Healthy and unhealthy communities - Microbiology Flashcards

1
Q

List the key factors determining the travel-related risk

A
  • Mode of destination
  • Destination (local infection epidemiology)
  • Season of travel
  • Duration of travel
  • Standards of accomodation, food hygiene and sanitation
  • Behaviour of the traveller / purpose of travel
  • Underlying health of traveller
    *
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2
Q

Describe the importance the destination a travellor goes to is

A
  • Destinations where accomodaton, hygiene, sanitations, water quality and medical care of a high standard result in ‘few risks to the health of travellers’
  • Visitng major cities and tourist centres pose few serious risks
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3
Q

Describe how the behaviour of a travellor can expose them to risks?

A
  • Going outdoors in the evenings in a malaria-endemic area without taking precautions
  • Swimming in schistosoma infested lakes
  • Exposre to insects, rodents, bats, and other animals
  • Ingestingcontaminated food/water
  • Unprotected sexual intercourse
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4
Q

a) What is gastroenteritis associated with?
b) Describe the epidiemiology of gastroenteritis
c) What are the two types?
d) What are the causative agents?

A

a) Associated with poor hygiene and sanitation
b) Worlwide in endemic areas, 1.5 million children die yearly due to infectious gasteroenteritis
c) Viral and bacterial gastroenteritis
c) Rotavirus, Norovirus, Astrovirus

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5
Q

List the bacterial gastroenteritis agents

A
  • Campylobacter jejuni
  • (Enterotoxigenic) E.coli
  • Salmonella
  • Shigella
  • Vibrio cholerae
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6
Q

Gastroenteritis

a) Presentation
b) Diagnosis
c) Treatment

A

a)

  • Anorexia
  • Nausea
  • Vomiting
  • Diarrhoea
  • Abdominal discomfort

b)

  • Clinical evaluation
  • Stool testing

c)

  • Oral or IV rehydration
  • Antibiotics in select bacterial cases if bacteraemia
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7
Q

Which viral hepatitis are enterically (food and waterbore) transmitted?

A
  • Hepatitis E
  • Hepatitis A
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8
Q

Infection charcteristics of hepatitis E

a) Transmission
b) Outbreak
c) Incubation
d) Attack rate
e) Mortalitiy
f) Severity of disease
g) Vaccine available

A

a) Faeces
b) Seasonal, often associated with monsoon period
c) 3-7 weeks
d) 1 in 2
e) <1% but 15-25% in antenatal women
f) Increases with age
g) Develope

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9
Q

a) What are the genotypes of hepatitis E
b) Which is the most prevalent genotype?

A

a) Genotype: 1,2,3 and 4
b) Genotype 1

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10
Q

Describe the prevention and control measures for travellers to hepatitis E endemic regions

A
  • Avoid drinking water (and beverage with ice) of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveller
  • Vaccine developed
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11
Q

Infection characteristics of hepatitis A

a) Transmission
b) Site of infection
c) Severity of disease
d) Epidemiology

A

a) Faecal-oral route
b) Acute, self-limiting infection of the liver
c) Infection may be asymptomatic in children and adults symptomatic. Rarely, fulminant hepatitis (Clinical syndrome of severe liver function impairment can ensue)
d) Every year there are 1.5 million symptomatic cases

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12
Q

Describe the prevention of hepatitis A

A

Good hgygiene

Pre-exposure

  • Active immunisation vaccine (killed whole virus - active within 14 days of first dose) for travellers to intermediate and high-risk areas

Post exposure

  • Vaccine (within 7 days)
  • Immunoglobulin HNIG (within 14 days of onset of disease in primary case)
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13
Q

There are athropod-associate travel infections.What is an anthropod?

A

Mosquitoes or ticks

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14
Q

List some examples of mosquito associated viral infections

A
  • Dengue type 1,2,3,4
  • Japanese encephalitis
  • Murray valey encephalitis
  • St louis encephalitis
  • West Nile virus
  • Zika virus
  • Yellow fever
  • Chikungunya virus
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15
Q

Dengue fever

a) Transmittance
b) Symptoms
c) Presentation of dengue haemorrhage fever
d) What are the severe consequences of fengue haemorrhage fever?
e) What are the differential diagnosis of fengue fever and why?

A

a) Transmitted to people by bite of Aedes mosquito that is infected with dengue virus

b)

  • High fever
  • Severe headache
  • Severe pain behind eyes
  • Joint pain
  • Muscle and bone pain
  • Rash
  • Mild bleeding (e.g., nose or gum bleeds, easy bruising)

c)

  • Fever that lasts 2-7 days, with general signs and symptoms consistent with dengue fever
  • When the fever declines, symptomsinclude persistent vomiting, sever abdominal pain, and dysponea (shortness of breath) may develop

d) Haemorrhage follows leading to failure of the circulatory system and shock. This leads to death if not corrected
e) Chikungunya and zika virus as they are prevalent in the same areas as denge virus (subtropical and tropical areas of the world)

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16
Q
A
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17
Q

List some examples of tick-borne infections

A
  • Tick-borne encephalitis
  • Kyasunar forest disease (Alkhumra)
  • Lounping ill
  • Omsk haemorrhage fever
  • Powosan
  • Crimean-congo haemarrhagic fever
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18
Q

Crimean-congo haemorrhagic fever

a) Cause
b) Case fatality
c) Incubation period
d) What type of outbreak does it cause?
e) Symptoms
f) Worrying signs and can they lead to?

A

a) Caused by an infection with Nairovirus (tick-borne virus) in the family Bunyavirdae
b) 10-40%
c) Short (1-3 days)d) Haemorrhagic fever

e)

  • Fever
  • Myalgia
  • Neck stiffness
  • Backache
  • Headache
  • Photophobia
  • Nausea
  • Vomiting
  • Diarrhoea
  • Abdominal pain
  • Mood swings
  • Confusion

f) Bleeding into the skin, mucosa, internal organs

19
Q

a) What are viral haemorrhagic fevers (VHFs)?
b) What is the term ‘viral haemorrhagic fever’ used to describe?
c) Characteristically,what occurs in viral haemorrhagic fevers?
d) Provide examples of some viral haemorrhagic fevers in Africa

A

a) Viral haemorrhagic fervers (VHFs) refer to a group of epidemc prone disease that are caused by several distinct families of viruses
b) The term “viral haemorrhagic fever” is used to describe a severe multi-system syndrome (multple organ systems affected)
c) Characteristcally, the overall vascular system is damaged and the body’s ability to regulate itself is weakened. Symptoms can oftern be accompanied with life-threatening bleeding
d) Marburg and Ebola haemorrhagic fevers, Crimean-congo haemorrhagic fever (CCF), Rift Valley fever (RVF), Lassa fever, yellow fever

20
Q

Tuberculosis

a) Causation? and what is the most common causative agent?
b) Transmission
c) Epidemiolgy
d) What do you call people who are asymptomatic and not infectious?
e) What vaccine provides partial prtoection against TB?
f) Treatment? What issues can arise?

A

a) Caused by various strains of mycobacteria. Most commonely mycobacterium tuberculosis
b) About 1/4 of the worl is infected with mycbacteria. 10 million people fell ill with TB in 2017
c) TB is transmited by people inhaling airborne droplets produced by infectious TB carriers
d) Latent TB infection (LTBI) carriers
e) BCG (Bacillus Calmette-Guerin) vaccine
f) Standard treatment of TB consists of six-month regimen of 4 first-line drugs (isoniazid, rifampicin, ethambutol and pyrazinamide)

Issue - variants of TB are resistant to antibiotics which makes TB more difficul and expensive to treat and have higher fatality rates. This is known as multidrug-resistant (MBR) and extensively drug-resistant (XDR) TB

21
Q

Middle East Respiratory Syndrome Coronavirus (MERS-CoV)

a) Case-fatality rate
b) Major reservoir host
c) Symptoms

A

a) 35.5% transission human-to-human
b) Dromedary camels

c)

  • Fever, cough, short of breath
  • Pneumonia is common but not always present
  • GI symptoms include diarrhoea
22
Q

Rabies

a) Transmittance
b) Wich animals are the main source of human rabies death?
c) Epidemiology
d) Managment and treatment

A

a) Direct contact with saliva (usually through a bite) or brain/nervous system tissue from an infected animal of a rabid animal, most commonly dogs
b) Dogs
c) Infections cause tens of thousands of deaths every year, mainly in Asia and Africa
d) Immediate thorugh wound washing with soap and water after contact with a suspected rabid animal and then followed by post-exposure prophylaxis [(rabies vaccine and rabies immune globulin (RIG)]

23
Q

Monkeypox

a) Transmittance
b) What is monkey pox similar to? What is the difference between them?
c) Case-fatality
d) Treatment

A

a) Viral zoonotic disease that is transmitted from various wild animals e.g., rodents and primates but has limited secondary spread from human-to-human transmission
b) The monkeypox virus is similar to huma smallpox (eradicated in 1980) however monkeypox is milder (still fatal)
c) 1-10% with most deaths occuring in younger age groups
d) There is no specific treatment or vaccine available although prior smallpox vaccination was highly effective in preventing monkeypox as well

24
Q

Malaria

a) Causative agents
b) Transmittance?
c) Where and when does it most occur?
d) Epidemiology

A

a) Plasmodium falciparum, P. vivax, P.ovale (subspecies curtisi and wallikeri), P.malariae, P.knowlesi
b) Transmitted by the bite of female anopheline mosquitoes
c) Occurs throughout tropics and sutropics at altitudes below 1500 metres. Malaria transmission occurs during or just after the rainy season
d) 240 k deaths per year. Between 2000-2015 global incidence reduce by 41% but still causes 200 million cases per year

25
Q

Describe the clinical presentation of malaria

A
  • Symptoms are non-specific and range from fever to fatal cerebral disease/multiorgan failure and are associated exclusively with the asexual blood stage and species of parasite
  • Splenomegaly occurs as ethryocytes burst due to osmotic fragility caused by parasitic infection
  • Various intrabdominal pain usually in severe casees
26
Q

When does fever in malaria follow? Describe what this means

A

Fever folllows after rupture of ethrocytic schizonts, therefore there is periodicity in the fever and characteristic patterns of fever - 48hr (tertian: days 1 and 3), 72hr (quartan: days 1 and 4), 24hr (quotidian-daily(rare))

27
Q

Describe the cynical syndrme of P.vivax

A

P.vivax develops into chronic febrile illness with severe mortality and causes malaria with pronounced anaemia and respiratory illness

28
Q

Describe the clinical syndromes of P.ovale and P.malariae

A

P.Ovale and P.Malariae are usually self-limitying but can reucur as they often form hypnozotites that can represent with anaemia even years after the original infection

29
Q

a) Describe the clinicial syndrome of P.falciparum malaria
b) Which people is complicated P.falciparum malaria most common in?

A

a) P.falciparum malaria is frequently fatal during first 2 weeks because of the variety of complications
b) In hyperendemic areas, complicated falciparum malaria is most common in children 6 months- 5 years and in pregnant women

30
Q

What are the main complications of malaria?

A
  • Cerebral malaria (most dangerous complication)
  • Seevere anaemia
  • Hypoglycaemia, lactic lordosis and actue renal failure
31
Q

a) Cerebal malaria is a complicaton of malaria. What are the features and consequences of cerebral malaria
b) Severe anaemia is a complicaton of malaria. What is this due to?
c) Hypoglycaemia, lactic lordosis and acute renal failure is a complication of malaria. What is this due to?

A

a) It occurs with convulsion and dimished level of consciousness leading to a coma
b) Due partly to red cell destruction and dyserythropoieses (defective development of erythrocytes) in the bone marrow
c) Due to acute tubular necrosis

32
Q

a) What is the first choice diagnsosis of malaria?
b) How else malaria can be diagnosed?
c) If malaria persists for several years what type of testing should be done?
d) Will a single negative blood film exclude malaria of any species? If no, what else would need to be done?

A

a) Thin and thick film - to find parasitized red cells
b) Lateral-flow devices (dipsticks)
c) Antibody testing
d) No - further blood films need to be done 24hr and 48hr continuum

33
Q

a) What is complicated falciparum malaria treated with?
b) If there is a delay in obtaining artensunate to treat complicated falciparum what is the next line drug? and what monitoring is required and why?

A

a) IV artesunate
b) IV quinone. Cardic monitoring and regular blood sugar levels as there are risks of arrythmias and hypoglycaemia

34
Q

What is uncomplicated falciparum malaria treated with?

A

Oral artemisinin combination therapy

35
Q

a) What is malaria due to P.vivax, P.ovale, P.knowlesi or P.malariae treated with?
b) What is severe or complicated malaria due to any of these species treated as?

A

a) Oral artemisinin combination therapy or oral cholroquine
b) Treated as complicated falciparum malaria so IV artesunate used

36
Q

a) What drug is used to prevent relapse of benign malarias (Pvivax and P.ovale)
b) What is this drug contraindicated in?

A

a) Primaquine
b) G6PD deficiency

37
Q

Which malaria is treated with IV artesunate or quinone?

A

Complicated falciparum

38
Q

Which malaria is treated with oral artemisinin combinations or oral chloroquine?

A

Artemisinin in uncomplicated P.falciparum

Artemisinin or chloroquine in malaria due to P.vivax, P.ovale, P.knowlesi, P.malariae

39
Q

Describe how malaria can be prevented

A
  • BED NETS impregnated with isecticides
  • In-dorr insecticide spraying > 80% of households
  • Antimalarial drugs
  • Pregnant women to take sulfadoxine-pyrimethamine
  • The RTS,S vaccine
40
Q

Describe the life cycle of malaria

A
  1. Infected anopheles mosquito bites and injects sporozoites from the salliva into huma blood stream
  2. Sporozites enter parenchymal cells of live where (in approximately 2 weeks) they mature into pre-erthyocytic schizonts
  3. They then rupture to produce 10000-40000 merozoites
  4. Merozoites enter the red blood cells to initate asexual blood stage. Some parasites remain in the liver to lie dormant as hypnozoites, which are the cause of relapses.
  5. In red blood cells, merozoites mature into trophozoite and schizont, which complete the cycle by maturing to release merozoites back into the circulation
  6. Some merozoites go on to initiate the sexual stage, maturing within the red blood cells to form and male female gametocytes, which can be taken up by the anaopheles mosquito on feeding
  7. On enterting the gut of the insect, the male gametocyte exflagellates to form male microgametes, which fertilize the female gamete to form the zygote
  8. This then invades the gut mucosa, where it develops into an oocyst
  9. This develops to produce thousands of sporozites, which are released and migrate to the salivary glands of the insect.
  10. The cycle begins again
41
Q

Describe the resistance of P.vivax malaria

A
  • The invasion of red blood cells requires 2 seperate receptor-ligand interactions. The lack of the duffy antigen (red cell surface receptor), explains the absence of P.vivax from most west africans, as there is a high prevalence of duffy negative people in the region
  • However, P.vivax infection of duffy-negative individuals has now been confirmed, indicating that this parasie is capable of using other receptors to invade ethrocytes, suggesting it is evolving rapidly
42
Q

Describe the resistance of P.falciparum malaria

A

P.falciparum has now become resistant to chloroquine and sulfadoxine-pyrimethamine, initially in South-east Asia and now throughout Africa

43
Q

What other genetic traits contribute to malaria resistance?

A
  • Sickle cell
  • Beta-thalassaemia deficiency
  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency
44
Q

a) What should you explain to patients seeking prophylaxis for malaria
b) What should you do if a patient is HIV positive?

A

a) A combination of mosquito avoidance and chemoprophylaxis will give significant protection against malaria, but no regime is 100% effective and prophylaxis should be obtained from reputable UK source
b) Refer to HIV physician