgG
44
Common viruses: Picornavirus
Enterovirus - CNS issues
Hepatovirus - Hepatitis A
Rhinovirus - common colds
Aphthovirus - Foot and Mouth in cattle
45
Poliovirus - Enterovirus: how is it spread, how long is incubation, what are the symptoms, and what are the treatments?
Spread by the faecal-oral route
Incubate for 1-2 weeks
Fever, malaise, sore throat, vomiting, constipation, 5% suffer from flaccid paralysis, and 1% suffer permanent paralysis and maybe death
Vaccination
46
Poliovirus - Rhinovirus: how is it spread, how long is incubation, what are the symptoms, and what are the treatments?
Spread by the respiratory route
Incubate for 2-4 days
Headache, sneezing, sore throat, and cough
Too difficult to isolate since it has very generic symptoms
47
Influenza viruses - Orthomyxovirus: how is it spread, how long is incubation, what are the symptoms, what are the notable features, and what are the treatments?
Spread by the respiratory route
Incubate for 1-4 days
Fever, chills, aching, anorexia, etc lasting 3-7 days (recovery in 2 weeks). Secondary pneumonia can kill the elderly/very young
* Most deaths occur when there are other risky conditions
* There are three main types, type A causes the most world epidemics
?
48
How many influenza antigens are there and which ones affect which species
16 Haemaglutinin and 9 Neuraminidase antigens
Humans affected by H1/H2/H3 and N1/N2/N3
Avians are affected by all H16 and N9 antigens
49
Why do influenza viruses mutate so frequently?
They are RNA viruses whgich mean they have no proofreading mechanics so, if a mutation occurs, it's likely that it is not fixed
50
Antiviral drugs for influenza
Tamiflu and relenza
Block viral exit from cells
51
Coronavirus
Respiratory route
Asymptomatic to life-threatening fevers and malaise
52
Viral vaccinations
After discovering how the virus operates when binding to and replicating in a cell, vaccinations aim to counteract these processes
53
Herpesviridae: how many types are there and how long does it take to lose these viruses
Contain 3 sub families with 120 viruses
These viruses establish lifelong latent infections which can reactivate and cause subsequent rounds of disease
54
Alphaherpesviruses: what are they, how similar are HSV1 and HSV2, how many people suffer from the virus, and what are its interesting features?
One subfamily of the herpes virus
Herpes simplex virus (HSV) type 1 and type 2 have 90% similarity
40-80% of the population have the virus
* Establish latency in host after primary infection by travelling up sensory nerves to the dorsal root ganglion
* Reactivation not fully understood (stress? Sunlight?)
* Icosahedral symmetry
* Contain ds DNA
55
HSV1: what is it and is there treatment?
Primary infection is often in childhoof and may result in gingivostomatitis
Acyclovir - blocks viral DNA synthesis (making HSV1 easy to treat)
56
Varicella zoster virus: what is one example, how long is its incubation, and how lethal is it?
Chickenpox
10-21 day incubation
Often easy to tolerate during primary infection unless immunocompromised but can reactivate in the 40s-50s where it is rather dangerous
57
Paramyxoviruses: what are some example, how long are their incubations, how are they spread, how lethal are they, and do they have treatment?
Measles/Mumps
9-12 days / 16-18 days
Virus is spread before rash appears / virus spread through the respiratory route
Can cause Encephalomyelitis, Pneumonia, SSPE etc and has a 10% mortality rate / Orchitis, Parotits, Meningitis, Pancreatitis, Encephalitis (rarely)
MMR vaccination
58
Togaviridae: what is one example, how is it spread, how lethal is it, and are there any treatments for it?
Rubella
Can cross placenta in early pregnancy
Mild as a child but congenital Rubella can cause hearing loss, retardation and other serious issues
MMR virus
59
MMR vaccine: what does it do?
Measles, Mumps, and Rubella containing a mixture of live attenuated viruses administered via injection which aims to be more efficient and less traumatic than being infected three separate times
60
Vaccine skeptism
Andrew Wakefield - vaccines lead to autism, causing vaccine administration to be reduced
61
Papilloma virus: where do they replicate, what are the symptoms, and is there treatment?
Replicate in squamos epithelium
Warts, some are oncogenic, may cause cervical cancer (4th most common cancer in womans)
Vaccine available
62
Zoonoses
Viruses crossing the species barrier
63
Major causes of crop loss since the start of the 21st century
Insect pests - 16%
Microbial infections - 18%
Weeds - 34%
64
What three conditions need to be fulfilled for disease to affect plants?
Susceptible host, favourable environment, and a pathogen
65
The economic cost of disease: Irish potato famine
Irish peasants relied heavily on one vairiety of potato
Phytophthera infestans (late blight fungus) infected potatoes and caused ~75% of potato crops to be lost, causing mass starvation, mass emigration, and the loss of 1/8 of the population
66
Disease process in plants
* The pathogens must recognize the host
* Penetrate host barriers
* Suppress host defence systems
* Move (invasion) through host tissues (phloem)
* Utilize host components (nutrition) for growth and reproduction
67
What do viruses produce for the infection
Enzymes - break down defence systems, penetrate the plant structures, movement, breakdown of macromolecules, and impair plant cell function
Toxins - interfere with plant cell functions and kill cells
Growth regulatory factors - make the plant grow in a way to benefit the pathogen
68
How are viral diseases spread to plants and what symptoms are there?
Vector (an organism that carries and transmits a disease) needed to transmit infection from plant to plant
Most transmitted through insects but also spread through grafting
Symptoms include leaf spotting, chlorosis, stunted growth, ring spots, flower break, vein clearing and, although death is not common, crop yields are reduced
69
CTV: what is it, how virulent is it, how is it transmitted, what are the symptoms, and what are some interesting facts?
Citrus tristeza (misery) virus is a + sense ssRNA virus; flexuous rod, helical symmetry; genome size 9.2kb
Number of strains of varied virulence
Transmitted by the brown citrus aphid and spreads through phloem
Symptoms: clear veins which turn corky include chlorosis followed by cupping of the leaf. and die back, severe outbreaks can kill trees, and 80 million trees have been killed since 1910
* Causes decline in growth and lower yields
* Severity affected by environmental conditions
70
TMV: what is it, how does it move through the plant, what are the symptoms, and what are the consequences ?
Tobacco mosaic virus is a + ssRNA virus with helical symmetry
Moves through phloem and from cell to cell
Symptoms: chlorosis -mosaic-like mottling on leaves; rugosity
Consequences: stunted growth of plant, lower crop yield, rarely causes death
71
Soft rots on vegetables caused by?
Erwinia carotovora.
Virulence factors: pectinases; proteases; cellulases degrade plant cell walls
72
Wilts: what are they and what causes them?
Clogs vascular tissue
e.g. Pierce’s disease of grapes caused by Xylella fastidiosa.
73
Blights: what are they and what causes them?
Rapid destruction of plant tissue.
e.g. Fire Blight of apples and pears caused by Erwinia amylovor
74
Cankers (sores): what are they and what causes them?
Infections where an open wound has been infected
e.g. Xanthomonas citri which causes Citrus canker
75
Plant tumours: what are they and what causes them?
Proliferated growth in certain parts of plants
e.g. Agrobacterium tumifaciens which causes Crown gall tumours.
76
Crown gall: what is it, how does it enter the plant, what does it do, and what species are affected by it?
A condition where plants have galls grow in certain parts of the plant
Enters the plant the plant through wounds in roots or stems amdtransfers and integrates part of its own DNA, the T-DNA, into the plant genome
Upregulates plant hormones auxin and cytokinin production which causes crown gall formation at junction between root and shoot which weaken and stunt the growth of the plant, and can usually cause total plant deat
a serious pathogen of walnuts, grape vines, stone fruits, nut trees, sugar beets, horse radish, and rhubarb.
77
Bacterial diseases of insects - Bacillus thuringiensis: what is it, when was it discovered, and what does it do?
A Gram +ve rod pathogen that is used as pest control
First discovered in 1911 as a pathogen of flour moths
Produces the botulinum toxin (Bt toxin) as it multiplies in the insect lymph
78
BT toxin: why is it safe to use and how does it affect insects?
Bt protein is highly insoluble in normal conditions (crystals), therefore harmless to humans and animals. It is highly insect specific as only activated by conditions in the insect gut.
Bacteria invades the haemocoel (body cavity), and is solubilised in reducing conditions of high pH (above 9.5) found in the mid-gut of lepidopteran larvae where it forms pores in the gut wall, paralysing the digestive tract - Insect stops eating and starves
79
Genetically-engineered crops
BT toxin expressed naturally in plants so the plants have increased insect resistance
80
entomopathogens: what are they and what do they do?
Entomophthorales - Fungal diseases of insects which can invade and kill a range of insect hosts
* Are often host-specific but can kill related insects
* Release spores applied as a biopesticide which spray germinate, invade and kill insects
81
Fungi as biopesticides
Metarhizium sp used in commercial cockroach bait stations as a (Greenguard approved) biopesticide against locusts, weevils and grasshoppers.
Beauvaria bassiana spores are used in commercial insecticides and are sprayed on plant foliage to protect against thrips, mealy bugs, weevils, and white fly aphids etc
82
Nematods-trapping fungi
Carnivorous fungi which can trap things when nitrogen levels are low
Can be an issue when attacking plants/parasitizing livestock so control is necessary
83
Tulip breaking virus: what is it and how does it work?
The virus infects the bulb and causes the cultivar to "break" its lock on a single color, resulting in intricate bars, stripes, streaks, featherings or flame-like effects of different colors on the petals. The color variegation is caused either by local fading, or intensification and overaccumulation of pigments in the vacuoles of the upper epidermal layer due to the irregular distribution of anthocyanin; this fluctuation in pigmentation occurs after the normal flower color has developed. Because each outer surface is affected, both sides of the petal often display different patterns.
As early as 1637 Dutch growers were able to produce new broken varieties through bulb grafting, by combining "broken" bulbs infected with the virus with healthy bulbs that produced uniformly colored flowers
