6 - One Health Flashcards

1
Q

What is One Health?

A

It is an integrated, unifying approach that aims to sustainably balance and optimise the health of people, animals and ecosystem

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2
Q

What kind of approaches and concepts do we have for One Health?

A

Concepts should be system dynamic (connectiveness between aspects) and the approaches should be ecological, despite anthropogenic drivers.

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3
Q

What is the scope of One Health?

A

One Health covers emerging zoonoses, food security/systems, international health/development, antimicrobial resistance, human-animal bond and more.

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4
Q

What are SDGs and how does One Health aid them?

A

SDGs are sustainable development goals which aim to improve food security, poverty alleviation, climate change, social justice, peace, environmental protection and health. One Health provides framework for achieving benefits which span many SDGs.

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5
Q

Describe the issue of underconsumption.

A

Childhood stunting rates are at high levels due to low consumption of animal-sourced foods - usually aids growth, cognitive performance, motor development and increased activity in children.

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6
Q

Describe reliance and issue with livestock.

A

Livestock is heavily relied on for food security and livelihoods, also aids crop production (manure, traction), and provides financial stability.
The issue with livestock is disease, which impacts income, and can cause malnutrition, zoonotic diseases, decreased education (SDG - break cycle) etc. Another issue is that livestock die during drought season and so people seek other forms of income/food like crops.
e.g. foot and mouth disease.

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7
Q

Describe the issue and main driver of zoonotic diseases and give an example of where we saw this.

A

Zoonotic diseases are hard to manage and diagnose due to prevalent symptoms. Land-use change like deforestation and irrigation is the major driver of zoonosis spillover - causing an increased zoonotic risk. It effects reservoir host distributions, pathogen prevalence and spread.
Example: Nipah virus was due to spillover from fruit bats to pigs - proximity of pig farm to mango plantation meant the bodily fluids secreted from bats when feeding contaminated the environment, and the virus then emerged in pigs.

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8
Q

What is spillover?

A

The transmission of a pathogen between animal species.

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9
Q

Describe the issue of endemic diseases.

A

Endemic diseases are most often found in poor and disadvantaged areas due to lack of resources and access to treatment/prevention. There is a cycle of neglect that occurs where there is a a lack of disease burden data, we face diagnostic challenges and then this affects these communities.

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10
Q

Describe the issues of febrile illnesses.

A

Febrile illnesses present with flu-like symptoms and are very common in children from low to middle income countries. These symptoms are an issue as so many diseases present with them, so tend to be misdiagnosed - often as Malaria.

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11
Q

What are the two ways we could tackle many One Health issues?

A
  1. Target animals for protection of people
  2. Lower/get rid of immunisation prices.
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12
Q

Describe what vaccinating animals would do.

A

This available intervention would treat the disease at the source (reservoir) and provides a broader safety net. It would reduce disease burden on both parties and is necessary for elimination of infections with these animal reservoirs - not confined to humans.

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13
Q

Describe one example of animal vaccination.

A

Rabies Management
Post-exposure prophylaxis (PEP) is given after a bite, and mass dog vaccination is done to prevent reservoir transmission. It has the highest disease case fatality, but PEP is expensive and so there are inequalities; Those most prone do not receive vaccination.
Rabies rates are lower in areas with high vaccination rates of both dogs and humans (PEP) - most cost effective and sustainable, causing the fewest deaths.
More funds should be allocated to dog vaccination.

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14
Q

What is MCF and the effects of livestock vaccination?

A

Malignant Catarrhal Fever is a wildebeest virus which spreads to cattle in the calving season due to spread via reproductive tissue (picked up from grazing). There are no vaccines available so pastoralists must move cattle from high-grazing land to avoid this season, meaning households gain less protein, cannot consume or sell milk, and it also causes rebuilding of cattle’s body conditions.
There is a potential vaccine which would provide partial protection, and focus groups of pastoralists were made. This would improve pasture quality, food security and reduce land conflict, but could increase predation, degrade land, increase human-wildlife conflict and affect wildebeest migration.

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15
Q

What is the effects of immunisation prices?

A

Childhood immunisation for polio is free, but not for rabies, and there are charging fees for animal interventions. These are not government funded and so aids the spread of rabies due to inaccessability.

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16
Q

What are the opportunities of One Health?

A
  • Recognises need for integrated and ecological approaches
  • Funding available
  • There is expertise for One Health
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17
Q

What are the challenges of One Health?

A
  • Very generalist, multidisciplinary approach so issues surrounding trust and control.
  • Community engagement
  • Challenges in funding for implementation of preventative measures.
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18
Q

What is a vaccine?

A

A vaccine gives a boost to the immune system to induce an antibody response which protects against an infection. It is a small harmless dose of the disease which initiates the response, meaning we have the necessary antibodies if we encounter the disease again.

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19
Q

What is the difference between prophylactic and therapeutic vaccines?

A

PROphylactic - given to healthy individuals to develop immunity.
Therapeutic - given to those previously infected and accelerates their immunity, training the immune system.

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20
Q

What is herd immunity and why is it important?

A

Herd immunity is when a large proportion of the population is vaccinated and so it is harder for infectious disease to spread.
It is important as it provides protection to communities, breaks chain of transmission and prevents unnecessary deaths. It is vital those who can get vaccinated do to ensure herd immunity as those immunocompromised and of age limitations cannot. The effort required is dependent on the R0 value - how many should be vaccinated.

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21
Q

What is the R0 number?

A

The R0 is the reproduction rate/number/ratio. It is an epidemiologic metric which describes the contagiousness and transmissibility of an infectious agent using estimations from mathematical models. It helps us see how many individuals must be vaccinated, whether we need any boosters and its efficacy.
R0 > 1 - outbreak continues
R0 <1 - ends.

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22
Q

What are the 5 contents of a vaccine?

A
  1. Water (bulk)
  2. Active ingredient (small harmless dose of disease)
  3. Adjuvant (extra boost if active isn’t sufficient to generate antibodies e.g. Aluminium)
  4. Preservatives/stabilisers (prevents contamination, prolongs shelf life, maintains quality)
  5. Residual traces (something used to make vaccine (egg))
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23
Q

What is the R0 value in terms of spread of infection?

A

It describes the average number of secondary infections caused by a single host in a completely susceptible population.
R0 = 2, every 1 infects 2, maintaining chain of infection.
R0 = 1, not exponential spread but sufficient to persist, every infection replaces itself (1=1).
R0 < 1, outbreak will end and pathogen will go extinct.

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24
Q

How are vaccinations carried out in the UK, give an example.

A

The UK uses strict routine immunisations which gives an order and age to when you should receive each vital vaccine for it to be effective.
e.g. MenACWY - four strains of meningitis (~12 years - before sexual activity)
MMR vaccine

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25
Q

Why may someone be given an extra vaccine (4)?

A

High risk groups:
- immunocompromised
- pregnant (antibodies can move to foetus too)
- born to HepB infected mother
- in high TB incidence area

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26
Q

What are the 8 factors we should consider in order to eradicate a virus?

A
  1. Effective and safe (cheap, stable (will not adapt to pressure) and little doses)
  2. Lifelong natural immunity induced
  3. Short period of communicability (confined to humans easier to vaccinate)
  4. Highly characteristic clinical symptoms
  5. Easy and reliable means of diagnosis
  6. No nonhuman/environmental reservoirs
  7. Genetically stable causative agent
  8. Seasonality of occurrence (more targeted)
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27
Q

What are three current vaccine candidates?

A

Polio, measles, and rubella.

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28
Q

What are the pros and cons of a replicating viral vaccine strategy?

A
  • live, attenuated (replicated in other systems so no longer infectious to humans)
    Pros: stimulate antibodies, T cells and mucosal immunity, single vaccine may be efficient, durable immunity.
    Cons: could restore virulence, persistence in immunosuppressed, cell culture low yielding or not possible and limited shelf life.
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29
Q

What are the pros and cons of a non-replicating viral vaccine strategy?

A
  • subunit, nucleic acid etc (small part of vaccine)
    Pros: no risk of infection and quicker to produce.
    Cons: less immunogenic, may require adjuvants/boosters, may not stimulate local IgA mucosal response.
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30
Q

What is Mpox and its components?

A

MPXV is a linear ds-DNA which is a brick-shaped virion that can be enveloped in host cell-derived membrane, and they have ITRs which ease replication via forming a ring.

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31
Q

What is a viral vector?

A

An unrelated harmless virus which is modified to deliver genetic material for the viral vaccine.

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32
Q

What is the poxvirus replication cycle?

A
  1. Bind
  2. Fuse/enter (mature - no membrane so taken in by vacuoles, enveloped - membranes fuse to enter)
  3. Nucleocapsid release
  4. Transcription
  5. Translation
  6. Replication (into viral proteins in cytoplasm)
  7. Lysis/budding
  8. Release (enveloped virions burst from cell to exit)
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33
Q

What is the difference between clade I and II mpox?

A

I - endemic to Central Africa, severe, more virulent, and can actively disable immune response
II - less virulent, endemic to West Africa.

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34
Q

What was MPXV declared by WHO and when?

A

MPXV was declared a public health emergency of international concern in 2022, but has been classified this on and off - different clades causing issue.

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35
Q

How does mpox spread - how does it enter, who?

A

Mpox can spread between animals and humans, infecting a variety of mammalian species, and it does not require an animal intermediate. It can spread from mother to foetus via placenta.
The virus enters via skin breaks, eyes, mouth, nose, and other respiratory tracts.
The animal reservoir is unknown and transmission is likely direct, but could be indirect (contamination of shared space etc).

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36
Q

How are mpox and smallpox linked (vaccination)?

A

The mpox outbreak began when smallpox was eradicated (1980s), and this could be due to the smallpox vaccine giving individuals an extra boost, and the natural antibodies for the related virus stopped being generated when we stopped vaccinating.

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37
Q

What are the clinical symptoms for mpox?

A
  • takes 7-21 days to show
  • mild as it is self-limiting (naturally cleared)
  • lasts 2-4 weeks
  • transmissible if pox lesions appear (distinctive)
  • aches, fever, exhaustion
  • differs from smallpox by swollen lymph nodes
  • centrifugal rash spreading to extremities
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38
Q

What are the five stages of mpox rash?

A
  1. macule (spotted)
  2. papule (raised)
  3. vesicle (blisters)
  4. pustule
  5. scabbing (scab falls off = no longer infectious)
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39
Q

What are the three methods we can use to diagnose mpox?

A
  1. Real-time PCR - how much virus is present in individual, highly sensitive, fast, determines clade.
  2. Eliza - look for present antibodies and vaccine efficacy - IgM best. Cannot determine if individual is infected or not as Ab may be present from a previous or current infection.
  3. Sequencing - which virus, how it is mutating, which clade. It is unsuitable for clinical use due to pricing and training needs - use MinION sequencers instead to increase number of sequences to tackle this.
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40
Q

What is the treatment for mpox?

A

Supportive care - milder symptoms so we treat these rather than infection.
Combination therapy of three drugs may be used as they may evolve and develop resistance.

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41
Q

Is there a vaccine for mpox?

A
  • smallpox vaccine protects against mpox
  • two approved vaccines for both clades: MVA-BN and LC16m8.
  • these are third generation smallpox vaccines which are live, attenuated.
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42
Q

How can we as a population prepare for an outbreak of mpox?

A

Community engagement, isolation, self-protection, limiting number of sexual partners, pre- and post-exposure vaccines.

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43
Q

What is epidemiology?

A

This is the study of the distribution and determinants of disease frequency and the application of this to control health problems - uses One Health at a population-level.

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44
Q

What is morbidity?

A

Frequency of disease within a population.

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45
Q

What is the incidence?

A

The number of new cases per unit time.

46
Q

What is the prevalence?

A

The proportion of a population that has the disease at a given moment.

47
Q

What is the seroprevalence?

A

The proportion of serum samples reacting positively - they contain the antibody.

48
Q

What is the case fatality rate?

A

The proportion of those with the clinical disease that die (varies with infectious agents)

49
Q

What is the mortality rate?

A

The relative number of deaths within a population per unit of time.
It is a combination of case fatality rate and prevalence (high fatality but low prevalence could yield a low mortality and vice versa).

50
Q

What is an epidemic?

A

When the outbreak of infections is growing exponentially (R0 > 1).

51
Q

What is a pandemic?

A

When the epidemic grows to a large scale which impacts populations globally.

52
Q

What is an endemic disease?

A

When the number of infections is remaining stable (R0~1).

53
Q

What is an emerging infectious disease?

A

These are diseases which are growing in incidence following the introduction to host populations or to an existing population due to epidemiological changes.

54
Q

What is the difference between micro- and macro-parasites?

A

Micro - single-celled
Macro - worms, ticks

55
Q

What are the main infectious disease killers in humans?

A

Diarrhoeal diseases, malaria, TB and HIV/AIDs.

56
Q

What is the impact of infectious disease on wildlife populations?

A
  • threat to rare/endangered
  • disease-induced mortality can regulate host populations
  • act as reservoirs (issue)
57
Q

What are the two methods of direct transmission?

A
  1. Vertical - parent to offspring
  2. Horizontal - via close contact
    (a) bodily fluids - Ebola, smallpox
    (b) sexually transmitted infections - HIV/AIDs, syphilis
    (c) aerosol/respiratory - influenza, TB
58
Q

What are the three methods of indirect transmission?

A
  1. Vector-borne (malaria, Lyme, dengue fever)
  2. Food-borne (E.coli)
  3. Environmental contamination (anthrax, cholera)
59
Q

What are multi-host pathogens?

A

These can infect more than one species and are the cause of most emerging diseases - transmission may involve wildlife, domestic animals and humans (variety of reservoirs).

60
Q

What is a reservoir and give an example?

A

A population which maintains the pathogen independently of the target community - elk and bison for brucella (spillover to cattle is target)

61
Q

What is a carrier?

A

An infected organism that may be part of a reservoir but presents no or limited clinical signs/symptoms of the disease.

62
Q

Why are reservoirs and carriers important for an infection?

A

They pose an issue surrounding prevention and eradication.
They are harder to detect and prevent, meaning the disease is able to persist in a population and ensure the pathogen does not go extinct.

63
Q

What is the epidemiological triad?

A

1 - Host - varying levels of susceptibility
2 - pathogen - differing virulence factors or resistance
3 - environment - interactions, affects both other factors

64
Q

How can we prevent/reduce infection generally?

A

We want to break chain of transmission - improved hygiene, sanitation, protective equipment, antibiotics, drugs, vaccination etc.

65
Q

What is surveillance?

A

The continuous, systemic collection, analysis and interpretation of health-related data needed for the planning, implementation and evaluation of public health practise.

66
Q

What is monitoring?

A

The routine collection of information at a population-level over a defined time period, may not lead to action.

67
Q

What is active surveillance?

A

Targeted form where we actively collect data on a specific notifiable disease - cannot be done for every disease as it is expensive and labour-intensive. It allows a more complete estimate of disease frequency.

68
Q

What is targeted surveillance?

A

It is an active form which is directed at particular at-risk individuals, helping to improve health outcomes via early detection - effective treatment.

69
Q

What is passive surveillance and what do we expect?

A

The regular reporting of observed cases but no active search. This is the minimum standard, tests are being carried out anyway so inexpensive. It contributes to active.
There is an expectation of underreporting (misdiagnosis or no record) and under ascertainment (healthcare not sought by individual) - so does not show true incidence.

70
Q

What are the issues with wildlife surveillance (3)?

A

Remoteness (irregular access), scavengers and topography.

71
Q

What is citizen science?

A

This is the role of the general public in reporting infectious disease - could be used to identify potential reservoirs.
Mobile phones - most have access, cheap, fast, current (detect trends early).

72
Q

What is syndromic surveillance and its issue?

A

Reporting based on symptoms/clinical signs but with no distinct cause. This can be useful for monitoring trends and can be done via nowcasting (use of media).
Potential for misdiagnosis - treatments less effective.

73
Q

What is laboratory-based surveillance?

A

This tells us the underlying cause and the associated pathogen - precise, diagnostic confirmation, more specific than syndromic as it detects antibodies etc.

74
Q

What is a notifiable disease?

A

Those which should be reported within 24-72 hours - high public health and economic implications - tend to be exotic, endemic or not etc.

75
Q

Give four examples of re-emerging diseases.

A

Ebola, yellow fever, cholera and Zika.

76
Q

How can genomic data contribute to surveillance?

A

Sequencing data and whole genomes can track the spread of infections - can support country of origin and information of multiple spread events (patterns).

77
Q

What are the two hypotheses of pathogen origin?

A

1 - co-evolution (from our ancestors).
2 - cross-species contamination - pathogen may be newly introduced from animals (like most)

78
Q

How can we rule in or out a transmission hypothesis?

A

Via separate spillover events from animal reservoirs or whether it was maintained by a human population (most likely at low levels)

79
Q

How can we predict emergence (2)?

A

1 - catalogue all wildlife pathogens and identify most likely to emerge
2 - better surveillance systems e.g. portable sequencing devices

80
Q

What is control (achievable)?

A

Transmission is ceased within a specific area by looking at incidence, prevalence, morbidity and mortality at a local-level.
- deliberate efforts
- continued intervention measures
e.g. diarrhoeal diseases

81
Q

What is elimination (achievable) (2)?

A

Disease
The reduction to zero of disease incidence in a defined area.
- deliberate efforts
- continued intervention
e.g. neonatal tetanus
Infections
The reduction to zero of disease incidence of an infection caused by a specific pathogen.
- deliberate
- continued measures to prevent reestablishment
e.g. measles

82
Q

What is eradication?

A

The permanent and global reduction to zero of global disease incidence caused by a specific agent - only seen twice (smallpox and rinderpest). It is more feasible to eliminate a disease in a restricted area with little to no movement.
- deliberate efforts
- intervention no longer required

83
Q

What is extinction?

A

The specific infectious agent no longer exists within nature or labs - this has never been achieved.
Tendency to have the pathogen within lab conditions from studies etc means it is tricky to achieve.

84
Q

What is a ‘news worthy’ disease (example)?

A

Ebola
- high mortality
- rapid spread
- lack of treatment
- global impact
- human interest
- public health response

85
Q

Describe Toxocara SSP (toxocariasis).

A
  • worm persists in muscle tissue, waits until immunosuppressed to act.
  • cysts
  • picking up dog waste, hygiene are prevention methods
  • difficult to control due to complex mode of transmission, multiple sources, variation in exposure (pet ownership, unclean veg) and complex general symptoms.
  • localised control possible (complex network)
86
Q

Describe Taenia Solium (taeniasis).

A
  • infects humans if close contact with pigs or consumption of undercooked/raw pork
  • prevalent in pig farmers, severe economic loss
  • simple life cycle (stronger candidate for eradication)
  • worms can become lost and insist in brain - death
  • treatment: drugs, health education, improved sanitation, sanitation, livestock vaccination, improved meat inspection.
  • lack of funding due to social determination
87
Q

Describe the guinea worm.

A
  • water-borne zoonotic disease
  • no reservoirs
  • comes out intestinal tract down leg, causing warm itch in foot
  • cold water caused eggs to release into water
  • transmitted via consumption of contaminated water
  • no drugs/vaccine available
  • extraction slow and fail could lead to secondary infection
  • host: dogs and baboons
88
Q

Was eradication successful for the guinea worm and how?

A

Efforts began in 1980s and could be first example of human parasitic disease to be eradicated without vaccines.
Measures involve mapping, community-based surveillance, case containment, safe water, health education etc.
(they now know not to bathe foot if they gain a warm sensation).

89
Q

Why has the guinea worm eradication goal been set back previously?

A

Goal - 2030
unknown reservoir, unexplained infections, conflicts (war) etc.

90
Q

What is the WHO certification process (3)?

A

(1) Interruption of transmission - 0 indigenous cases over calendar month
(2) pre-certification - 0 indigenous cases 3 years later via active surveillance
(3) certification - ICT visits ensuring reports strong and true.

91
Q

Describe cholera.

A
  • infection of intestine by Vibrio cholerae
  • acute diarrhoeal
  • mild symptoms
  • rice water stools, leg cramps, vomiting, poor skin elasticity, severe dehydration
  • symptoms present after 3 hours due to release of CT toxin
  • contaminated water or food (faecal matter)
  • mainly endemic
  • seasonal
  • mainly due to those lacking pre-existing immunity
92
Q

What is the virulence factor of cholera and its process?

A

The cholera toxin (CT) is made of A (enzymatic) and B (attach) subunits. It penetrates the intestine and prevents absorption of water and food - aiming to increase cAMP levels.
CT binds to host cells via B and forms a toxin-containing vacuole which moves towards the ER where A cleaves into A1 and A2 by protease. A1 is exported to cytoplasm where it attaches to G protein, causing constant stimulation of adenylate cyclase - produces cAMP.
High cAMP levels activate ion channels, moving various electrolytes (ions) with water out of the cell into the intestinal lumen - symptoms arise.

93
Q

How does pathogenicity occur in V. cholerae?

A
  • facultative anaerobe
  • occurs due to toxin and pilus (TCP allows the cell to aggregate to form microcolonies which protect the host - difficult to clear and CT secreted at high levels).
  • horizontal gene transfer - pass on virulence genes encoding toxic subunits by infecting non-pathogenic V. species.
94
Q

Describe the serogroups and biotypes of V. cholera.

A

2 toxic serogroups - 01 and 0139.
01 biotype –> classical and El Tor (survives longer and produces haemolysins).
Biotype serotypes –> Ogawa (B), Inaba (C) and Hikojima (all) - differ in antigenic determinant depending on methylation.

95
Q

How can we treat cholera?

A

Oral rehydration, delivery of clean water, and sanitation.

96
Q

What role does the environment play in cholera?

A
  • V. cholerae naturally inhabits aquatic environments - coasts.
  • emerged in Bay of Bengal
  • can survive coastal waters for long time periods before human infection
  • complex life cycle means it can exist in various physiological states and can interact with other natural inhabitants
  • exists in free living culturable state or viable but non-culturable state (winter).
97
Q

What relationship do copepods and V. cholerae have?

A
  • type of zooplankton whose gut and egg masses colonised by V. cholerae
  • commensal association
    > form biofilms on surface
    > multiply during algal blooms
    > provides protective environment from external stress - would be bad for free-living
    > enables induction and transfer of genes
    > allows it to enter hyper-infectious state
    (key for epidemiology)
98
Q

What is the filtration method for V. cholerae?

A

Different types of sari can cause a reduction of cholera cases in a population via efficient removal of copepods - old cotton more effective as it has smaller holes for bacteria

99
Q

How can we predict future cholera outbreaks (2 methods)?

A
  • satellite sensing allows detection of microbes by the use of space-based sensors providing a view of our oceans (direct - optical properties, indirect - physical or physiological properties (chlorophyll))
  • cholera incidence decreases in sub-optimal conditions (less rainfall, improved sanitation)
  • predict based on sea temperature and phytoplankton abundance
  • coastal flooding - increase in cholera
  • remote sensing - potential parameters combined for predictions like sea temp, height and chlorophyll levels (predicted is similar to actual incidence).
100
Q

Why is climate change a threat in terms of cholera?

A

A favourable environment is being created for V. cholera to thrive and grow - physical environment drivers - more regions are becoming suitable for inhabitation.

101
Q

Describe the Haiti natural disaster.

A
  • 2010 epidemic
  • following earthquake
  • UN peacekeepers called to Nepal during cholera epidemic and experienced sanitation issues
  • Haiti infected by UN peacekeepers who never tested again before leaving Nepal and underreported.
  • allowed no investigation of source or access to samples
  • UN apologised 6 years later for their role in Haiti outbreak (claimed thousands of lives in 18 months)
102
Q

What are the two aims for cholera?

A

(1) reduce cholera deaths by 90%
(2) 20 countries to be cholera free by 2030

103
Q

What are the three conclusions we have made surrounding EIDs?

A

(1) response is not enough - prepare
(2) technology advancements could map spread, outbreaks etc
(3) cities (due to travel and work) are hubs of transmission and so we require better interventions

104
Q

What are the four main categories of EIDs?

A

Newly emerging, re-emerging (historically infected humans and continues to reappear in new locations or in resistant form), deliberately emerging (intent to harm, bioterrorism - mass panic) and accidentally emerging (created in labs and unintentionally released).

105
Q

What is the disease risk factors for EIDs?

A
  • evolution and adaptation occurs quickly, especially in RNA viruses
  • point mutations by recombination and reassortment
  • not main driver
    > viruses stable in particular ecological niches, it is only when you upset this that they evolve/mutate
106
Q

Why are human EID risk factors so potent?

A
  • main driver for emergence
  • changing virus conditions so it is no longer stable
  • knock-on effect
    > people, food, travel, high transmission rate
    e.g. urbanisation, population growth, movement etc.
107
Q

Why is human travel an EID risk factor?

A
  • can carry any disease to any part of the world in a short time period
  • biggest cause
  • more accessible than past
108
Q

Why is vector travel an EID risk factor and give an example.

A
  • hitchhikers
  • survival enhanced by climate change
  • transport via aircraft, livestock movement, luggage
    e.g. West Nile virus outbreak in NYC
109
Q

Why is hunting an EID risk factor and give an example.

A
  • close contact with nonhuman primates
  • HIV has a zoonotic origin but is not a zoonotic disease
    > no longer requires reservoir
  • SIV in primates
110
Q

Why is pasturage an EID risk factor and give a countries example.

A
  • promotes susceptibility to infections
  • developing countries have less legislation and closer proximity
  • China - live markets for cultural food
    > cross-species contamination from animal to handler (lack of sanitation in animal housing)
111
Q

Why are generalist viruses a risk factor and give a current example.

A
  • Generalist viruses do not require an intermediate host for evolution - general in nature.
  • although intermediate aids host switching
  • SARS-CoV-2 new strain emerged which required quick action
    > can be transmitted by pangolins but makes them ill
    > reservoir: horseshoe bats.
112
Q

What are the two ecological risk factors of EIDs and briefly explain them, giving examples.

A

(1) El Nino Southern Oscillation (ENSO)
- general fluctuations in ocean and atmospheric temperature
- warm phase
e.g. HPS (hantavirus pulmonary syndrome) due to hot and wet conditions (increased precipitation) increase pinon nuts for deer mice (HPS carrier population explosion - more contact).

(2) Global warming
- small increase in temp = explosion of insect (vector) populations
e.g. West Nile in NYC - milder conditions, natural predation reduction, mosquito-to-bird transmission (local reservoir).