Medicinal microbiology Flashcards

1
Q

What is the name of the bacterium that causes diptheria?

A

Corynebacterium diptheriae

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2
Q

What causes symptoms of diptheria?

A

The toxins produced by corynebacterium diptheriae

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3
Q

What are the symptoms of a diptheria infection?

A

The toxins cause a grey/white ‘false membrane’ to form starting from an ulcer. This can cover the back of the throat and cause suffocation if not treated. Other symptoms include a fever, swollen glands and a sore throat.

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4
Q

What is the 6 in 1 vaccine and when is it given?

A

The vaccine is given to babies at 8,12 and 16 weeks.
It covers diptheria, hepatitis B, Haemophilus influnzae Type B, polio, tetanus and whooping cough.

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5
Q

Aside from the 6 in 1, 4 in 1 and 3 in 1 vaccine when else may a diptheria vaccine be administrated?

A

You may receive a booster vaccine if you are travelling to an area with high prevalence of diptheria such as Indonesia.

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6
Q

What type of bacteria is Corynebacterium dipetheriae?

A

Gram postitive (aerobe)

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7
Q

What is the bacterium called that causes tetanus?

A

Clostridium tetani

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8
Q

What type of bacteria is clostridium tetani?

A

Gram positive (anaerobic) rod shaped

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9
Q

How can you become infected with clostridium tetani?

A

Wounds come into contact with soil or manure. The bacterium is a specific type of soil bacterium.

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10
Q

What causes the symptoms of tetanus to appear?

A

Clostridium tetani produces endospores under certain conditions. When these spores enter our bodies they produce neurotoxins which causes symptoms of tetanus.

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11
Q

What are some of the symptoms of tetanus?

A

Stiffness of jaw muscle
Painful muscle spasms
Stiffness in neck and back
Fever
Sweating
Rapid heart rate

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12
Q

What is the 4 in 1 vaccine and when is it administrated?

A

It is also known as the pre school booster and is given at the age of 3 years and 4 months.
It includes killed strains of:
Diptheria
Tetanus
Whooping cough
Polio

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13
Q

What is the 3 in 1 vaccine and when is it administrated?

A

It is given in Year 9 and includes protection from:
Diptheria
Tetanus
Polio

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14
Q

What are the main symptoms of a UTI?

A

Burning sensation on urination
Increased urinary frequency
Blood in urine
Lower back pain

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15
Q

What bacterium causes a UTI?

A

In the community over 80% of UTIs are caused by E. coli

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16
Q

What type of bacterium is E coli?

A

Gram negative

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17
Q

List Gram negative specific antibiotics.

A

-Ureidopenicillins (piperacillin)
-Third- or fourth-generation cephalosporins (cefotaxime, ceftazidime)
-Carbapenems (imipenem, meropenem)
-Fluorquinolones (ciprofloxacin)

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18
Q

What sort of infections does Gram negative bacterium cause?

A

Usually affects GI tract, UTIs and pelvic inflammatory diseases

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19
Q

What sort of infections does Gram positive bacterium cause?

A

Causes infections of the skin and soft tissue, wound infections and osteomyelitis

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20
Q

What sort of infections does anaerobic bacterium cause?

A

Normally responsible for infections in the mouth, teeth, throat, sinus in addition to the lower bowel and appendicitis

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21
Q

What is the difference between staphylococcus and streptococcus bacterium?

A

Both are gram positive bacterium. Staphylococcus infections are the leading cause of boils, abscesses, conjunctivitis, impetigo and cellulitis. Streptococcus infections cause strept throat and scarlet fever.

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22
Q

When should nitrofurantoin not be prescribed for a UTI?

A

If the patient has poor renal function (under 45 mL/min)

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23
Q

What is a severe drug interaction with Trimethoprim?

A

Should NOT be given alongside methotrexate

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24
Q

What is the empiric treatment for a UTI? (non-pregnant women)

A

Trimethoprim 200mg twice a day for 3 days or 100mg Modified release Nitrofurantoin twice a day for 3 days.

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25
Q

What should be given for a severe UTI?

A

IV Gentamycin

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26
Q

How would you diagnose a UTI in over 65s?

A

Only based on symptoms present

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27
Q

How would you diagnose a UTI in under 65s?

A

Symptoms in addition to a dipstick test of urine sample to test for the present of nitrates which indicates an infection.

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28
Q

What is the difference between horizontal and vertical transmission of a pathogen?

A

Horizontal transmission a person passing on the pathogen to others in a community or exposing the pathogen to others in a community. Vertical transmission is exposing the pathogen inter-generationally.

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29
Q

What is an example of vertical transmission (antibodies)?

A

Passing of antibodies via the placenta (IgG in the third trimester) or breast milk (IgA).

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30
Q

What diseases can be transmitted vertically?

A

Hepatitis B, HIV, rubella

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31
Q

Explain opportunistic infections.

A

Opportunistic infections are pathogens that infect us but do not causes an immune response, they do not make us ill. Only if you are immuno-suppressed would cause a disease.

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32
Q

What is the name of bacterium that causes opportunistic infections?

A

Pseudomonas

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33
Q

What type of bacterium is pseudomonas?

A

Gram negative rod shaped bacterium, respiratory mode of metabolism

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34
Q

What is a disease where psuedomonas is the primary pathogen?

A

Cystic fibrosis, secondary invader in severe burns

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35
Q

How does borrelia burgdorfen spread?

A

Bites of ticks

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36
Q

Describe the three stages a patient would experience with borrelia burgdorfen?

A

The first stage is the appearance of an expanding rash at the site of the tick bite.
Then the dissemination phase with fever and a headache.
Lastly if untreated a persistent infection would occur affecting the nervous system.

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37
Q

What is the clinical name associated of Borrelia Burgdorfen?

A

Lyme disease

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38
Q

What type of bacterium is Borrelia burgdorferi?

A

It is a gram negative spirochete bacterium

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39
Q

What is the first line treatment of Lyme Disease? Explain you choice.

A

Course of oral doxycycline (broad spectrum antibiotic covering both Gram positive and Gram negative bacterium).

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40
Q

If a patient is presenting with symptoms of central nervous system involvement what is the first line treatment? (Lyme disease)

A

IV Ceftriaxone,
If not suitable then oral doxycycline

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41
Q

When should a microbiological samples and blood culture sample be taken for a patient with suspected sepsis?

A

Before administrating any IV antibiotics. Therefore at least within an hour of the patient being diagnosed with suspected sepsis.

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42
Q

What does the ‘SEPSIS’ acronym stand for?

A

Symptoms of Sepsis:
S- slurred speech or confusion
E- extreme shivering/muscle pain
P-passing no urine
S-severe breathlessness
I-it feels like you are going to die
S-skin mottled or discoloured

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43
Q

How is sepsis transmitted?

A

Normally sepsis is caused by an infection that then develops. It is not contagious.

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44
Q

What are examples of bacterium that causes sepsis?

A

The three most common sepsis-causing bacterium are:
Staphylococcus aureus
E. coli
Streptococcus

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45
Q

What is the first line treatment of a patient with suspected sepsis?

A

IV empirical anti-microbial which is given in line with local or national guidelines.

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46
Q

How is legionella pneumophilia normally spread?

A

When the bacteria enters water sources and can rapidly multiply in warm, moist conditions such as air conditioners.

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47
Q

When does hospital acquired pneumonia usually occur?

A

Symptoms develop 48-72 hours of being in hospital

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48
Q

How does the first line treatment of CAP differ with HAP?

A

First line treatment in CAP:
Amoxicillin 500mg three times a day for 5 days
HAP:
Doxycycline 200mg on Day 1 then 100mg for the four following days (5 days treatment)

Can increase to 7 days, depending on severity

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49
Q

What is the main cause of pneumonia? (fungi, bacteria, virus etc.)

A

In children mainly due to a viral infection or secondary bacterial, in adults it is bacterial.

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50
Q

How can neonates develop pneumonia?

A

If they inherit chlamydia from the Mother they can develop interstitial pneumonitis

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51
Q

What are the main identifiable symptoms of pneumonia

A

Chest pain
A persistent cough which can be dry or productive
Loss of appetite
High temperature
Rapid heart rate
Shivering or sweating

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52
Q

Main bacterium that causes community acquired pneumonia?

A

Streptococcus pneumoniae

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53
Q

What diagnostic measures would you use for a suspected CAP presenting patient?

A

Chest X-ray- if CAP is present there is likely to be shadowing on the lungs (basal consolidation).

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54
Q

What key symptom is NOT present in CAP?

A

Sore throat

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55
Q

When is clarithomycin prescribed in pneumonia?

A

When the bacterium causing CAP is atypical bacteria such as Legionella pneumophilia or mycoplasma pneumoniae

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56
Q

Should clarithomycin be administrated by IV or orally?

A

It has no increased efficacy when given by IV therefore if possible orally

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57
Q

How is celluitis monitored?

A

Draw around the red area, to see it shrinking once antibiotics are administrated

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58
Q

What are the main pathogens causing celluitis?

A

Group A streptococcus
Staphylococcus auerus

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59
Q

What is the first line treatment for celluitis?

A

IV flucoxacillin or clarithomycin

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60
Q

How do you diagnose celluitis?

A

Taking a wound swab

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61
Q

What clinical interventions should be made before starting patients on antibiotics? (START SMART)

A

Take medication record, making note of allergies
Begin antibiotics as soon as possible, normally broad spectrum
Record indication and drug chart
Note review date or duration
Comply with local guidelines
Take microbiological specimens

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62
Q

When should a clinical review of antibiotics take place?

A

48 hours after treatment has begun

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63
Q

What are the five decisions made at antibiotic review?

A

STOP
IV to oral switch
Change to narrow spectrum
No change, review in another 24 hours
OPAT

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64
Q

What are some of the investigations used to detect and monitor patient infections?

A

Haemotology results
Biochemistry results
Body temperature
X-rays

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65
Q

When is the meningoccocal type B vaccine given?

A

It is given to babies a 8 weeks, 16 weeks and then at one years old.

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66
Q

What are the four vaccines given when a baby turns 1?

A

Hib/MenC (1st dose)
MMR (1st dose)
Pneumococcal vaccine (2nd dose)
MenB (3rd dose)

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67
Q

What are three teenage jabs?

A

HPV vaccine (12-13 years)
3 in 1 teenage booster (13-15 years)
MenACWY vaccine (13-15 years)

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68
Q

When is the second MMR vaccine given?

A

3 years 4 months alongside the 4 in 1 booster

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69
Q

How is the rotavirus vaccine administrated?

A

It is given orally

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70
Q

What age is the rotavirus vaccine administrated?

A

At 8 weeks and 12 weeks

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71
Q

What antibodies are crucial for polio protection?

A

IgA antibodies

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72
Q

Which demographics would be unable to receive live attenuated vaccines and why?

A

Immunosuppressed patients in the fear that they will not be able to produce a sufficient immune response
Pregnant women due to potential fecal damage

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73
Q

What is the difference in mechanisms between live and killed vaccines?

A

Live vaccines contain a weakened form of the antigen causing the pathogen, the antigen can infect cells but not cause the illness. Killed vaccines contain a killed form of the antigen so they cannot infect cells but can still trigger an immune response.

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74
Q

What are the advantages of live attenuated vaccines?

A

Only one single dose is required
Low cost
Immunity last for years rather than months

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75
Q

What is the potential safety risk of live attenuated virus?

A

In live attenuated vaccines the antigen present is often a mutated form of the actual virus. Therefore in some individuals the antigen can re-mutate back into the original form inducing the disease.

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76
Q

What are some examples of live attenuated vaccines?

A

MMR and the rotavirus

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77
Q

What are some of the advantages of using killed vaccines?

A

There is no risk of reverting back into the original virus.

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78
Q

What are the disadvantages of using a killed vaccine?

A

Usually quite expensive
Requires multiple injections as the immune system is not activated therefore multiple doses of antibodies are required.

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79
Q

The conditions required to propose global eradication of a disease? (6 conditions)

A

The disease must be limited to humans
No long term carrier status possible
The disease must be easily recognisable
Must only be one or a few serotypes
There must a cheap, stable and effective vaccine available
The eradication program is cost effective

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80
Q

Describe the difference between the two polio vaccines.

A

The Salk vaccine is a killed vaccine whereas the Sabin vaccine was a live vaccine.

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81
Q

Which polio vaccine is no longer used and why?

A

The Sabin virus (live virus) is no longer used once the disease has been eradicated, this was due to the side effects induced by the vaccine.

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82
Q

Why has no vaccine for HIV been developed yet?

A

Because epitopes of the viral envelope are too variable. Furthermore HIV attacks the immune system so there is no effective cell-mediated immunity.

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83
Q

When are additional vaccines given at birth?

A

When the mother is Hep B positive or the baby is at risk of developing tuberculosis. They are given BCG or Hep B vaccine.

84
Q

Are the hepatitis vaccines live or killed vaccines?

A

They are killed vaccines. Normally given at 8,12 and 16 weeks unless the mother is screened during pregnancy and is positive and then the vaccines are administrated at birth.

85
Q

Why is the influenza vaccine given every year?

A

This is because it mutates annually so a vaccine is given to protect against the predicted mutated strain.

86
Q

Who receives the varicella vaccine?

A

Healthcare workers who have no evidence of immunity.

87
Q

In addition to Clostridium tetani what are the two other types of Clostridium bacterium?

A

Clostridium perfringens which causes food poisoning, and anaerobic wound infection.
Clostridium difficle causes a severe form of colitis

88
Q

What causes the symptoms of tetanus?

A

Continuous stimulation of the excitatory neurotransmitter means there is constant contraction of the muscles which results in ‘locking’.

89
Q

What is enteric bacterium?

A

Enteric bacterium is rod shaped Gram negative bacterium which lives in the intestinal tract of animals.

90
Q

Describe the mechanism of the cholera pathway.

A

Once inside the lumen of the epithelial cell cholera release the toxins called choleragen which is made of 1 alpha subunits and 5 beta subunits. The B sub-unit of the choleragen binds to the GMI ganglioside receptor on the surface of the target intestinal epithelial cell.
The alpha sub-unit is then released and endocytosed into the cell.
The A subunit then catalyses the addition of a ADP-ribose on the G (as) sub-unit causing it to lose its GTP hydrolysis activity, causing permanent activation. This causes an increase in adenylyl cyclase activity which results in an increase in cAMP concentration inside the intestinal cells. cAMP binds to and activates protein kinase A . Protein kinase A phosphorylates the cystic fibrosis transmembrane conductance regulator (CFTCR) which enables the efflux of chloride ions out of the cell down their electrochemical gradient into the intestinal lumen. Sodium and hydrogen ions follow causing an increase in osomotic pressure out of the cell. Water molecules diffuse across the membrane following the net flow of the salts. Therefore the combined effect, results in a loss of sodium, chlorine, potassium and water from the cells into the lumen resulting in watery diarrhea and dehydration.

91
Q

Describe the bacterium that causes cholera.

A

Vibrio cholerae causes cholera and it is curved rod shaped Gram negative bacterium (aerobic) and basic conditions .

92
Q

How do most people get cholera?

A

Eating or drinking contaminated food or water containing feces of someone who had cholera.

93
Q

Why do symptoms occur in the small intestine for cholera?

A

Any toxins that have survived the acidic conditions in the stomach, pass to the intestine which is more basic and begin to thrive and infect epithelial cells there.

94
Q

Aside from diarrhea, what are some of the other symptoms of cholera?

A

Abdominal pains, sweating, nausea and vomiting

95
Q

What is the incubation time of cholera and duration of the infection? How does this differ to salmonella?

A

Incubation time of cholera is 2-3 days and symptom duration can be up to 7 days. This differs to salmonella which has an incubation time of 6 hours to 2 days and a duration of 48 hours to 7 days.

96
Q

What are some examples of gram positive pyogenic cocci?

A

Staphylococcus aureus
Streptococcus pygenes

97
Q

What does MRSA stand for?

A

Methicillin resistant staphyloccus aureus

98
Q

How is salmonella caused?

A

Eating raw or undercooked meat
Drinking unpasteurized milk

99
Q

Describe the patho-physiological pathway of salmonella.

A

The bacterium salmonella enteriditis is indigested. The bacterium is absorbed into epithelial cells in the small intestine. The bacteria penetrates the cells and migration into the lamina propria layer causing hyperplasia and hypertrophy after the bacterium multiplies in the lymphoid follicles. This triggers an inflammatory response causing the release of prostaglandins which activate the cAMP signalling pathway aand therefore protein kinase A. Protein kinase A phosphorylates and deactivates the Na/H anti-porter which inhibits sodium re-absorption into the cell. It also opens Cl- channels, down their electrochemical gradient to the outside of the cell. Water molecules diffuse across the membrane following the net flow of the salts. Therefore the combined effect, results in a loss of sodium, chlorine, potassium and water from the cells into the lumen resulting in watery diarrhea and dehydration.

100
Q

What is Shigella dysenteriae?

A

Causes bacillary dysentery, which results in severe diarrhea. It is a rod shaped gram negative bacterium.

101
Q

Which STIs cause gential warts? Which causes genital herpes?

A

Gential warts are caused by the papillomavirus (most common STI).
Genital herpes are caused by HSV 1 and 2

102
Q

Describe the different types of chlamydia.

A

Chlamydia trachomatis, Chlamydia pneumoniae and Chlamydia psittacci are the three different sub-types of chlamydia.
Chlamydia pneumoniae and Chlamydia psittacci cause respiratory infections whereas Chlamydia trachomatis causes infections of the eyes, urogenital or pneumonia in infants with infected mothers.

103
Q

What are the different serotypes of chlamydia trachomatis?

A

Chlamydia trachomatis (D-K) sub-types infect gential tract epithelial cells resulting in pelvic inflammatory disease, etopic pregnancies.
Chlamydia trachomatis (L1-L3) causes Lymphogranuloma which within a couple of weeks of infection causes bleeding, pus and constipation from the rectum.

104
Q

Demographic affected by lymphogranuloma?

A

Rarely seen in heterosexual men and women. More common among gay and bisexual men.

105
Q

What bacterium causes syphilis?

A

Treponema pallidum

106
Q

What are some of the symptoms of syphilis in men?

A

Ulcers on the penis
Rashes on palms of the hands and soles of the feet
Hair loss
Fever
Swollen lymph glands
White or grey warty growths on penis or anus

107
Q

What is chancroid?

A

A bacterial condition caused by Haemophilus ducreyi causing open sores on or around the genitals. Most prevalent in parts of Africa or the Caribbean.

108
Q

What bacterium causes vaginitis and what symptoms does it present?

A

Vaginitis is just inflammation of the vagina causing redness or soreness. A bacterium that causes this is trichomonas vaginalis (STI) but it can be caused by other factors such as reduced estrogen levels after menopause.

109
Q

What type virus causes polio?

A

Poliovirus which is a single stranded RNA viruses.

110
Q

What are some of the potential effects of polio?

A

In 90% of infections the patient has no symptoms (they are asymptomatic).
5% of cases result in abortive poliomyelitis which causes non-febrile symptoms such as fever, headache, sore throat.
In 1-2% non-paralytic or aseptic meningitis where the virus spreads to other parts of the body.
Paralytic polio occurs 1-2 days after the first symptoms have subsided such as a fever and a headache.

111
Q

Describe how poliomyelitis paralytic polio occurs?

A

When the virus spreads to the central nervous system it can replicate and destroy motor neurons in the spinal, cord, brain stem. Spinal polio occurs due to the invasion of motor neurons in the anterior horn cells eventually leading to paralysis.

112
Q

What are the four possible outcomes of a measles infection?

A

Recovery and lifelong immunity
Post-infectious encephalitis- inflammation of the brain
Sub-acute sclerosing panencephalitis- progressive neurological disorder that can affect the CNS.
Death

113
Q

What factors can affect the outcome of a measles infection?

A

Age - children and elderly are most vulnerable to develop complications
Social history- malnourished children are more likely to develop more severe complications or for longer

114
Q

How does transmission of hepatitis A and B differ?

A

Hepatitis A transmitted by faecal-oral route (e.g drinking contaminated water)
Hepatitis B transmitted sexually or by a blood transfusion.

115
Q

Is hepatitis A a serious condition?

A

No particularly, usually self-limiting to 2 months but symptoms are unpleasant. It is an acute infection.

116
Q

What measures can be implemented to stop spread of hepatitis A?

A

Keeping child or adult off school or work until they are no longer infectious (7 days after the symptoms appear).
Promote good hygiene (hand washing and practicing safe sex).

117
Q

What are the most common symptoms of Hepatitis A?

A

Nausea, vomiting, diarrhea, fever, abdominal pain and most recognisably jaundice

118
Q

What are the different routes of transmission of hepatitis?

A

Hepatitis A and E are faecal to oral transmission.
Hepatitis B, C and D are transmitted either parentally, sexually or by the exchange of bodily fluids

119
Q

Describe the structure of Hepatitis D.

A

Negative-sense enveloped single stranded RNA virus

120
Q

Is it possible to get Hepatitis A twice?

A

No, usually immune after first infection

121
Q

Explain the immunological response of an infected hepatocyte with hepatitis.

A

As part of the viral replication of all types of hepatitis, the virus uses the host cell’s own ribosomes to synthesize its own proteins including antigens. These antigens can become presented on the infected hepatocyte’s cell surface by a MHC-1 complex. At the same time when infected a hepatocyte secretes IFN-Y which attracts macrophages. These macrophages then attract cytotoxic T cells as part of the immunological response, specifically CD 8 (+) T cells which bind to the MHC-1 complex on the antigen. If the CD 8 TCR (+) doesn’t recognise the antigen present it secretes perforin, creating pores in the infected hepatocyte before releasing granzyme which induces apotosis.

122
Q

Which type of Hepatitis viruses are single stranded RNA?

A

Type A, Type C, Type D and Type E

123
Q

What is the mechanism of Hepatitis A?

A

The virus is indigested and is carried in the blood to its target - the liver. The single strand RNA viral strand enters hepatocytes by endocytosis and sheds its coating (viral envelope and capsomeres). The virus then uses the host’s ribosomes to synthesis its own proteins such as more capsomeres (make capsids), antigens for viral surface or RNA/DNA polymerases. These are then sent to Golgi apparatus or endoplasmic reticulum for synthesis which produces the proteins enclosed in vesicles. The RNA dependent RNA polymerase uses the single strand for replication producing more of the viral RNA. This combines with the vesicles to produce the viral cell which can be released from the cell to infect other hepatocytes.

124
Q

What is a consequence of nausea and vomiting as a result of hepatitis?

A

Dehydration
Electrolyte imbalance
Weight loss (over time)

125
Q

What are the symptoms of the prodromal phase in hepatitis?

A

Fever
Nausea and vomiting
Diarrhea

126
Q

Explain how jaundice and urine discolouration occur as a result of hepatits infection?

A

Haemogloblin breakdown results in heme before further breakdown to unconjugated bilirubin. This unconjugated bilirubin is transported to hepatocytes which contain a enzyme called uridine diphospho-glucuronate glucuronosyltransferase which converts it to normal bilirubin. Due to hepatitis there is a reduced number of hepatocytes able to carry out the catalysis of the bilirubin reaction causing an increase in concentrations of unconjugated and conjugated bilirubin in the blood. This causes a deposition of the bilirubin in the sclera tissue in the eye and epithelial tissue in the palms of hands and soles of feet causing a discolouration to a yellow colour (jaundice). Furthermore the kidney is responsible for excreting conjugated bilirubin. An increased concentration of serum conjugated bilirubin causes an increase in secretion resulting in urine discolouration (darker).

127
Q

What is a result of decreased billary production?

A

A decreased bile secretion from the liver results in a decreased bilirubin concentration in the intestines. This means there is less bacteria breaking down the bilirubin into urobiliergen and then less stercobillan. Sterocobillan causes the brown pigmentation of feces so it can result in clay coloured stools.

128
Q

What are the eneteric phase symptoms of hepatitis?

A

Jaundice
Urine discolouration
Clay coloured stools
Liver inflammation (hepatomegaly) resulting in right upper quadrant abdominal pain

129
Q

Describe the process when hepato-toxins build up.

A

When the liver is infected with hepatitis, hepato-toxins build up and enter the bloodstream travelling to the CNS specifically the brain. In the brain the bind to receptors on the chemo trigger zone activating it. Upon activation it then stimulates the emetic centre causing reteroparesaultic action in the GI system, causing nausea and vomiting and diarrhea.

130
Q

How can hepatitis B and C affect other organs?

A

Plasma cells produce antibodies which form complexes with the antigen presenting infected cells. These can be deposited in the tissue such as blood vessels (vasculitis) , myo or paracardiam of the heart (myocarditis or paracarditis), cyanovial joints (arthritis), globelum basement membrane (kidney).

131
Q

What other substances do the hepatitis antigens bind to?

A

Platlets (thrombocytopenia)
Red blood cells (hemolytic anaemia)
Neutrophils (Neutropenia)
Increase lymocytes

132
Q

Describe the convolescent phase of hepatitis.

A

Decrease in symptoms, back to normal. However B and C causes extra hepatic manifestations (affecting other organs and immunological mediators).

133
Q

Explain how fever is caused as a result of a hepatitis infection?

A

Infected hepatocytes releases cytokines such as IL-1, IL-6 and TNF-alpha. These enter the bloodstream and migrate to the CNS. The mediators trigger a prostaglandin response by the production of Prostaglandin E2 and Prostaglandin F2 which affects the hypothalmic thermostat causing fever.

134
Q

What other enzymes are released as a result of liver failure? (enteric phase)

A

Alanine transaminase
Aspartate transaminase
Clotting proteins
GGT
ACP

135
Q

What symptom of hepatitis A is less commonly seen in children?

A

Only 10% of children infected with hepatitis A experience jaundice but it is much more commonly seen in adults (70-80%).

136
Q

Describe the downstream effect of hepatitis A in the body.

A

HAV is ingested and enters the bloodstream through the oropharynx or the epithelial
lining of the intestines
* target cells are parenchymal cells in the liver
* virus replicates in hepatocytes and Kupffer’s cells
* virus is produced in these cells and released into the bile and from there into stool
* virus is shed into stool

137
Q

What food is commonly associated with hepatitis A infection?

A

Shellfish

138
Q

What is the incubation period of Hepatitis A?

A

10-14 days before symptoms appear

139
Q

What type of virus is Hepatitis B?

A

Double stranded DNA virus

140
Q

What are some of the complications arising from a Hepatitis B infection?

A

Cirrhosis (liver scarring)
Liver damage

141
Q

How is Hepatitis B transmitted?

A

Mother to baby transmission
Sexual activity
Exchange of needles
Exchange of bodily fluids including blood, saliva, or seminal, menstrual and vaginal fluid

142
Q

What some of the symptoms of hepatitis B?

A

Urine discolouration
Fatigue
Jaundice
Abdominal pain
Nausea
Vomiting

143
Q

How does viral replication occur in Hepatitis B?

A

The viral partially double stranded DNA cell binds to the receptor on the surface of the hepatocyte before it is endocytosed into the cell. The virus then undergoes uncoating causing the release of antigens. The virus then enters the nucleus and DNA repair enzymes complete the double strand. RNA polymerase transcribes the DNA to two types of RNA. Viral mRNA uses the host cells ribsomes to synthesise its own proteins including RNA/DNA polymerases, antigens and capsomeres. All are sent to the golgi apparatus where the enzymes are enclosed in vesicles. The other type of mRNA (pre-genomic RNA) has reverse transcriptase which converts the RNA back into the partially stranded DNA. The RNA and vesicles containing enzymes combine forming the virus so it can infect other cells. The partially stranded DNA is then incorporated into the host cell genome. The virus uses DNA polymerase to amplify and uses RNA polymerase to make even more proteins and more pre-genomic RNA is produced causing more reverse transcriptase and the viral cell lifestyle continues.

144
Q

What cells are involved in the cell mediated response of hepatitis B?

A

Cytotoxic T lymphocytes bind to MHC (anitgen presenting cells). Abolish viral replication in the liver.

145
Q

Which two cytokines mediate the CD8+ T-cells?

A

IFN-Y and TNF

146
Q

What are the percentage outcomes of Hepatitis C?

A

15% have a complete recovery
15% have a rapid onset of cirrhosis
Remaining 70% have a persistent infection

147
Q

What is the outcome of hepatocyte apotosis?

A

Fibrosis tissue formation
Regeneration of hepatocytes (mitosis)

148
Q

What are the additional symptoms of a chronic hepatitis B or C infection?

A

Increase in fibrosis which can result in cirrosis (liver scarring) and increase in mitosis causes cellular dysplasia increases risk of cellular carcinoma.

149
Q

What are some of the symptoms of Hepatitis C?

A

Muscle aches
Fever
Feeling tired all the time
Loss of appetite
Stomach ache
Nausea and vomiting

150
Q

When do the symptoms of Hepatitis C usually appear?

A

When there has already been significant liver damage

151
Q

Which types of influenza virus causes disease in humans?

A

Influenza virus types A and B

152
Q

What type of virus is the influenza virus?

A

Virus is enveloped and has a segmented negative-sense RNA genome

153
Q

How is the influenza virus spread?

A

Via airborne droplets from breathing, sneezing and coughing

154
Q

What are the two types of influenza mutation?

A

Antigenic drift and antigenic shift.

155
Q

Explain how the influenza virus undergoes seasonal mutation?

A

The influenza virus undergoes seasonal mutation via antigenic drift. This occurs when the negative sense RNA produces its own RNA dependent RNA polymerase. It causes point mutations to occur in the hemagglutinin and neuraminidase which changes the glycoprotein expression on the cell surface, which makes the virus unrecognisable to previous strains of antibodies.

156
Q

Explain the process of mutations in the influenza virus which causes widespread pandemics.

A

It occurs when the influenza strain undergoes antigenic shift. Occurs when an organism is infected with two different influenza viral strains. The eight gene segements from each strain undegoes reassortment, where different hemagglutinin and neuraminidase are combined and then expressed on the surface as glycoproteins making a new strain of influenza.

157
Q

What is the key functional difference between hemagglutinin and neuraminidase?

A

The functional difference between hemagglutinin and neuraminidase is that hemagglutinin binds with cell surface sialic acid on target cells to facilitate viral attachment to host cells while neuraminidase cleaves sialic acid from viral receptors (glycoproteins) to release the progeny viruses from the host cells.

158
Q

What is the structure of hemagglutinin?

A

Hemagglutinin forms a H shaped trimer

159
Q

What is the structure of neurominidase?

A

Forms a tetramer

160
Q

How is influenza usually diagnosed?

A

Normally based on symptoms in addition to the season and spread of the virus in the community (are other patients developing symptoms).

161
Q

What are the two diagnostic tests for influenza?

A

Rapid antigen assay which can detect influenza A or B
Reverse transcriptase PCR can detect and distinguish between Influenza types A and B

162
Q

What are the key differences between symptoms of influenza and of the common cold?

A

A fever is usually present in influenza whereas it is less likely in the common cold.
Usually get a severe headache and chest pain with influenza normally more mild with the common cold.
Do not normally get a stuffy nose, sore throat or sneezing with influenza.

163
Q

What is the incubation period of rhinoviruses?

A

8-10 hours

164
Q

What is the second cause of the common cold?

A

Coronavirus

165
Q

What is the incubation period of coronavirus?

A

3 days

166
Q

Why do you experience less common colds as you get older?

A

There are more than 100 serotypes of the rhinovirus and coronavirus, each one has specific antigens and therefore antibodies that develop. By the time you have reached middle-aged/elderly you have been exposed to/ developed antibodies for so many of the viruses that you are immune due to prior antibody development.

167
Q

How is coronavirus spread?

A

Large droplets and aerosols

168
Q

What were some of the symptoms of the SARS 2003 endemic?

A

Symptoms of atypical pneumonia such as fever, chills, rigors and breathing difficulties

169
Q

Explain the concept of zoonosis.

A

Any disease which can be transmitted from animals to humans

170
Q

What are the four transmission mechanisms of zoonosis?

A

Through feces
Through bites or scratches
Through contact
Through vector carrying pathogens

171
Q

What is the Marburg virus?

A

It is a severe hemorrhagic fever virus causing fever and hemorrhage. Belongs to the same family as the Ebola viruses.

172
Q

How is the Marburg virus transmitted?

A

Transmitted by exposure to fruit bats and from human to human by the exchange of bodily fluids either through sex or by broken skin.

173
Q

What type of viruses are Ebola and Marburg viruses?

A

Filamentous, enveloped, negative-strand RNA viruses

174
Q

What is the incubation period of Ebola?

A

2 to 21 days

175
Q

What are the initial symptoms of Ebola virus?

A

High temperature
Fever
Sweating
Nausea
Vomiting
Severe weakness/ exhaustion
Sore throat
Dizziness

176
Q

What happens in late stage Ebola?

A

Internal bleeding so internal bleeding from every opening in the body. This can cause:
Low blood pressure
Fast but weak pulse
Organ damage
Proteinuria (proteins in urine)

177
Q

What are retroviruses?

A

Enveloped, positive-strand RNA genome

178
Q

When do the symptoms of Hepatitis C usually appear?

A

When there has already been significant liver damage

179
Q

When do the symptoms of Hepatitis C usually appear?

A

When there has already been significant liver damage

180
Q

What type of virus is HIV?

A

Retrovirus

181
Q

What cells does HIV target?

A

CD 4 positive cells such as:
Macrophages
Monocytes
T-lymphocytes
Dendritic cells

182
Q

How is HIV transmitted?

A

Either by sexual intercourse, parentally or by vertical transmission

183
Q

Describe the gene structure of HIV.

A

Three of the 9 genes that encode HIV include:
GAG, Pol and ENV.

GAG contains the core proteins such as nucleic acids, group specific antigen, capsid (all the core proteins).

Pol: (enzymes) polymerase, protease, integrase

ENV: contains the envelope glycoproteins.

Either side of the genes there are long terminal repeats containing oncogenes, promoter genes, enhancers

184
Q

What are the 8 broad steps of HIV replication inside a cell?

A

Attachment
Fusion
Reverse transcriptase
Integration
Transcription
Translation
Assembly and release
Maturation

185
Q

Describe the viral envelope.

A

The outermost layer of the virus and protects its genetic material. Composed of a lipid bilayer with glycoprotein spikes.

186
Q

What are the responsibilities of glycoprotein gp120 and gp41?

A

gp120 is a glycoprotein on the HIV envelope that interacts with the CD4 complex on host cells and the co-receptor CCR5 or CXCR4 which causes the fusing of the two membranes.
gp41 causes the fusing of the envelope with the cell wall.

187
Q

Once the HIV virus has entered the cell what happens next?

A

HIV sheds its envelope and uses its own reverse transcriptase to convert RNA to pro viral DNA.

188
Q

What enzyme is responsible for inserting the pro-viral DNA into the host cell’s DNA?

A

Intergrase, it attaches to the end of the pro viral DNA stand and carries it to the nucleus where it inserts it into the host strand.

189
Q

Once the virus has been inserted into the host DNA what are the two possible following possibilities?

A

Either uses the host cell machinery to replicate or
Remains dormant

190
Q

When does transcription occur?

A

Once the infected cell becomes active

191
Q

What happens in the transcription step?

A

The HIV uses the host cell RNA polymerase to read off the gene producing two types of mRNA.
Viral mRNA and pre-genomic mRNA.

192
Q

What is the function of viral mRNA?

A

Uses the host ribosomes to synthesise proteins such as capsomeres, antigens and RNA/DNA polymerase. All are sent to the golgi where they are then encased in vesicles.

193
Q

What is the function of pre-genomic mRNA in HIV?

A

It makes reverse transcriptase which converts the RNA back into the HIV DNA.

194
Q

How does the HIV virus leave the cell?

A

Pushes through the cell wall and encases itself with the viral envelope, taking glycoprotein spikes as well.

195
Q

Describe the maturation step in HIV replication.

A

The viral HIV protease cleaves the precusors forming the final HIV viral structure

196
Q

What is the immunological response of HIV?

A

Some dendritic phagocytose the antigen and present it on its cell surface with a MHC-2 complex. These migrate to the lymph nodes and are presented to CD 4 positive cells. The CD 4 complex reacts with the MHC-2 complex and the antigen reacts with the TCR. This causes activation of B-cells (plasma cells) which produces antibodies and CD 8 cells which when bind to the CD4 MHC-2 complex induce a apotosis mechanism through perfornin and granzyme.

197
Q

What occurs in an acute HIV infection?

A

Increase in viral load
HIV p24 antibody detected
CD8 activation
Seroconversion

198
Q

How does the HIV for mutations?

A

Downregulate MHC-2 expression causing the infected CD 4 cells to become unrecognisable.

199
Q

Describe the asymptomatic phase of HIV infection.

A

Can be asymptomatic for about 10 years. HIV remains dormant and reduces the CD 4 count slowly. The viral load remains constant due to CD 8 (+).

200
Q

When does HIV become symptomatic again?

A

When the CD 4 count drops below 200 per ml3, then at risk of AIDS and getting opportunistic infections.

201
Q

What are some of the anti-retroviral targets of HIV?

A

Protease inhibitors
Entry inhibitors
Reverse transcriptase inhibitors
CCR5 and CXCR4 inhibitors

202
Q

How can you detect HIV?

A

Using a combination assay.
Firstly test for p24. If positive, they are HIV positive and then you can complete additional tests to determine whether they are HIV 1 or 2 positive.
Then if they are negative test for their viral load, if positive they are HIV positive if negative then they do not have HIV.

203
Q

How does the discharge differ for certain infections?

A

Watery, grey, fishy smelling discharge- Bacterial vagnosis
Yellow/green foul smelling- Trichmonas vaginitis
Cottage cheese texture, no smell- Thrush
Pus, mucus, milky, can be yellow and a bit smelly- Chlamydia

204
Q

What is the recommended treatment for bacterial vagnosis and trichomonas vaginitis?

A

Prescribe oral Metronidazole 400–500 mg twice a day for 5–7 days, or Metronidazole 2 g as a single oral dose

205
Q

What are the two types of enteric bacterium and describe the shape of the bacterium?

A

E coli and Shigella dysenteriae

Both are gram negative rod shaped and anaerobic shape of metabolism

206
Q

What are some of the advantages of using RNA vaccines?

A

RNA viruses mutate very quickly due to inability of the RNA polymerases to proof read during transcription unlike DNA polymerases. Therefore the same can be replicated for the vaccines to respond to mutations in the virus.

207
Q

How do RNA vaccines work?

A

They work by injecting a patient with mRNA strand which inside the body encodes for a specific viral antigen. Inside the body they stimulate the innate immune system. Normally given in vehicles with lipid nanoparticles.