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Microbiology & Immunology > Global Influences of Microbes > Flashcards

Global Influences of Microbes Flashcards

1
Q

What are the main protagonists of climate change?

A

CO2, methane and N2O

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2
Q

Which organisms can fix carbon?

A
  • Photoautotrophs (e.g. Cyanobacteria)
  • Lithoautotrophs
  • Facultative anaerobic purple bacteria
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3
Q

What do photoautotrophs do?

A

Use energy from sunlight to convert CO2 and water into organic materials to be used in cellular functions such as biosynthesis and respiration

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4
Q

Bind and convert Co2 into biomass

A
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5
Q

What are the 2 parts to Co2 fixation by photoautrotrophs?

A
  1. Generation of energy
  2. Assimilation of Co2 through the Calvin cycle
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6
Q

How does cyanobacteria generate energy for part 1 of Co2 fixation?

A

Through the light dependent reaction

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7
Q

Describe the light dependent reaction

A
  • Uses light energy to make energy storage molecule ATP and the reduced electron carrier NADPH
  • Takes place in the thylakoid membranes of organelles (chloroplasts)
  • Light is absorbed by pigments in PSII and passed between pigments to the reaction center
  • Energy is transferred to P680, boosting an electron to a high energy level
  • The high energy electron is passed to an acceptor molecule and replaced with an electron from water
  • The splitting of water releases O2
  • The high energy electron travels down an ETC, losing energy
  • Some released energy drives the pumping of H+ ions from the stroma into the thylakoid interior, building a gradient
  • As H+ ions flow down their gradient into the stroma, they pass through ATP synthase, driving ATP production (this is known as chemiosmosis)
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8
Q

Describe the light independent (dark) reaction

A
  • The electron from PSII arrives at PSI and joins the P700 special pair of chlorophylls in the reaction center
  • Light energy absorbed by the pigments and passed into the reaction center boosts the electron in P700 to a very high energy level and it is transferred to an acceptor molecule
  • The special pair’s missing electron is replaced by a new electron from PSII
  • The high energy electron travels down a short second leg of the ETC where it is passed to NADP+ to make NADPH
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9
Q

What are some impacts of climate change on oceans?

A
  • influences composition, location and existence of carbon fixing microbes
  • increased temperatures affects water salinity (ice cap melting) and wind
  • may increase/decrease phytoplankton growth
  • increase in surface runoff of nutrients (can lead to cyanobacterial blooms)
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10
Q

What are cyanobacterial blooms?

A

Huge mat-like structures of organisms

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11
Q

What are the 2 major consequences of cyanobacterial blooms?

A
  1. Biochemical O2 debt
  2. creation of anoxic regions
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12
Q

What is biochemical O2 debt?

A

A decrease in O2 in the water due to microbial proliferation

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13
Q

How are anoxic regions created?

A
  • organisms sink to the floor when they die and are degraded by bacteria
  • decaying plankton consume O2
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14
Q

How does facultative anaerobic purple bacteria fix CO2?

A

Using the Calvin cycle

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15
Q

How do Lithoautotrophs fix carbon?

A

Mostly under anaerobic conditions, generating their energy through the use of compounds (eg. hydrogen sulphide)

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16
Q

True or False, both lithoautotrophs and facultative anaerobic purple bacteria use RuBisCo

A

True

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17
Q

Describe the process of carbon cycling

A
  1. Primary fixers are consumed by grazers and decomposers
  2. Grazers are consumed by predators which are then consumed by higher predators
  3. Decomposers consume predators and higher predators
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18
Q

Describe the role of the ocean as a carbon sink

A
  • Co2 is absorbed by phytoplankton which sink to the ocean floor when they die
  • These are not degraded fully as O2 is scarce
  • This carbon has been compressed over millions of years => FOSSIL FUELS
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19
Q

What are some ways carbon is released into the environment?

A
  • Fossil fuels
  • Respiration
  • Methanogenesis
  • Melting ice caps releases undecomposed organisms which then release carbon upon decomposition
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20
Q

What are methanogens?

A

They are obligate anaerobes and chemoautotrophs

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21
Q

How are methanogens chemoautotrophs?

A

They use H2 as a terminal electron acceptor during anaerobic respiration
(Generate energy by reducing Co2 to methane)

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22
Q

Where do methanogens live?

A

In anoxic environments such as swamps and marshes, and the guts of most mammals

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23
Q

What is the role of termites in relation to methanogens?

A
  • Their gut contains a protist called Mixtricha paradoxa which degrades lignin to form acetate and organic acids
  • ## The Co2 and H2 produced using fermentation are consumed by methanogens to make methane
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24
Q

How can microbes be used as biofuels?

A
  • A by-product of microbial fermentation is the production of alcohol
  • Co2 is still produced but is carbon neutral (carbon fixed by plants = carbon used as fuel)
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25
Q

Advantages of bioethanol production

A
  • Renewable energy source
  • Carbon neutral
  • Can be used alone or mixed with other liquid fuels
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26
Q

Disadvantages of bioethanol production

A
  • Uses land to grow fuel crops that could have been used to feed people
  • Production requires energy input
  • Bioethanol can be damaging in non-compatible fuel systems
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27
Q

Rank the following feedstocks for ethanol production in order of easiest, harder, and hardest:

Sugar crops, Lignocellulosic material, Starch crops

A

Easiest = sugar crops
Harder = Starch crops
Hardest = Lignocellulosic material

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28
Q

Name the 4 diseases of cattle

A
  • Bovine Tuberculosis (TB)
  • Nagana
  • Rinderpest
  • Ringworm
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29
Q

What was the economic impact of Foot and Mouth disease?

A
  • 6 million animals culled
  • consequences to tourism, transport
  • loss of £8 billion to economy
  • Changes in food security practices
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30
Q

What are the symptoms of TB in cattle?

A
  • Infected lymph nodes in head
  • tubercles in the chest cavity and lungs
  • weakness
  • coughing
  • weight loss
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31
Q

How is a mycobacterium killed by the immune system?

A
  • Is phagocytosed into a phagosome (vacuole)
  • The phagosome fuses with the lysosome
  • Need activated macrophages to kill mycobacteria (activate by immune molecules to change the phenotype)
  • T cell response produces cytokines which activate macrophages and eliminate bacteria
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32
Q

How does mycobacterium evade the immune system?

A
  • They secrete protein and lipid factors that block phagosome maturation and prevent phagolysosome fusion
  • Mycobacteria are resistant to acidification and reactive oxygen species
  • Inhibits apoptosis and autophagy
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33
Q

How does TB evade the immune system long term?

A

Infected macrophages are phagocytosed by other macrophages and accumulate, forming lesions. This continues until death.

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34
Q

How is TB spread?

A
  • Many potential reservoirs exist: deer, fox, rodents
  • Badgers thought to transmit directly to cows
  • Difficult to monitor and control spread from wildlife to cattle
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35
Q

Which strain of TB is used to vaccinate humans?

A

The Bacillus Calmette-Guerin (BCG) strain

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36
Q

What TB vaccines are available to cattle?

A

Vaccines are not successful in cattle, however injectable badger BCG vaccine has been working well so far in badgers

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37
Q

Which animals are affected by African animal trypanosomes (Trypanosomiasis)?

A

Cattle and other livestock

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38
Q

What are the symptoms of Trypanosomiasis in cattle?

A
  • Swelling
  • Fever
  • Reduced milk production
  • Fertility issues
  • Weight loss
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39
Q

Which trypanosomes are responsible for Trypanosomiasis?

A
  • T. congolense
  • T. vivax
  • T. brucei spp.
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40
Q

How do trypanosomes evade the immune response?

A

Antigenic variation

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41
Q

How does antigenic variation allow immune evasion of trypanosomes?

A
  • Variant surface glycoprotein (VSG) switching alloes trypanosomes to change their coat protein, making it difficult to find one vaccine that will recognise all.
  • Trypanosomes first induce an immune response and then change their antigen coat to prevent clearing
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42
Q

How is Trypanosomiasis treated?

A

Using drugs like diminazene aceturate, homidium bromide/chloride, isometamidium chloride

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43
Q

What are some measures used to prevent Trypanosomiasis?

A
  • Breed trypanotolerant cattle
  • Control vectors: remove fly using traps, bush clearing and insecticide
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44
Q

What is Rinderpest?

A

An acute, highly contagious viral disease of cattle, water buffalo and other wildlife

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45
Q

What virus is responsible for Rinderpest?

A

Morbillivirus

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46
Q

How is Rinderpest spread?

A

Through close contact - breath, secretions, excretions

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47
Q

What are some symptoms of Rinderpest?

A

Fever, diarrhoea, oral lesions

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48
Q

What is the long lasting effects of infection with Rinderpest?

A

Infected individuals develop a long lasting specific immune response to morbilliviruses:

  • Reduced B cells, monocytes, neutrophils and some T cell types
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49
Q

Is Rinderpest eradicated?

A

Yes

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50
Q

What is ringworm?

A

It is a fungal infection of hair and keratinised layers of the skin (also known as dermatophytosis) (is a cattle infection)

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51
Q

Can zoonosis occur in ringworm from cattle to humans?

A

Yes, theough direct contact/bites

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52
Q

What is the name of the Ringworm fungi?

A

Trichophyton verrucosum

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53
Q

How do you treat ringworm?

A

Vaccines are available

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54
Q

What is the Foot and Mouth disease virus?

A

A picornavirus of cloven hoofed livestock (pigs, cows, sheep, goats)

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55
Q

How many serotypes of Foot and Mouth disease are there?

A

7, with serotype O responsible for 70% of global outbreaks

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56
Q

Describe how Foot and Mouth disease virus enters the cell

A
  • The virus capsid protects the RNA genome while outside of the host cel and also allows entry into cells by binding to specific receptors
  • RNA genome is then released into the cytoplasm of the cell
  • Translation occurs to produce viral proteins, including non-structural proteins
  • +ve sense RNA are packaged by capsid proteins to generate new virus particles
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57
Q

What are the symptoms of Foot and Mouth disease in cows?

A
  • High fever
  • loss of appetite and increased salivation
  • depression
  • drop in milk yield
  • temporary immunosuppression
58
Q

What are the long term effects of Foot and Mouth disease in cows?

A

Reduced milk production and lameness

59
Q

Where is the primary site of infection and replication of FMDV?

A

In the mucosa of the pharynx

60
Q

Describe the pathogenesis of FMDV in cows

A
  • Virus can enter through skin lesions or GI tract
  • Is then distributed throught lymphatic system
  • Virus replicates in the epithelium of the mouth, muzzle, teats, feet, and areas of damaged skin
  • Vesicles develop and rupture within 48 hours
  • Animals that have been infected and recovered and those who have been vaccinated can become carriers
61
Q

How is FMDV transmitted?

A
  • Direct contact with infected animals
  • Indirect contact with secretions or excretions from infected animals
  • Mechanical vectors (people, horses, dogs, cats, birds, vehicles)
  • Air movement over land or water
62
Q

What makes FMDV so easily spread?

A

The virus is shed into milk in cows before clinical signs develop which means it can spread easily from farm to farm and cow to calf

63
Q

Name 3 diagnostic tests used for FMDV?

A
  • ELISA
  • qPCR
  • sequencing
64
Q

Is there a vaccine for FMDV?

A

Yes, but immunity is short-lived

65
Q

Name 4 challenges faced in vaccination against FMDV

A
  • Existing vaccines are live, chemically attenuated so production is risky and costly
  • There are 7 seeotypes, each with many variants due to a high mutation rate so it is challenging to produce a universal vaccine
  • Intact virus is fragile and so costly to store and distribute
  • Subunit vaccines are in development
66
Q

What is Feline Immunodeficiency Virus (FIV)?

A
  • Infection of T helper cells and thus impairs the immune system
  • Is the cat equivalent of HIV so is a good model for HIV studies
67
Q

What is a vaccine used against FIV?

A

Fel-O-vax, a chemical inactivated whole virus

68
Q

What is Feline Leukaemia Virus (FeLV)?

A

Causes immunosuppression/deficiency, anaemia and lymphoma in cats

69
Q

How is FeLV transmitted?

A

Through saliva, bites and licks

70
Q

What are some symptoms of FeLV in cats?

A
  • Loss of appetite
  • Enlarged lymph nodes
  • Persistent fever
  • Pale gums
  • Secondary infections
  • Persistent diarrhoea
  • Abortion
  • inflammation of the gums
71
Q

What are some treatments of FeLV?

A
  • Vaccines (but not 100% effective)
  • Treat secondary infections
  • Keep cats indoors
72
Q

How do you diagnose FeLV?

A
  • ELISA
  • PCR
  • Virus culture
73
Q

Why are diseases transmitted more easily in birds?

A

Because they travel much greater distances

74
Q

What are the subtypes of avian influenza based off of?

A

Different combinations of haemagglutinin (H) and neuraminidase (N)

75
Q

What is the role of haemagglutinin in avian influenza?

A

It recognises and binds to the host

76
Q

What is the role of neuraminidase in avian influenza?

A

Release of new viral particles

77
Q

Name some natural carriers of avian influenza that are resistant to severe infection

A

Wild migratory birds such as ducks, geese, gulls and shorebirds

78
Q

How does direct infection occur?

A

Through exposure to saliva, mucus or faeces from infected birds

79
Q

What are the two types of Avian influenza A viruses?

A
  • Low pathogenicity avian influenza (LPAI) A viruses
  • High pathogenicity avian influenza (HPAI) A viruses
80
Q

What is the difference between LPAI and HPAI in terms of amino acids at the cleavage site?

A

LPAI do not contain a series of basic amino acids at the cleavage sites, whereas HPAI have multiple basic amino acids

81
Q

What are some symptoms of avian influenza?

A
  • Swollen head
  • Closed, excessively watery eyes
  • Lethargy, depression
  • Loss of balance/tremors
  • Drooping wings
  • Twisting of head and neck
  • Reduced egg production
  • Respiratory distress
  • Fever
  • Loss of appetite
82
Q

How is avian influenza diagnosed?

A

Based on history, clinical signs and post mortem analysis

83
Q

How do you treat avian influenza?

A

There are no readily available treatments and it is difficult to treat all chickens due to vast number

84
Q

What is trichomonosis?

A

A bird disease caused by the protozoan parasite Trichomonas gallinae

85
Q

What are the signs of trichomonosis in birds?

A

Yellow deposits and lesions in the oral cavity which leads to malnutrition (can’t eat properly) and then death

86
Q

How is trichomonosis spread?

A

Via unwashed bird feeders

87
Q

How do you prevent trichomonosis spreading?

A

Allow bird feeders to dry out

88
Q

What is eimeria?

A

A parasitic infection that causes coccidosis in poultry and goats

89
Q

How is eimeria transmitted?

A

Via the faecal-oral route

  • is ingested, proliferates in the gut and is pooped out
  • can be introduced through farmer’s boots or new infected stock
90
Q

What is the pathology of coccidosis?

A
  • Replicates in intestinal epithelial cells
  • Causes tissue damage, bloody diarrhoea, malabsorption of nutrients and death
91
Q

What are some treatments of coccidosis?

A
  • Chemotherapy
  • Live-attenuated vaccine
  • Housing of chickens that is not too warm, humid or crowded and ensure litter is cleared
92
Q

Name 7 viruses that cause cancer in humans

A
  • Epstein-Barr virus (EBV)
  • Hepatitis B virus (HBV)
  • Hepatitis C virus (HCV)
  • Human papillomavirus (HPV)
  • Kaposi’s sarcoma herpesvirus (KSHV)
  • Human T-lymphotrophic virus-1 (HTLV-1)
  • Merkel cell polyomavirus (MCV)
93
Q

What are some examples of cancer that EBV causes?

A

Burkitt’s lymphoma, some Hodgkin’s lymphoma, post-transplant lymphoma, and nasopharyngeal carcinoma

94
Q

What type of cancer does HBV and HCV cause?

A

Liver cancer

95
Q

Is there a vaccine available for HBV?

A

Yes

96
Q

Is there a vaccine available for HCV?

A

No

97
Q

Out of HBV and HCV, which is more prevalent?

A

HBV

98
Q

What type of cancer does HPV cause, and is there a vaccine available?

A

Cervical cancer and yes

99
Q

What are 2 examples of cancers that KSHV causes?

A

Kaposi’s sarcoma and primary effusion lymphoma

100
Q

Is there a vaccine against KSHV?

A

No

101
Q

What cancer does HTLV-1 cause and is there a vaccine available?

A

Adult T-cell leukaemia and no vaccine

102
Q

What cancer does MCV cause and is there a vaccine available?

A

Merkel cell carcinoma and no vaccine

103
Q

Name 3 characteristics of a tumour causing virus

A
  1. Persists in the host for a long time
  2. Long interval before tumour development
  3. Different mechanisms - direct or indirect
104
Q

Name 3 viruses that have direct mechanisms of causing cancer

A
  • Retrovirus
  • KSHV
  • HPV
105
Q

Name 4 viruses that have indirect mechanisms of causing cancer (i.e. a side effect of infection)

A
  • Retrovirus
  • HCV
  • HBV
  • HIV-1
106
Q

What are the 2 hypotheses that hypothesise why a virus would interfere with cell regulation?

A

The limited resource hypothesis and the anti-antivirus hypothesis

107
Q

What is the limited resource hypothesis in cancer-causing viruses?

A

Where a virus infecting a cell to make a new virus uses a lot of amino acids and makes the cell utilise all of its resources into making new viral particles

108
Q

What is the anti-antivirus hypothesis in cancer-causing viruses?

A

Where the virus combats the cell’s anti-viral response (which is to go into senescence and die) to prevent the cell from dying

109
Q

How does KSHV target cell growth pathways?

A
  • Produces virus interleukin (makes new immune cells so virus can infect more cells)
  • Sends signals for cells to constantly grow
  • ## It controls apoptosis signals to keep the cell alive for production of more virus
110
Q

What is p53 and what does it do?

A

It is a major anticancer that causes cells to go into apoptosis

111
Q

How many types of HPV as cancer-causing?

A

There are 14 high-risk types

112
Q

Which 2 HPV types cause 70% of cervical cancer and precancerous cervical lesions?

A

Types 16 and 18

113
Q

Which levels are new viral HPV particles produced in the cervical epithelium?

A

L1 and L2

114
Q

Which 2 E layers does differentiation occur in?

A

E2 to E1 layers

115
Q

What are E6 and E7 and what do they do?

A

They are proteins of the HPV virus that interact with p53. E7 promotes cell proliferation E6 inhibits cell apoptosis

116
Q

What happens when the HPV virus becomes integrated into the genome?

A

The E2 protein that normally controls E6 and E7 becomes disrupted and leads to aggressive tumours due to the now uncontrolled proliferation

117
Q

How does cervical screening work in the UK?

A
  • Sample cells from the cervix surface to look for signs of the basal layer at the top of epithelial cells
  • If HPV is detected, the sample is checked under a microscope to look for abnormal cells
  • If abnormal cells are detected then the patient is referred for a coloscopy
118
Q

Which HPV types are the major causes of genital warts?

A

HPV 6 and 11

119
Q

Which types if HPV does gardasil 9 protect against?

A

Types 6, 11, 16, 31, 33, 45, 52, and 58

120
Q

How good is the HPV gardasil 9 vaccine?

A

Very good if given before the age of 17

121
Q

What are 3 mechanisms that retroviruses use to create cancer?

A

Transducing, cis-activating, and trans-activating

122
Q

What do transducing retroviruses have in their gene transcript?

A

A viral oncogene (v-onc) and sometime v-src

123
Q

Name 3 things that cis-acting retroviruses do

A
  1. Activate cellular oncogenes
  2. Make RNA from DNA
  3. Target regions of the genome that have roles in active transcription
124
Q

Give 2 examples of cis-acting retroviruses

A

Avian leukosis virus and mouse mammary tumour virus

125
Q

What occurs during viral insertional mutagenesis of cis-acting retroviruses?

A

Promoters and enhancers are inserted, which increases the amount of protein transcribed

126
Q

What viral protein does trans-acting retroviruses contain?

A

Tax

127
Q

What is Tax?

A

It is a transcriptional activator of LTR and a viral protein

128
Q

What does Tax do to cause cancer?

A
  • Regulates transcription of specific cellular genes
  • Used by virus to turn on virus producer and own gene to drive growth
  • Accidentally activates proliferator genes (e.g. rof-regulators in white blood cells)
129
Q

Is HIV-1 an oncogenic virus?

A

No, it does not directly cause cancer itself

130
Q

How does HIV-1 cause cancer?

A

It is an immunosuppressive disease which means that cancer cannot be eliminated by the immune system

131
Q

What type of virus is HBV?

A

A DNA virus (double and single-stranded)

132
Q

What is HBV?

A

It is a viral infection that attacks the liver and causes acute and chronic disease

133
Q

What factor influences an individual’s ability to clear HBV?

A

Age - young children have a weak immune system whereas >95% of adults clear infection

134
Q

What conditions can develop in adults who are chronically infected with HBV?

A

Cirrhosis and/or liver cancer

135
Q

What type of virus is HCV?

A

A cytoplasmic RNA virus

136
Q

What is HCV?

A

A viral infection that attacks the liver can cause chronic or acute hepatitis

137
Q

What is there a risk of within 20 years of HCV infection?

A

Cirrhosis

138
Q

What can chronic HCV infection cause?

A

Hepatocellular carcinoma

139
Q

How does HBV and HCV cause hepatocellular carcinoma?

A
  • They drive the liver to a stage where cells are constantly dying and others are replicating to replace them
  • Dysregulation of the mitochondria produces ROS free radicals
  • The subsequent genome instability causes the cancer
140
Q

Why does it take so long for cancer to develop in HBV and HCV?

A

Because the cells are constantly dying and being renewed

141
Q

What vaccine is available for HBV?

A

The HBsAg vaccine

142
Q

What long term therapy is available for HBV?

A

HBV antiviral drugs - reduces but does not eliminate risk of cancer

Microbiology & Immunology (5 decks)

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