Microbio Flashcards
1
Q
Define pathogen
A
Organism that causes or is capable of causing disease
2
Q
Commensal
A
Organism which colonises the host but causes no disease in normal circumstances
3
Q
Opportunist Pathogen
A
Microbe that only causes disease if host defences are compromised
4
Q
Virulence definition
A
The degree to which a given organism is pathogenic
5
Q
Asymptomatic carriage
A
When a pathogen is carried harmlessly at a tissue site where it causes no disease
6
Q
what color do gram-positive vs gram negative bacteria stain
A
+ve - purple
-ve - red
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
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
9
Q
what is bacterial conjugation
A
how bacteria swap genetic material
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
11
Q
What is coagulase
A
enzyme produced by bacteria that clots blood plasma. Fibrin clot formation around bacteria may protect from phagocytosis.
12
Q
how do coagulase +ve staphylococci protect themselves from phagocytosis
A
Fibrin clot formation around bacteria may protect from phagocytosis.
13
Q
what is the normal habitat of staphylococci
A
Nose and skin
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
15
Q
name two coagulase-negative streptococci
A
S.epidermidis and S.saprophyticus
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
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
18
Q
how do the streptococci clum up compared to the staphylococci
A
streptococci form chains
staphylococci form clumps
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
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
21
Q
What are the group A and group B beta-haemolytic species?
A
S. pyogenes and S. algalactiae
22
Q
what is the optochin test
A
used to differentiate between S pneumoniae and Viridas strep in alpha-haemolytic streptococci groups
23
Q
name two gram-positive cocci
A
streptococcus and staphylococcus
24
Q
what problems do the viridans group of bacteria cause
A
infective endocarditis
deep organ abscesses
25
name a gram-positive bacilli
listeria monocytogenes, clostridium, corynebacterium
26
What test could be done to distinguish between different streptococci?
Blood agar haemolysis.
27
give an example of gamma haemolysis bacteria
streptococcus bovis
28
give examples of gram-negative bacilli
Salmonella, Helicobacter, Vibrio, E. coli
29
What is the difference between enteropathogenic, enterohaemorrhagic, and enteroinvasive e.coli infection?
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
30
what is the difference between Shigella and E. coli?
name what gram shigella is and what type
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
31
what allows shigella and e.coli to pass through the GI tract and infect a person
they are acid tolerant --> can pass through the stomach
32
what bacteria is responsible for salmonellosis
s. enterica
33
what are the 3 types of infections caused by S. enterica
Gastroenteritis/enterocolitis --> cause of food poisoning
Enteric fever/ typhoid fever
Bacteraemia
34
Why is vibrio cholerae so dangerous?
You’re losing huge amounts of water which can result in hypovolemic shock and severe dehydration, which can lead to death.
35
how do you test for mycobacteria and what part of the bacterial tree are they from
Zieehl-Neelsen stain test and they are bacilli
36
what causes TB
mycobacterium tuberculosis
37
virulence of TB
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
38
how is TB transmitted?
aerosol transmission
39
explain the pathophysiology of TB in its 3 steps
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)
40
how does our body defend itself from mycobacteria?
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.
41
how does TB stay in the body and when does it manifest
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
42
How do you detect TB
Nucleic acid detection
43
what is the tuberculin skin test?
called Mantoux
44
define a virus
An infectious intracellular parasite, totally dependent on its host cell for replication and existence
45
what is the genetic material in viruses surrounded by
protein coat
46
virus vs bacteria
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
47
different shapes of viruses
Helical
Icosahedral
Complex
48
what are the stages of virus replication?
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
49
how do viruses cause disease and give examples for each way
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
50
define meningitis
inflammation of the meninges (membranes) which cover the brain and spinal cord
51
what are the layers of the meninges
dura mater
arachnoid mater
pia mater
52
what are causes of meningitis
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.
53
define protozoa
one-celled organisms (animals). But they are bigger than bacteria and contain a nucleus and other cell structures, making them more like animal cells.
54
what causes invasive meningococcal disease and is the most common BACTERIAL cause of meningitis
Infection with Neisseria meningitidis
55
what are the characteristics of Neisseria meningitis, how is it transmitted, and how does it manifest?
Gram-negative diplococci
Transmission by respiratory droplets/ naso-pharyngeal secretions --> requires FREQUENT and PROLONGED contact
manifests as Meningitis or Septicaemia
56
How many serogroups of Neisseria meningitis are vaccine-preventable
5
57
what are risk factors of meningitis?
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
58
Meningococcal meningitis symptoms
fever
stiff neck
headache
confusion
increased sensitivity to light
nausea and vomiting
59
Symptoms of any septicaemia
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)
60
what is Brudzinski's neck sign
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.
61
what are petechiae
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
62
Name and explain two results of sepsis
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
63
how do you diagnose meningitis
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
64
what is chemoprophylaxis for meningitis
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)
65
does chemoprophylaxis stop infection
No!!!! It stops spread!
66
define virions
Viruses that have not yet infected a cell and live without a current host
67
define toxoid
a chemically modified toxin from a pathogenic microorganism, which is no longer toxic but is still antigenic and can be used as a vaccine.
68
what is typhoid fever and what is it caused by
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)
69
what causes tetanus and how does it manifest
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
what are the sterile sites in the body?
blood
csf
joints
bladder
lower resp tract
pleural fluid
peritoneal cavity
71
what are the non-sterile sites of the body
GI
skin
oral cavity
vagina
urethra
72
what is the classification of S pneumoniae?
alpha haemolytic streptococcus
73
what bacteria is optochin resistant
viridans
74
which is the least selective agar
blood agar
75
what is diphtheria and what causes it (include genus and type)
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
what is pertussis
whooping cough
77
what are the 2 types of fungi
yeast and moulds
78
Yeast vs. Mould
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
why are there few fungi which cause infections
most fungi are unable to grow at 37 degrees
80
what does the plasma membrane in fungi contain
ergosterol
81
what do you call fungi which exist as both yeasts and moulds
dimorphic fungi
82
how do dimorphic fungi behave at different temperatures
Mould at ambient temperature (25-30 degrees)
Convert to yeast form at 37 degrees
83
what is the most common fungal infection
candida albicans
84
what is invasive candidiasis most commonly caused by
infection of prosthetic devices in intra-abdominal disease
85
what is a medicine to treat fungal infections
fluconazole
86
name two different strains of fungi
candida and aspergillus
87
what is the biggest risk factor for fungal infections
immunosuppression
88
what are the 5 major groups of protozoa
Flagellates
Amoebae
Sporozoans
Ciliates
Microsporidia
89
what are the two main symptoms of malaria
fever and haemolysis
90
what are the consequences of malaria
Anaemia
Jaundice
Hepatosplenomegaly --> enlarged liver AND spleen
Haematoglobinurea --> due to haemolysis
91
what is thrombocytopenia
decreased platelets in the blood
92
what is aciclovir
Anti-herpesvirus drug
93
what is the aciclovir method of action
Pro-drug when activated gets 3 phosphates
Aciclovir triphosphate competitively inhibits herpesvirus specific DNA polymerases
94
what are the 2 types of herpes infection
HSV1 and HSV2
95
what are different types of herpes infections
genital herpes, oral herpes, chickenpox/shingles
96
how does shingles happen and what causes it
primary chicken pox infection
virus stays dormant in the DRG
Reactivation leads to dermatomal shingles
caused by Herpes Zoster virus
97
what is rituximab
a type of targeted cancer drug called a monoclonal antibody
98
measles symptoms
high fever
morbilliform rash
koplik spots
cough
diarrhoea
conjunctivitis
99
what is an antibiotic
Antibiotics are molecules produced by a micro-organism that work by binding a target site on a bacteria
100
what do you use to treat staph aureus
flucloxacillin
101
what are HIV transmission routes
Blood
Sexual
Vertical
102
what is the likelihood that if you are untreated HIV positive and pregnant you give the baby HIV
30%
103
can HIV-positive mothers have natural delivery?
yes; with retroviral therapy 2% chance of transmission (very small)
104
when are HIV PrEP most effective?
PrEP = pre-exposure prophylaxis
before sexual intercourse
105
what are risk factors for HIV
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
symptoms of HIV
Acute generalized rash
Glandular fever
Indicators of immune dysfunction
Unexplained weight loss or night sweats
Recurrent bacterial infections including pneumococcal pneumonia
107
if a person has undetectable levels of HIV virus and they are HIV positive can they still pass the virus through sex
NO
108
what are the examples of HIV PrEP
Truvada and Descovy
109
what is vertical transmission
from mother to child in uterus
110
how can HIV PrEP be administered
pill or injection
111
what is PEP and how does it compare in effectiveness compared to PrEP
PEP = post-exposure prophylaxis
it is not as effective as PrEP
112
what is the fastest HIV-detecting test and what are it's advantages and disadvantages
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
how do you manage a negative and positive HIV POCT pin prick test
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
Which are the more accurate HIV tests
venous blood sample tested for p24 antigen
115
what cells does HIV infect
CD4 cells
116
what group of viruses is HIV from and what type of virus is it
family = lentivirus
type of virus = retrovirus
117
what enzyme does HIV use to replicate
reverse transcriptase
118
what are the 2 markers used to monitor HIV infection
CD4 cell count
HIV viral load
119
when do HIV symptoms start
2-4 weeks of infection
120
what do you have to ask a patient with fever, rash and non-specific symptoms
Ask about sexual history
Think of HIV seroconversion
121
how long can the period of HIV clinical latency last and what is it
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
when should you do an HIV test
when faced with a common problem:
In an unexpected patient
That is recurring
That has no clear underlying cause
123
what defines a state of AIDS in terms of CD4 count
CD4 < 200
124
what is pneumocystis pneumonia and what are the symptoms and how do you treat it?
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
what is the most common opportunistic infection
PCP - pneumocystis pneumonia
126
what are possible opportunistic diseases which can take control of you when you have HIV
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
what test for another disease do you need to do if you have TB
HIV
128
what causes Kaposi's sarcoma and how does it manifest
Human Herpes Virus 8
manifests as single or multiple lesions on the skin
129
how do you treat HIV after diagnosis?
HAART - Highly Active Anti-Retroviral Therapy
involves the use of 3+ antiretroviral drugs to attack different points of the replication cycle of HIV
130
what are the HIV drug classes
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
how does HIV develop drug resistance?
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
What are the repercussions of HIV prescription non-adherence
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
what are the steps of HIV CD4 infection
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
what is cytomegalovirus (CMV)
herpes virus, which causes a glandular fever-type illness in the immunocompetent individual.
135
When should you do a lumbar puncture in someone diagnosed with HIV
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
what is the AIDS part of HIV
it is after clinical latency when you start to develop symptoms, you are very immuno-suppressed, and you are getting repetitive infections
137
what type of genetic material do you get after viral replication?
Double-stranded RNA - dsRNA
138
what are the steps of HIV virus infection in cell
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
what are the different types of HIV meds
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
what are 3 features which make HIV very good at evolving
1) error-prone replication
2) rapid viral replication
3) large population sizes
141
what features of HIV contribute to its virulence
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
what are Carbapenemase producing Enterobacteriaceae
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
what are carbapenems
Carbapenems are one of the broadest spectrum antibiotics available
Previously used as the antibiotic of last resort, now commonly used
144
what is Norovirus
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
what are the virulence factors of gram negative bacteria
1) use of colonisation factors like adhesins, invasins, defence against host
2) secretion of toxins
146
describe coliforms
gram negative bacteria
enterobacteria --> colonise the GI
rod-shaped
motile (have flagella)
aerobic
147
what does e.coli cause
primary cause of UTIs in women
gastroenteritis
traveller's diarrhoea
sepsis
meningitis in infants (rare in UK)
148
what is cystitis
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
what is cellulitis
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
what is shigellosis
severe bloody diarrhoea caused by shigella virus
151
what is salmonellosis and what are the 3 presentations of this disease
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
decribe vibrio cholerae
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
campylobacter vs helicobacter
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
what is neisseria gonorrhoeae
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
what does borrelia burgdorferi cause
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
what does treponema pallidum cause
syphillis
leads to genital infection (ulcer)
skin rash
swollen lymoh nodes
fever
headaches
joint pains
granulomas in bone and soft tissues
neural damage
157
describe chlamydia classification
obligate intracellular --> can only detect by serology; can't culture in media
gram negative
158
what are beta lactams
antibiotics used mainly for gram positive bacteria because they target peptidoglycans (gram positive have thick peptidoglycan wall)
159
give examples of beta-lactams
penicillin
flucloxacillin
amoxicillin
chephalosporins
160
what is the difference between beta-lactams and cephalosporins
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
a patient has a pencillin allergy and is infected with gram positive bacteria. what other beta-lactam would you give him?
a cephalosporin or vancomycin
162
what is MRSA
methicillin resistant staph aureus
163
what is a major complication of methicillin
kidney failure
164
what is vancomycin
antibiotic for gram positive bacteria resistant to beta-lactams
165
what are the 5 categories of antibiotics with examples
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
give an example of cephalosporins
Cefuroxime
Cefotaxime
Ceftriaxone
167
what are trimethoprim and nitrofurantoin used for
UTIs
168
give an example of a carbapenem
Meropenem
169
what are the 2 determinants of antibiotic effect?
concentration and time that the antibiotic remains at the binding site
170
what is horizontal gene transfer?
when some bacteria can take up free DNA from the environment or from other bacteria and incorporate it in their DNA
171
what antibiotic is administered for infectious endocarditis
amoxicillin with optional gentamicin
172
which one is in chains? staph or strep
strep
