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phase 2 medicine > Microbio > Flashcards

Microbio Flashcards

1
Q

Define pathogen

A

Organism that causes or is capable of causing disease

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2
Q

Commensal

A

Organism which colonises the host but causes no disease in normal circumstances

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3
Q

Opportunist Pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

Virulence definition

A

The degree to which a given organism is pathogenic

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5
Q

Asymptomatic carriage

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease

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6
Q

what color do gram-positive vs gram negative bacteria stain

A

+ve - purple
-ve - red

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7
Q

gram +ve vs gram -ve

A

+ve
thick peptidoglycan membrane
stains purple
single membrane

-ve
thin peptidoglycan membrane
have capsule
stains red
double membrane
endotoxin secretion from lipopolysaccharide layer

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8
Q

endotoxin vs exotoxins in bacteria

A

ENDOTOXIN
Component of the outer membrane of bacteria, eg lipopolysaccharide in Gram negative bacteria
released when the bacterial cells lyse

EXOTOXIN
Actively secreted proteins of Gram positive and Gram negative bacteria

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9
Q

what is bacterial conjugation

A

how bacteria swap genetic material

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10
Q

what factors give bacteria genetic variation

A

1) Mutation
Base substitution
Deletion
Insertion
2) Gene transfer
Transformation eg via plasmid
Transduction eg via phage
Conjugation eg via sex pilus

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11
Q

What is coagulase

A

enzyme produced by bacteria that clots blood plasma. Fibrin clot formation around bacteria may protect from phagocytosis.

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12
Q

how do coagulase +ve staphylococci protect themselves from phagocytosis

A

Fibrin clot formation around bacteria may protect from phagocytosis.

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13
Q

what is the normal habitat of staphylococci

A

Nose and skin

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14
Q

outline how staphylococcus aureus spreads, it’s virulence factors, what it is resistant to, and whether it is gram +ve/-ve

A

Spread by aerosol and touch
carriers & shedders (can infect wounds) - some people are specific carriers of staph aureus on skin

Virulence factors

Pore-forming toxins (some strains)
Proteases
Toxic Shock Syndrome toxin (stimulates cytokine release)
Protein A (surface protein which binds Ig’s in wrong orientation)

MRSA (Methicillin-resistant Staphylococcus aureus) – resistant to
beta-lactams
gentamicin, erythromycin,
tetracycline

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15
Q

name two coagulase-negative streptococci

A

S.epidermidis and S.saprophyticus

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16
Q

what kind of infections is S.epidermidis good at and what is its virulence factor

A

Infections in debilitated, prostheses (opportunistic)
Main virulence factor - ability to form persistent biofilms

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17
Q

what kind of infection is S. saprophytic good at and what is its virulence factor

A

common in UTI
Acute cystitis –> infection of the bladder
has hemagglutinin for adhesion and produces urease to neutralise acidic environment for bladder

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18
Q

how do the streptococci clum up compared to the staphylococci

A

streptococci form chains
staphylococci form clumps

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19
Q

what are the 3 haemolytic groups of streptococci and how do you tell them apart

A

alpha - haemolytic –> you get greening

beta-haemolytic –> You get transparent rim around colony

non-haemolytic –> no lysis

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20
Q

what is sero-grouping and what is the name of the test used

A

used in beta-haemolytic groups to tell apart bacteria based on their antigens
test used: Lancefield A-H and K-V

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21
Q

What are the group A and group B beta-haemolytic species?

A

S. pyogenes and S. algalactiae

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22
Q

what is the optochin test

A

used to differentiate between S pneumoniae and Viridas strep in alpha-haemolytic streptococci groups

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23
Q

name two gram-positive cocci

A

streptococcus and staphylococcus

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24
Q

what problems do the viridans group of bacteria cause

A

infective endocarditis
deep organ abscesses

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25
Q

name a gram-positive bacilli

A

listeria monocytogenes, clostridium, corynebacterium

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26
Q

What test could be done to distinguish between different streptococci?

A

Blood agar haemolysis.

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27
Q

give an example of gamma haemolysis bacteria

A

streptococcus bovis

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28
Q

give examples of gram-negative bacilli

A

Salmonella, Helicobacter, Vibrio, E. coli

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29
Q

What is the difference between enteropathogenic, enterohaemorrhagic, and enteroinvasive e.coli infection?

A

EP - Chronic watery diarrhoea; invasion of cells in the small intestine
EH - Bloody diarrhoea respectively
EI - Watery diarrhoea due to invasion of cells in the large intestine

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30
Q

what is the difference between Shigella and E. coli?

name what gram shigella is and what type

A

they both cause similar manifestations of diseases (watery diarrhoea, fever, pain in straining) but the toxin released is different to the ecoli toxins –> Shiga toxin

gram negative bacilli

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31
Q

what allows shigella and e.coli to pass through the GI tract and infect a person

A

they are acid tolerant –> can pass through the stomach

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32
Q

what bacteria is responsible for salmonellosis

A

s. enterica

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33
Q

what are the 3 types of infections caused by S. enterica

A

Gastroenteritis/enterocolitis –> cause of food poisoning
Enteric fever/ typhoid fever
Bacteraemia

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34
Q

Why is vibrio cholerae so dangerous?

A

You’re losing huge amounts of water which can result in hypovolemic shock and severe dehydration, which can lead to death.

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35
Q

how do you test for mycobacteria and what part of the bacterial tree are they from

A

Zieehl-Neelsen stain test and they are bacilli

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36
Q

what causes TB

A

mycobacterium tuberculosis

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37
Q

virulence of TB

A

Thick lipid rich cell wall making immune cell killing and penetration of drugs challenging
SLOW growth
Gradual onset of disease
Takes much longer to diagnose
Takes longer to treat

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38
Q

how is TB transmitted?

A

aerosol transmission

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39
Q

explain the pathophysiology of TB in its 3 steps

A

Primary tuberculosis
aerosol transmission
initial contact with alveolar macrophages
Bacilli taken in lymphatics
to hilar lymph
nodes

Latent TB
Cell mediated immune (CMI) response from T-cells but symptoms not present yet

Pulmonary TB
Granulomas forms around bacilli that have settled in apex
In apex of lung there
Is more air and less blood supply (fewer defending white cells to fight) –> TB spreads in lungs causing lesions

TB can spread to other places (pleura, bones, genital system, meningitis)

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40
Q

how does our body defend itself from mycobacteria?

A

Mycobacteria are phagocytosed by macrophages and trafficked to a phagolysosome to be killed

however, mycobacteria are able to withstand macrophage killing and can escape into the cytosol of the macrophage where they can chill

the most effective way to kill macrophages is via T-cell and mycobacteria interaction
requires CD4 T-cells which generate INF-y and this helps activate intracellular killing by macrophages.

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41
Q

how does TB stay in the body and when does it manifest

A

The mycobacteria form a granuloma and they stay dormant if our immune system is strong and fighting.
Macrophages and type 1 helper T lymphocytes (Th1) are capable of synthesising IFN-γ and other cytokines such as TNFα to maintaining granuloma and keep it stable.
When you are immuno-compromised then granuloma turns into a cavity full of live mycobacteria and starts leads to disseminated disease –> 2 hit hypothesis

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42
Q

How do you detect TB

A

Nucleic acid detection

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43
Q

what is the tuberculin skin test?

A

called Mantoux

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44
Q

define a virus

A

An infectious intracellular parasite, totally dependent on its host cell for replication and existence

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45
Q

what is the genetic material in viruses surrounded by

A

protein coat

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46
Q

virus vs bacteria

A

virus
dependant on host cell
NO:
cell wall
organelles
DNA and RNA
alive

bacteria:
NOT dependent on host cell
HAVE:
cell wall
organelles
DNA and RNA
alive

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47
Q

different shapes of viruses

A

Helical
Icosahedral
Complex

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48
Q

what are the stages of virus replication?

A
  1. attachment to receptor on host cell
  2. cell entry –> Uncoating of virion within cell
  3. HOST CELL INTERACTION + REPLICATION –> involves migration of genome to nucleus of host cell
  4. assembly of virion –> all of the replicated viral particles will reassemble to a new virus
  5. release of new virus via exocytosis –> results in host cell death
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49
Q

how do viruses cause disease and give examples for each way

A

a) Direct destruction of host cells
ex.: poliovirus

b) Modification of host cell
ex.: rotavirus –> atrophies villi and flattens epithelial cells so you have less absorption of nutrients in small intestine –> hyperosmotic state and diarrhoea

c) “Over-reactivity” of immune system
ex.: Hep B, Sars-CoV-2

d) Damage through cell proliferation
ex.: HPV –> leads to expression of oncoproteins and neoplasia –> cancer

e) Evasion of host defences –> there are a couple different mechanisms
ex.: herpesviridae, varicella zoster virus
1- latency (lies dormant and later reactivated)
2- cell to cell spread –> avoids immune system
3 - ability to change surface antigens to evade host’s immune system –> you can be reinfected all the time (ex.: the common cold)
4- prevention of host cell apoptosis –> by preventing apoptosis this allows the cell to continue replicating the virus –> more virus produced before release
5- down regulation of interferons and other host defence proteins
6- interfering with host cell antigen processing –> doesn’t let it display antigen on surface

many viruses use more than one method of causing disease

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50
Q

define meningitis

A

inflammation of the meninges (membranes) which cover the brain and spinal cord

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51
Q

what are the layers of the meninges

A

dura mater
arachnoid mater
pia mater

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52
Q

what are causes of meningitis

A

Bacteria
e.g. meningococcus, pneumococcus

Viruses
e.g. coxsackievirus, echovirus, herpes virus, mumps virus, influenza, HIV etc

Less common infective causes like fungi, protozoa, and other parasites.

Non-infectious causes:
Medications e.g. antibiotics (amoxicillin, trimethoprim/sulfamethoxazole), carbamazepine, lamotrigine, NSAIDs, ranitidine

Cancers e.g. melanoma, lung cancer, breast cancer, lymphoma, leukaemia

Autoimmune disease e.g. Systemic lupus erythematosus (SLE), Behçet’s syndrome.

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53
Q

define protozoa

A

one-celled organisms (animals). But they are bigger than bacteria and contain a nucleus and other cell structures, making them more like animal cells.

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54
Q

what causes invasive meningococcal disease and is the most common BACTERIAL cause of meningitis

A

Infection with Neisseria meningitidis

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55
Q

what are the characteristics of Neisseria meningitis, how is it transmitted, and how does it manifest?

A

Gram-negative diplococci
Transmission by respiratory droplets/ naso-pharyngeal secretions –> requires FREQUENT and PROLONGED contact
manifests as Meningitis or Septicaemia

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56
Q

How many serogroups of Neisseria meningitis are vaccine-preventable

A

5

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57
Q

what are risk factors of meningitis?

A

Extremes of age
Immunocompromised (e.g. HIV) or immunosuppressed (e.g. chemotherapy)
Asplenia/hyposplenia
Cancer – people with leukaemia and lymphoma
Sickle cell disease
Organ dysfunction – e.g. liver or kidney disease
Cranial anatomical defects
Cochlear implants –> breaching of one of the bodily defences
Contiguous infection - e.g. otitis media, sinusitis, mastoiditis, pneumonia
Smokers
Living in overcrowded households, college dormitories or military barracks
People who have had contact with a case
Travellers abroad to high risk area - increased risk of encountering the pathogen

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58
Q

Meningococcal meningitis symptoms

A

fever
stiff neck
headache
confusion
increased sensitivity to light
nausea and vomiting

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59
Q

Symptoms of any septicaemia

A

Fever and chills
Fatigue
Vomiting
Cold hands and feet
Severe aches or pain in the muscles, joints, chest, or abdomen
Rapid breathing
Diarrhoea
Non blanching rash (petechiae)
In the later stages, a dark purple rash (purpura)

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60
Q

what is Brudzinski’s neck sign

A

In simple terms, Brudzinski’s sign is when a person lying on their back involuntarily bends their knees and hips when their neck is gently bent forward by a doctor. This reflex movement happens because the protective membranes around the brain are irritated, causing the person’s body to respond by bending their legs to relieve the discomfort.

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61
Q

what are petechiae

A

the rash that is due to sepsis (does NOT FADE when you press on it) –> they are micro-clots that appear everywhere on skin because the body is bleeding randomly

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62
Q

Name and explain two results of sepsis

A

Purpura and DIC

Sepsis can cause Disseminated Intravascular Coagulation (DIC) – the activation of coagulation pathways that results in formation of intravascular thrombi (clots) and depletion of platelets and coagulation factors.
These clots can cause arterial occlusions leading to gangrene of extremities & auto-amputations (spontaneous detachment of an appendage from the body)

Purpura is a worse version of petechiae –> main difference is bigger red spots

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63
Q

how do you diagnose meningitis

A

Blood sample for blood culture & PCR
Cerebrospinal fluid (CSF) for microscopy, culture and PCR

For other localised infections, aspirate from a sterile site (e.g. joints) for microscopy, culture, PCR

Throat swab for culture - provides important information about the infecting strain

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64
Q

what is chemoprophylaxis for meningitis

A

Antibiotics given to eradicate throat carriage

Ciprofloxacin (recommended for all age groups and in pregnancy)
single dose
doesn’t interact with oral contraceptives
readily available

Rifampicin (alternative)

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65
Q

does chemoprophylaxis stop infection

A

No!!!! It stops spread!

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66
Q

define virions

A

Viruses that have not yet infected a cell and live without a current host

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67
Q

define toxoid

A

a chemically modified toxin from a pathogenic microorganism, which is no longer toxic but is still antigenic and can be used as a vaccine.

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68
Q

what is typhoid fever and what is it caused by

A

disease caused by insect bites which have been infected with typhoid bacteria
leads to severe fever and systemic disease

insect examples: lice, fleas, mites (capusa)

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69
Q

what causes tetanus and how does it manifest

A

caused by Clostridium tetani which produces a toxin which affects the NS

Symptoms:
muscle stiffness and spasms, particularly in the jaw muscles (resulting in “lockjaw”), neck, and abdominal muscles. It can lead to severe muscle rigidity and difficulty breathing

THERE IS NO CURE IT SUCKS

70
Q

what are the sterile sites in the body?

A

blood
csf
joints
bladder
lower resp tract
pleural fluid
peritoneal cavity

71
Q

what are the non-sterile sites of the body

A

GI
skin
oral cavity
vagina
urethra

72
Q

what is the classification of S pneumoniae?

A

alpha haemolytic streptococcus

73
Q

what bacteria is optochin resistant

A

viridans

74
Q

which is the least selective agar

A

blood agar

75
Q

what is diphtheria and what causes it (include genus and type)

A

it is a bacterial infection which manifests as a cold but can get very aggressive –> vaccinated against at 8 weeks
caused by Corynebacterium Diphtirae –> gram +ve aerobic bacilli

76
Q

what is pertussis

A

whooping cough

77
Q

what are the 2 types of fungi

A

yeast and moulds

78
Q

Yeast vs. Mould

A

Yeasts are small single celled organisms that divide by budding
Account for <1% of fungal species but include several highly medically relevant ones
Moulds form multicellular hyphae and spores

79
Q

why are there few fungi which cause infections

A

most fungi are unable to grow at 37 degrees

80
Q

what does the plasma membrane in fungi contain

A

ergosterol

81
Q

what do you call fungi which exist as both yeasts and moulds

A

dimorphic fungi

82
Q

how do dimorphic fungi behave at different temperatures

A

Mould at ambient temperature (25-30 degrees)

Convert to yeast form at 37 degrees

83
Q

what is the most common fungal infection

A

candida albicans

84
Q

what is invasive candidiasis most commonly caused by

A

infection of prosthetic devices in intra-abdominal disease

85
Q

what is a medicine to treat fungal infections

A

fluconazole

86
Q

name two different strains of fungi

A

candida and aspergillus

87
Q

what is the biggest risk factor for fungal infections

A

immunosuppression

88
Q

what are the 5 major groups of protozoa

A

Flagellates
Amoebae
Sporozoans
Ciliates
Microsporidia

89
Q

what are the two main symptoms of malaria

A

fever and haemolysis

90
Q

what are the consequences of malaria

A

Anaemia
Jaundice
Hepatosplenomegaly –> enlarged liver AND spleen
Haematoglobinurea –> due to haemolysis

91
Q

what is thrombocytopenia

A

decreased platelets in the blood

92
Q

what is aciclovir

A

Anti-herpesvirus drug

93
Q

what is the aciclovir method of action

A

Pro-drug when activated gets 3 phosphates
Aciclovir triphosphate competitively inhibits herpesvirus specific DNA polymerases

94
Q

what are the 2 types of herpes infection

A

HSV1 and HSV2

95
Q

what are different types of herpes infections

A

genital herpes, oral herpes, chickenpox/shingles

96
Q

how does shingles happen and what causes it

A

primary chicken pox infection
virus stays dormant in the DRG
Reactivation leads to dermatomal shingles

caused by Herpes Zoster virus

97
Q

what is rituximab

A

a type of targeted cancer drug called a monoclonal antibody

98
Q

measles symptoms

A

high fever
morbilliform rash
koplik spots
cough
diarrhoea
conjunctivitis

99
Q

what is an antibiotic

A

Antibiotics are molecules produced by a micro-organism that work by binding a target site on a bacteria

100
Q

what do you use to treat staph aureus

A

flucloxacillin

101
Q

what are HIV transmission routes

A

Blood
Sexual
Vertical

102
Q

what is the likelihood that if you are untreated HIV positive and pregnant you give the baby HIV

A

30%

103
Q

can HIV-positive mothers have natural delivery?

A

yes; with retroviral therapy 2% chance of transmission (very small)

104
Q

when are HIV PrEP most effective?

A

PrEP = pre-exposure prophylaxis
before sexual intercourse

105
Q

what are risk factors for HIV

A

High-risk behaviours
Sexual contact with people from high prevalence groups – MSM, sub-Saharan African/ Thailand
Multiple sexual partners
Rape in high-prevalence localities

106
Q

symptoms of HIV

A

Acute generalized rash
Glandular fever
Indicators of immune dysfunction
Unexplained weight loss or night sweats
Recurrent bacterial infections including pneumococcal pneumonia

107
Q

if a person has undetectable levels of HIV virus and they are HIV positive can they still pass the virus through sex

A

NO

108
Q

what are the examples of HIV PrEP

A

Truvada and Descovy

109
Q

what is vertical transmission

A

from mother to child in uterus

110
Q

how can HIV PrEP be administered

A

pill or injection

111
Q

what is PEP and how does it compare in effectiveness compared to PrEP

A

PEP = post-exposure prophylaxis
it is not as effective as PrEP

112
Q

what is the fastest HIV-detecting test and what are it’s advantages and disadvantages

A

HIV POCT - finger prick blood test
Advantages
Immediate result
Outreach to community settings
Increased patient testing
Earlier diagnosis in unaware individuals

Disadvantages
Lower sensitivity and specificity –> change of false positives or false negatives

113
Q

how do you manage a negative and positive HIV POCT pin prick test

A

Negative –> you repeat it within a window period

Positive –> you phone sexual health for advice, explain that the test is REACTIVE, NOT POSITIVE, and that further investigations are needed

114
Q

Which are the more accurate HIV tests

A

venous blood sample tested for p24 antigen

115
Q

what cells does HIV infect

A

CD4 cells

116
Q

what group of viruses is HIV from and what type of virus is it

A

family = lentivirus
type of virus = retrovirus

117
Q

what enzyme does HIV use to replicate

A

reverse transcriptase

118
Q

what are the 2 markers used to monitor HIV infection

A

CD4 cell count
HIV viral load

119
Q

when do HIV symptoms start

A

2-4 weeks of infection

120
Q

what do you have to ask a patient with fever, rash and non-specific symptoms

A

Ask about sexual history
Think of HIV seroconversion

121
Q

how long can the period of HIV clinical latency last and what is it

A

5-7 years
it is the period after primary infection where you do not have many symptoms because your immune system can cope with the infection

122
Q

when should you do an HIV test

A

when faced with a common problem:
In an unexpected patient
That is recurring
That has no clear underlying cause

123
Q

what defines a state of AIDS in terms of CD4 count

A

CD4 < 200

124
Q

what is pneumocystis pneumonia and what are the symptoms and how do you treat it?

A

fungal infection of lungs which results in inflammation of alveoli

associated with late stage of HIV

symptoms:
Fevers, SOB (shortness of breath), dry cough, pleuritic chest pain,exertional drop in oxygen saturations on movement

treatment: Co-trimoxazole
combined antibiotic and antifungal

125
Q

what is the most common opportunistic infection

A

PCP - pneumocystis pneumonia

126
Q

what are possible opportunistic diseases which can take control of you when you have HIV

A

TB
Kaposi’s sarcoma
Shingles
fungal infections
viral associated cancers
recurrent pneumonia
Oral candidosis
PCP - pneumocystis pneumonia
CNS lymphoma –> due to reactivation of EBV
different variations of CMV infections; most commonly CMV renitis

127
Q

what test for another disease do you need to do if you have TB

A

HIV

128
Q

what causes Kaposi’s sarcoma and how does it manifest

A

Human Herpes Virus 8
manifests as single or multiple lesions on the skin

129
Q

how do you treat HIV after diagnosis?

A

HAART - Highly Active Anti-Retroviral Therapy
involves the use of 3+ antiretroviral drugs to attack different points of the replication cycle of HIV

130
Q

what are the HIV drug classes

A

HIV enters the CD4 cell by binding to the CD4 molecule and a co-receptor (CCR5 or CXCR4)

Two classes of drugs stop the virus entering the cell
- entry inhibitors
- fusion inhibitors

After HIV enters the cell, it uses reverse transcriptase to transform from RNA to DNA.

ARVs which inhibit reverse transcriptase:
- NRTIs: Nucleoside reverse transcriptase inhibitors (-dines and -bines)
-NNRTIs: Non-nucleoside reverse transcriptase inhibitors.

The viral DNA then uses integrase to integrate its genome into the host cell’s DNA. This gives us another opportunity to block HIV replication with…
- Integrase inhibitors “INSTIs”

After hijacking the nuclear DNA, the RNA product then uses protease to exit the CD4 cell.

  • Protease inhibitors block HIV proteases to prevent HIV from becoming a mature virion
131
Q

how does HIV develop drug resistance?

A

1)
1 mutation every 2 new viruses –> natural selection
that is why we need to prescribe at least 3 drugs at a time

2)
non-adherence

3)
drug-drug interactions

132
Q

What are the repercussions of HIV prescription non-adherence

A

Missing one or two doses with some regimes can cause resistance, as copying can occur and then spontaneous drug resistance mutations can occur
Excellent adherence prevents relapses and resistance

133
Q

what are the steps of HIV CD4 infection

A

HIV enters the CD4 cell by binding to the CD4 molecule and a co-receptor (CCR5 or CXCR4)

After HIV enters the cell, it uses reverse transcriptase to transform from RNA to DNA.

The viral DNA then uses integrase to integrate its genome into the host cell’s DNA.

After hijacking the nuclear DNA, the RNA product then uses protease to exit the CD4 cell –> bursts out

134
Q

what is cytomegalovirus (CMV)

A

herpes virus, which causes a glandular fever-type illness in the immunocompetent individual.

135
Q

When should you do a lumbar puncture in someone diagnosed with HIV

A

EVEN IF YOU HAVE THE SMALLEST SUSPICION OF MENINGITIS

it can manifest as a simple headache as first and gets bad fast; even if there is a small headache you MUST do a lumbar puncture

136
Q

what is the AIDS part of HIV

A

it is after clinical latency when you start to develop symptoms, you are very immuno-suppressed, and you are getting repetitive infections

137
Q

what type of genetic material do you get after viral replication?

A

Double-stranded RNA - dsRNA

138
Q

what are the steps of HIV virus infection in cell

A

1) HIV fuses to CD4 cell
2) Reverse transcriptase used to replicate HIV virus
3) Viral DNA goes into nucleus and gets integrated in cellular DNA
4) Production of viral proteins and contents in cell
5) New HIV virus budding from CD4 cell

139
Q

what are the different types of HIV meds

A

think HIV cell replication steps

1) Fusion Inhibitors
2) Reverse transcriptase inhibitors
3) Integrase inhibitors –> inhibits integration of HIV DNA in cell DNA
4) Protease inhibitors –> inhibits budding of new HIV from cell

140
Q

what are 3 features which make HIV very good at evolving

A

1) error-prone replication
2) rapid viral replication
3) large population sizes

141
Q

what features of HIV contribute to its virulence

A

1) the surface of the virus is derived from the host cell membrane –> can trick and hide from the immune system
2) the virus is very good at replicating and mutating –> evolution
3) HIV infects CD4 cells, which leaves CD8 cells (T-cytotoxic) for the main immune response –> can’t cope with the rate of infection
4) HIV infects a wide range of immune cells, not only CD4
5) HIV can pass directly from cell to cell –> relatively inaccessible to antibodies in the blood
6) The small HIV genome encodes a range of genes that enable the virus to evade human immune system responses

142
Q

what are Carbapenemase producing Enterobacteriaceae

A

Include E. coli, Klebsiella, Proteus, Serratia, Enterobacter

Colonisers of large bowel, skin below waist and moist sites

Most common causes of UTI, intra-abdominal infection

carbapenemase = Enzyme which inactivates carbapenem antibiotics

143
Q

what are carbapenems

A

Carbapenems are one of the broadest spectrum antibiotics available

Previously used as the antibiotic of last resort, now commonly used

144
Q

what is Norovirus

A

Norovirus is a highly contagious virus that causes gastroenteritis, leading to symptoms like vomiting, diarrhoea, nausea, and stomach cramps. It’s often referred to as the “stomach flu”. Norovirus is commonly spread through contaminated food, water, surfaces, or direct contact with an infected person. The illness is usually self-limiting and resolves within a few days, but it can be severe, especially in vulnerable populations like the elderly or those with weakened immune systems.

145
Q

what are the virulence factors of gram negative bacteria

A

1) use of colonisation factors like adhesins, invasins, defence against host
2) secretion of toxins

146
Q

describe coliforms

A

gram negative bacteria
enterobacteria –> colonise the GI
rod-shaped
motile (have flagella)
aerobic

147
Q

what does e.coli cause

A

primary cause of UTIs in women
gastroenteritis
traveller’s diarrhoea
sepsis
meningitis in infants (rare in UK)

148
Q

what is cystitis

A

Cystitis refers to inflammation of the bladder, usually caused by a bacterial infection. It’s a type of urinary tract infection (UTI) that commonly affects women

149
Q

what is cellulitis

A

Cellulitis is a bacterial skin infection that affects the deeper layers of the skin and subcutaneous tissues. It’s characterized by redness, swelling, warmth, and pain in the affected area of the skin. Cellulitis typically occurs when bacteria enter the skin through a break or crack, such as a cut, wound, or insect bite.

150
Q

what is shigellosis

A

severe bloody diarrhoea caused by shigella virus

151
Q

what is salmonellosis and what are the 3 presentations of this disease

A

salmonellosis is an infection due to Salmonella virus –> S. enterica

It can cause:
1) gastroenteritis
2) enteric fever (also known as typhoid fever)
3) Bacteraemia (presence of bacteria in the bloodstream)

152
Q

decribe vibrio cholerae

A

gram negative rod
aerobic
causes cholera –> most severe diarrhoeal disease
due to poor sanitation
release of cholera toxin causes disease
treated with rehydration therapy (oral or iv)

153
Q

campylobacter vs helicobacter

A

they are both gram negative aerobic bacteria
campylobacter is the most common cause of food poisoning in the UK
helicobacter is much more dangerous; leads to gastritis, peptic ulcer, gastric adenocarcinoma, or even lymphoma

154
Q

what is neisseria gonorrhoeae

A

a strain of neisseria
gram negative cocci
aerobic
leads to gonorrhoea –> second most common STD worldwide
asymptomatic particularly in women
can lead to yellow or bloody discharges from vagina/penis
painful urination
pelvic pain
sore throat

155
Q

what does borrelia burgdorferi cause

A

lyme disease
transmitted to humans by tick nymphs
characterised by bull’s eye rash at the site of the tick bite
fever
fatigue
headache
disseminates through lymphatics and blood
over time leads to neurological problems like facial muscle weakness and meningitis
arrhythmias
arthritis

156
Q

what does treponema pallidum cause

A

syphillis
leads to genital infection (ulcer)
skin rash
swollen lymoh nodes
fever
headaches
joint pains
granulomas in bone and soft tissues
neural damage

157
Q

describe chlamydia classification

A

obligate intracellular –> can only detect by serology; can’t culture in media
gram negative

158
Q

what are beta lactams

A

antibiotics used mainly for gram positive bacteria because they target peptidoglycans (gram positive have thick peptidoglycan wall)

159
Q

give examples of beta-lactams

A

penicillin
flucloxacillin
amoxicillin
chephalosporins

160
Q

what is the difference between beta-lactams and cephalosporins

A

cephalosporins are a subtype of beta-lactams, but compared to general beta-lactams they can also be used on gram negative bacteria because they have a broader spectrum of activity –> used to treat a very wide range of bacteria

161
Q

a patient has a pencillin allergy and is infected with gram positive bacteria. what other beta-lactam would you give him?

A

a cephalosporin or vancomycin

162
Q

what is MRSA

A

methicillin resistant staph aureus

163
Q

what is a major complication of methicillin

A

kidney failure

164
Q

what is vancomycin

A

antibiotic for gram positive bacteria resistant to beta-lactams

165
Q

what are the 5 categories of antibiotics with examples

A

1) inhibitors of cell wall synthesis: beta-lactams - penicillin
glycopeptides - vancomycin and Teicoplanin

2) Inhibitors of protein synthesis:
GRAM POSITIVE
macrolides - clarithromycin and erythromycin
lincosamides - clindamycin
tetracyclines - doxycycline

GRAM NEGATIVE
aminoglycosides - gentamicin

3) Inhibitors of nucleic acid synthesis
quinolones - ciprofloxacin

4) Anti-metabolites
Trimethoprim

5) Inhibitors of membrane function

166
Q

give an example of cephalosporins

A

Cefuroxime
Cefotaxime
Ceftriaxone

167
Q

what are trimethoprim and nitrofurantoin used for

A

UTIs

168
Q

give an example of a carbapenem

A

Meropenem

169
Q

what are the 2 determinants of antibiotic effect?

A

concentration and time that the antibiotic remains at the binding site

170
Q

what is horizontal gene transfer?

A

when some bacteria can take up free DNA from the environment or from other bacteria and incorporate it in their DNA

171
Q

what antibiotic is administered for infectious endocarditis

A

amoxicillin with optional gentamicin

172
Q

which one is in chains? staph or strep

A

strep

phase 2 medicine (15 decks)

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