Microbiology Flashcards
Define pathogen
An organism that causes or is capable of causing disease
Define commensal
An organism which colonises the host but causes no disease in normal circumstances (cause disease when displaced)
What is an opportunistic pathogen?
A microbe that only causes disease if the host defences are compromised (e.g. immunosuppressed or AIDS patients)
Define virulence/pathogenicity
The degree to which a given organism is harmful/pathogenic
What is asymptomatic carriage?
When a pathogen is carried harmlessly at a tissue site where it causes no disease
Describe the differences between the cell walls of gram positive and gram negative bacteria
Gram +ve bacteria have a large layer of peptidoglycan, and contain strands of lipoteichoic acids
Gram -ve bacteria have a thin layer of peptidoglycans, and their outer membrane contains projections of lipopolysaccharides (LPS) known as the endotoxin
What are the conditions that bacteria can survive in?
Temperatures between -80 and +80
pH between under 4 and 9
Water/desiccation, ranging from 2 hours to 3 months (>50 years for spores)
UV light
What is the difference between endotoxin and exotoxin?
Endotoxin is a component of the outer membrane (LPS) of gram-ve bacteria only, with non-specific action and weak antigenicity
Exotoxin is secreted proteins from any bacteria, with specific action and strong antigenicity
How does genetic variation occur in bacteria
DNA mutation (or chromosome or plasmid)… base deletion, substitution, insertion
Gene transfer… conjunction (via sex pilus), transformation (via plasmid), transduction (via bacteriophage after viral infection)
What are obligate intracellular bacteria? List 3 examples
Bacteria which require a host cell to replicate
- Rickettsia spp.
- Chlamydia spp.
- Coxiella spp.
Give an example of a bacteria with no cell wall
Mollicutes (mycoplasma and ureaplasma spp.)
List 3 bacteria which grow as filaments
Actinomyces spp.
Nocardia spp.
Streptomyces spp.
List 3 spirochetes
Leptospira spp.
Treponema spp.
Borrelia spp.
Which bacteria stain positive with Ziehl-Neelsen stain?
Mycobacteria e.g. Mycobacteria. tuberculosis
Name an anaerobic gram -ve cocci
Veillonella spp.
Name a species of aerobic gram -ve cocci
Neisseria spp.
Give two examples of bacteria from the Neisseria species
- N. gonorrhoeae (cause gonorrhoea, infects urethra, rectum, throat, fallopian tubes, can be asymptomatic)
- N. meningitidis (causes meningitis by invading CSF, virulence factor = anti-phagocytic capsule, LPS)
Name an anaerobic gram +ve cocci
Peptostreptococcus spp.
Name three aerobic gram +ve cocci
Staphylococcus spp.
Streptococcus spp.
Enterococcus spp.
Name two bacteria from the Staphylococcus species
S. aureus… coagulase +ve, virulence factors = pore-forming toxins, proteases
S. epidermidis… coagulase -ve, virulence factors = forms persistent biofilms, infections are opportunistic
How can you tell the difference between Staphylococcus and Streptococcus
Staphylococcus grows in clusters, catalase positive
Streptococcus grows in chains, catalase negative
What are the two categories of Streptococcus
Alpha-haemolytic - partial/greening haemolysis
Beta-haemolytic - complete haemolysis
Give two examples of alpha-haemolytic Streptococcus, and how they are told apart
S. pneumoniae (optochin sensitive)… normal commensal in oropharynx, but causes pneumonia and meningitis, virulence factors = anti-phagocytic capsule
Viridians groups e.g. S. oralis. S. sanguinis (optochin resistant)… can cause dental abscesses or infective endocarditis
Give an example of a beta-haemolytic Streptococcus
S. pyogenes group A… causes scarlet fever, infection of the respiratory tract, skin, soft tissue, virulence factors = streptokinase, streptolysin, erythrogenic toxins, M protein
How are beta-haemolytic Streptococcus grouped?
Grouped by carbohydrate cell-surface antigens using Lancefield grouping A-H, K-V
Give an example of a bacteria from the enterococcus species
E. faecalis… (gut commensal, but can can endocarditis, meningitis, UTIs, sepsis)
Name an example of anaerobic gram-ve bacilli
Bacteroides… commensal flora, cause opportunistic infections in tissue injury
What groups of aerobic gram -ve bacilli are there?
Enterobacteriaceae/coliforms (present in GI tract)
Pseudomonads (commonly found in water and soil)
Vibrios (curved-rod shaped, commonly found in food/water)
Parvobacteria (need blood products for growth)
List 7 Enterobacteriaceae/coliforms
Escherichia spp.
Shigella spp.
Salmonella spp.
Proteus spp.
Klebsiella spp.
Yersinia spp.
Citrobacter spp.
Even severe snow practically kills young cats
Which gram -ve aerobic bacteria are lactose fermenting and non-lactose fermenting, and how is this tested?
Tested on MacConkey agar, or CLED agar for urine
Lactose fermenting (stains pink): Escherichia, Klebsiella
Non-lactose fermenting (stains yellow/clear): Salmonella, Shigella, Proteus, Pseudomonas (oxidase positive)
How are Shigella and Salmonella told apart?
XLD agar
Shigella grows red
Salmonella grows red with black centres
Give an example of a bacteria from the Escherichia species
E. coli… can cause wound infections, UTIs, diarrhoea, there are several pathovars with different pathogenesis e.g. toxin-induced, or cytotoxic damage and inflammation
Give an example of a bacteria from the Shigella species
S. dysenteriae… causes severe bloody diarrhoea, frequent passing of stools, prevalent in developing countries, virulence factor = shiga toxin
Give an example of a bacteria from the Salmonella species
S. enterica… causes gastroenteritis/food poisoning in a local infection, or enteric fever/typhoid in a systemic infection, virulence factors = enters and survives within macrophages
Give an example of a bacteria from the Proteus species
P. mirabilis… causes catheter-associated UTIs, differentiates into elongated hyperflagellated form, produces urease which causes kidney/bladder stones to develop and block the catheter
Give an example of a bacteria from the Yersinia species
Y. pestis… causes bubonic plague, systemic infection, spread by animals
How does the Citrobacter species cause disease?
Can cause UTIs, meningitis, in neonates, sepsis
Closely related to salmonella
Give an example of a bacteria from the Pseudomonas species
P. aeruginosa… causes localised infections of UTIs/burns/surgical wounds, or systemic infections of sepsis, virulence factor = toxins
Opportunistic, resistant to many anti-biotics and disinfectants
Can cause chronic infection in CF patients
Which species of bacteria belong to the vibrio group?
Vibrio spp.
Campylobacter spp.
Helicobacter spp.
Give an example of a bacteria from the Vibrio species
V. cholerae… causes cholera from drinking contaminated water, virulence factor = cholera toxin causing loss of water from epithelial cells
Give an example of a bacteria from the Campylobacter species
C. jejuni… most common cause of food poisoning, causes mild to severe diarrhoea often with bleeding, virulence factor = toxins
What agar plate is specific to Campylobacter?
CCDA
Give an example of a bacteria from the Helicobacter species
H. pylori… causes gastritis and peptic ulcers, virulence factors = toxins causing metaplasia and damage to mucosa
Which species of bacteria belong to the Parvobacteria group?
Haemophilus spp.
Brucella spp.
Bordetella spp.
Pasteurella spp.
Give an example of a bacteria from the Haemophilus species
H. influenzae… nasopharyngeal carriage in 25-80% of population, opportunistic infection of pneumonia, meningitis, sepsis in patients with COPD, CF, HIV/AIDS, virulence factors = capsule which can penetrate nasopharyngeal epithelium and is resistant to phagocytes
Give an example of a bacteria from the Bordetella species
B. pertussis… causes whooping cough, virulence factors = toxins
How does the Brucella species cause disease?
Infected animals or animal products cause brucellosis
How does the Pasteurella species cause disease?
Commensals of animals, infections from dog/cat scratches/bites
List three examples of anaerobic gram +ve bacilli
Clostridia spp.
- C. tetani… from infected wounds, causes tetanus (muscle contractions and spasms progressing from head to body)
- C. botulinum… from infected wounds or contaminated food, causes botulism (paralysis spreading from head to toe)
- C. difficile… causes antibiotic associated diarrhoea
List three examples of aerobic gram +ve bacilli
Listeria spp. (e.g. L. monocytogenes)
Corynebacterium (e.g. C. diphtheriae)
Bacillus spp. (e.g. B. anthracis)
List 4 medically important mycobacteria and what they cause
M. tuberculosis… TB
M. avium complex (MAV)… disseminated infection in AIDS, chronic lung infection
M. ulcerans… buruli ulcers
M. leprae… leprosy
Describe the structure of mycobacteria
Slightly curved, beaded bacilli which are aerobic, non-motile, and non-spore forming
They have high content of lipids and mycolic acids in the cell walls which makes them resistant to Gram staining (Ziehl-Neelsen stain is used instead)
Their cell wall has a high molecular weight lipids, which means they are very well protected and slow growing (doubling time = 24h)
How have mycobacteria adapted to immunology
They have adapted to withstand phagolysosomal killing by surviving in the cytoplasm of macrophages after being phagocytosed
The body allows these macrophages to travel around the body, so the mycobacteria are transported too, allowing them to survive in the body latently for a long time
A granuloma forms around the infected macrophage (recruiting Th1 cells, IFN, TNFa), but this can become unstable in T-cell depletion (e.g. AIDS) and allow the mycobacteria to reactivate
How can mycobacteria be detected?
Solid or liquid culture (time consuming)
Nucleic acid detection using PCR (rapid)
Why are viruses medically important?
They are a common and significant cause of human disease nationally and globally (outbreaks, cancer, morbidity, mortality)
Define virus
An infectious obligate intracellular parasite comprising of genetic material (DNA/RNA) surrounded by a protein coat and/or membrane
Describe the varied structures of viruses
Viruses come in different shapes: helical, icosahedral (ball), complex
They can be non-enveloped (e.g. adenovirus, parvovirus), or enveloped (e.g. influenza, HIV) so surrounded by a lipid coat derived from the host cell plasma membrane
They can be different sizes: 20-260nm
How do viruses differ from bacteria?
Viruses have no cell wall or organelles
Viruses cannot feed, respire, or reproduce independently
Viruses are not alive, they are dependent on a host cell
Describe the 5 steps of viral replication
- attachment to a specific receptor - dictates which cells a virus can enter
- cell entry - uncoating of the virion (core of nucleic acids and proteins) into the host cell
- host cell interaction + replication - migration of viral genome to cell nucleus and transcription to mRNA using host materials, to produce the viral genome and proteins
- assembly of the virion - occurring in different places depending on the virus (e.g nucleus = herpes viruses, cytoplasm = poliovirus, cell membrane = influenza)
- release of new virus particles - by bursting out of the cell and killing it (e.g. rhinovirus), of by budding/exocytosis (e.g. HIV, influenza)
List 5 ways that viruses cause disease
direct destruction
modification of host cell
over-reactivity of the immune system
damage through cell proliferation
evasion of host cell defences (cellular or molecular level)
Give an example of a virus which causes disease by direct destruction of the host cell
poliovirus - causes lysis of the neuron host cell, leading to loss of function (paralysis)
Give an example of a virus which causes disease by modification of the host cell
rotavirus - causes atrophy and flattening of the epithelial cells, so decreases the intestinal surface area and absorption of nutrients, leading to a hyperosmotic state and diarrhoea
Give an example of a virus which causes disease by over-reactivity of the immune system
hepatitis B - expression of antigens on hepatocyte surface leads to T lymphocytes attacking and killing hepatocytes, leading to jaundice, fever, itching, etc
Give an example of a virus which causes disease by damage through cell proliferation
human papillomavirus (HPV) - dysplasia and metaplasia of infected epithelium leading to cancer of the cervix, anus, penis, head, and neck
In what ways can viruses evade host defences on a cellular level, give an example for each
Latency… after the primary disease the virus is undetectable but viral DNA lies latent and can reactivate (e.g. varicella zoster virus -> chicken pox -> shingles)
Cell to cell spread… avoids random release to the environment and immune system detection, and speeds up the spread within tissues (e.g. measles, HIV)
In what ways can viruses evade host defences on a molecular level, give an example for each
Antigenic variation… antigen changes to avoid detection so the host can be reinfected with the same virus (e.g. influenza)
Prevention of host cell apoptosis… allows virus to continue replicating so more are produced and released (e.g. herpes virus)
Down regulation of interferon and other intracellular defence proteins… stops and antiviral state being established in neighbouring cells (many examples)
Interference with host cell antigen presenting pathways… to avoid immune detection (e.g. herpes viruses, measles, HIV)
What tests are used to detect viruses?
- Direct detection:
- electron microscopy (visualise morphology of virus, but requires time and effort)
- cytopathic effect, CPE (look at effect on cell culture over 2-4 weeks, but also requires time and effort)
- nucleic acid amplification tests (NAATs) e.g. PCR (detects copies of RNA/DNA, sensitive and quick, can only detect the virus you’re testing for) - Indirect detection:
- serology = detecting antibody (IgG/IgM) response in the serum e.g. ELSIA
What is a protozoa
Protozoa are one-celled eukaryotic organisms
They have a nucleus and a relatively complicated internal structure
They can be parasitic (live in humans) and cause disease
What are the 5 major classifications of protozoa
Flagellates
Amoebae
Ciliates
Sporozoa
Microsporidia
List 4 flagellates
Trypanosoma spp.
Leishmania spp.
Trichomonas spp.
Giardia spp.
List an example of an amoebae
Entamoebae histolytica
List three examples of sporozoa
Cryptosporidium spp.
Toxoplasma spp.
Plasmodium spp.
Which microorganism is the most common cause of malaria and how is it spread?
Plasmodium falciparum, spread through the bite of female anopheles mosquitos
What are the signs and symptoms of malaria?
Signs = anaemia, jaundice, hepatosplenomegaly, haemoglobinuria
Symptoms = fever, headaches, myalgia, fatigue, diarrhoea, vomiting, abdominal pain
What are the complications of malaria?
Infected red blood cells stick to endothelium causing…
- cerebral = vascular occlusion -> drowsiness, seizures, increased intracranial pressure, coma, death
- respiratory = shortness of breath due to anaemia, lactic acidosis, increase vascular permeability
- renal = hypoperfusion, due to dehydration/hypotension, haemolysis ->haematuria
- bleeding = thrombocytopenia, increased activation of coagulation cascade -> worsening anaemia, abnormal bleeding
- cardiovascular = anaemia, bleeding, increased vascular permeability, sepsis, pro-inflammatory cascade -> hypotension, tachycardia, shock
What is the treatment for malaria?
IV artesunate for complicated malaria
Supportive measures (oxygen, fluids, blood products, antiepileptics, antibiotics, diuretics)
Describe the lifecycle of malaria
- a mosquito bites an infected human and ingests plasmodium gametocytes
- within the mosquito, gametocytes undergo development and end as sporozoites in the salivary glands
- the mosquito bites someone and injects sporozoites
- the sporozoite infects a liver cell to become a schizont, which ruptures (causing abdominal pain), and goes on to infect red blood cells
- the plasmodium becomes a trophozoite within the red blood cell, which can be seen on blood film
- the trophozoite develops into a schizont, which ruptures and re-infects another red blood cell (this haemolysis causes anaemia, jaundice, and haemoglobinuria)
- some of the trophozoites develop into gametocytes, which are taken up by another mosquito and the cycle begins again
What does the immune response to bacteria depend on?
The number of organisms and their level of virulence…
- low number/virulence = phagocytes,
- high number/virulence = whole immune response
Whether the bacteria is intra or extracellular…
- intracellular = cellular response (T cells/macrophages),
- extracellular = humoral response (antibodies)
What components does the host defence to bacteria involve?
Complement - causing cell lysis and opsonisation, to prevent proliferation
Antibodies - neutralise toxins
IgA - blocks the attachment to host cells
Th cell activation - delayed type hypersensitivity
Secretion of IFN, TNF, IL2
Macrophage recruitment - continued activation leads to granuloma formation and tissue damage from lytic enzymes
What dose the immune response to protozoa depend on?
The location of the parasite within the host…
- blood stage = humoral immunity (antibodies)
- tissue stage = cell-mediated immunity (T cells/macrophages)
Describe the immune response to malaria
IgE triggers degranulation and cytokine release from mast cells/basophils/eosinophils
Production cytokines (TNF), done excessively leads to the symptoms of malaria
Antibody production against sporozoites (poor response, only in the blood for a short time)
Describe the humoral immune response to viruses
Antibodies - block binding of virus to host cell and involved in opsonisation
IgM - agglutinates particles
Complement - involved in opsonisation and cell lysis
Describe the cell-mediated immune response to viruses
Cytotoxic T lymphocytes kill infected cells
IFN from Th or Tc cells has direct antiviral action, and induces antiviral proteins for bystander cells
Natural killer cells and macrophages are involved in antibody-dependent cellular cytotoxic killing
Describe the immune response to helminths (worms)
The body has a poor immune response to helminth infections, which is not sufficient to kill them
They trigger an IgE response, where mast cells/basophils/eosinophils degranulate and release cytokines
How do bacteria evade an immune response, give an example for each
- antigenic variation (N. gonorrhoea)
- polysaccharide capsule preventing phagocytosis (S. pneumoniae)
- coagulase forms a fibrin coat around the organism (Staphylococci)
- escape from phagolysosome and live in cytoplasm (mycobacteria)
How do viruses evade an immune response, give an example for each
- antigenic variation (HIV, rhinovirus)
- changing haemagglutinin (HA) and neuraminidase (NA) glycoproteins in the coat (influenza)
- immune suppression by destroying/altering lymphocytes/macrophages (HIV, measles)
- inhibiting classical complement cascade (vaccinia protein from small pox)
How do protozoa evade an immune response?
Surface antigen variation, by switching VSG (variable surface glycoprotein)
How do helminths (worms) evade an immune response?
Establish hypo-responsiveness by supressing T cells and decreasing antigen expression
Define antibiotic
An antimicrobial agent that is active against bacteria
Define antimicrobial
An agent which kills pathogens
What is an antibiotic target site, give three examples
Antibiotic target sites are a points of biochemical reactions that are crucial to the survival of the bacteria
- cell wall synthesis
- nucleic acid synthesis
- protein synthesis
What antibiotics target cell wall synthesis?
Beta lactams…
- penicillins (penicillin, benzylpenicillin, piperacillin, flucloxacillin, amoxicillin)
- cephalosporins (cefuroxime, ceftriaxone, cefotaxime)
- carbapenems (meropenem)
- monobactams (aztreonam)
Glycopeptides…
- vancomycin
- teicoplanin
How do beta-lactams work?
Disrupting the peptidoglycan production by binding covalently and irreversibly to the penicillin binding proteins, resulting in lysis of the bacteria
Are beta-lactams more effective on gram positive or negative bacteria?
They are more effective on gram-positive bacteria (due to the larger peptidoglycan layer), and they have a variety in their spectrum and activity due to different binding affinities to different penicillin binding proteins
Why are beta-lactams ineffective on intracellular bacteria?
They poorly penetrate human cells
Give three examples of antibiotics which target nucleic acid synthesis, and how they work
Rifampicin (inhibits RNA polymerase)
Metronidazole (blocks DNA synthesis in aerobic bacteria and protozoa)
Ciprofloxacin (a type of fluoroquinolone which prevents DNA replication in gram-negative bacteria)
Which groups of antibiotics target protein synthesis, give an example for each and what they target
Macrolides (e.g. clarithromycin - treats gram +ve bacteria and atypical pneumonia pathogens)
Lincosmaides (e.g. clindamycin - treats gram +ve and aerobic bacteria)
Tetracyclines (e.g. doxycycline - broad spectrum but mainly gram +ve)
Aminoglycosides (e.g. gentamicin - treats gram -ve bacteria and staphylococci)
What alternative mechanisms are targeted by some antibiotics, give two examples
Trimethoprim = anti-metabolite (folate antagonist), broad spectrum but mostly gram -ve bacteria
Nitrofurantoin = inhibits TCA cycle, DNA, RNA, and protein synthesis, treats gram +ve and -ve bacteria, commonly used for lower UTIs
What are bactericidal antibiotics and what are they used for?
These are agents which kill bacteria
They are useful if there will be poor penetration, or in infections which need to be eradicated quickly
They are the antibiotics which inhibit cell wall synthesis (beta lactams, glycopeptides)
What are bacteriostatic antibiotics, and how do they work?
These are agents which will inhibit the growth of bacteria to give time and support to the immune system to deal with the infection
They work by inhibiting protein or DNA synthesis, or metabolism
What is the minimum inhibitory concentration of bacteriostatic antibiotics, and how does this affect time or concentration dependent killing?
MIC is the dose above which is required for the antibiotic to be effective
- time dependent killing = where the key parameter is the time that the serum concentration remains above the MIC (t>MIC)
- concentration-dependent killing = where the key parameter is how high the concentration is above the MIC (peak concentration/MIC ratio)
What are the 4 ways in which bacteria resist antibiotics, give an example of each
Change the antibiotic target - change the molecular configuration or mask the antibiotic binding site (MRSA, VRE)
Destroy or inactivate the antibiotic (bacterial enzyme beta-lactamase hydrolyses the lactam ring of penicillins or cephalosporins)
Prevent antibiotic entry - bacteria modifies its membrane porin channel size, number, or selectivity (gram -ve bacteria against aminoglycosides)
Removing the antibiotic from the bacteria - proteins in bacteria act as pumps on membrane to export antibiotic (e.g. S. aureus or S. pneumoniae resistances to fluroquinolones)
What are cephalosporins used for?
People with a non-severe penicillin allergy
Works against some resistant bacteria
What are glycopeptides used for?
People with a severe penicillin allergy
Works against some resistant bacteria but gram +ve
How do bacteria develop resistance?
Intrinsic/natural resistance - e.g. vancomycin cannot penetrate the outer membrane of gram -ve bacteria
Spontaneous gene mutation - nucleotide changes amino acid sequence which changes cell/enzyme structure, reducing the affinity or activity of the antibiotic
Horizontal gene transfer - by conjugation (sharing plasmids e.g. ESBLs), by transduction (insertion of viral DNA by bacteriophages e.g. MRSA), or by transformation (picking up naked DNA e.g. spreading penicillin resistance from S. mitis to S. pneumonia)
What does MRSA stand for?
Methicillin resistant Staphylococcus aureus
How did MRSA become antibiotic resistant?
Bacteriophage mediated transduction of Staphylococcus cassette chromosome mec (SCC mec) which contains the resistant gene mecA
MecA encodes for penicillin binding protein 2a, so gives resistance to all beta-lactams
What does VRE stand for?
Vancomycin-resistant enterococci
How did VRE become antibiotic resistant
Plasmid mediated acquisition of a gene encoding for altered amino acid on the peptide chain which prevents the binding of vancomycin (promoted by cephalosporin use)
What does ESBLs stand for?
Extended spectrum beta lactamases
How are ESBLs antibiotic resistant, and what can they be treated with?
ESBLs hydrolyse the oxyimino side chains of cephalosporins and monobactams
They can be treated by also using a beta-lactamase inhibitor (e.g. amoxicillin + clavulanate = co-amoxiclav)
What do CRE/CPE stand for, and what are they?
Carbapenem resistant enterobacteriaceae
Carbapenemase producing enterobacteriaceae
These are bacteria which are able to break down carbapenem (invented to be highly resistant to degradation by beta-lactamase), so have very limited treatment options
What are fungi?
Fungi are eukaryotic organisms which can be unicellular or multicellular and complex
They are heterotrophic (can’t make their own food, rely on other sources of carbon and nitrogen)
Their cell wall is made of chitin, which provides strength and rigidity
What two forms are fungi found in?
Yeast = small single celled organisms that divide by budding (account for <1% of fungi, but the most medically relevant)
Mould = form multicellular hyphae (long branching filaments) and spores
Why do only a small proportion of fungi cause human infection?
Because of their inability to grow at 37 degrees
Because of the innate and adaptive immune response
List 4 common fungi which cause disease
Aspergillus
Pneumocystis
Candida
Cryptococcus
List some common superficial fungal infections
Vulvovaginal candidiasis (vaginal thrush/yeast infection)
Tinea pedis (athlete’s foot)
Onychomycosis (fungal nail infection)
Otitis externa (external ear infection)
List some rare invasive fungal infections
In immunocompromised patients… candida line infections, invasive aspergillosis, pneumocystis pneumonia (PCP)
In post-surgical patients… intra-abdominal fungal infections
In healthy hosts… fungal-exacerbated asthma, post-influenza aspergillosis, travel associated fungal infections
How are fungal infections diagnosed?
Radiology (insensitive in the early stages)
Microscopy (usually insensitive)
Culture (ok for yeasts, poor for moulds)
Molecular…
- PCR (mixed results)
- Antigen tests (cryptococcal Ag is the best)
Why is treating fungal infections harder than treating bacterial infections?
Treatment relies on identifying molecules with selective toxicity for the organism targets, which is more difficult for fungi than bacteria because they are eukaryotic (closer to human cells)
What different types of treatment targets are there for fungal diseases?
Targeting DNA/RNA/protein synthesis - not commonly used as these are similar to the human process (e.g. flucytosine)
Targeting cell wall - doesn’t exist in humans so good target (e.g. echinocandins = safe + effective against candida and some aspergillus)
Targeting cell membrane - contains ergosterol not cholesterol like human cells so good target (e.g. amphotericin = very broad spectrum, barrier to resistance, azoles = most common treatment, different drugs have different spectrums, toxicities, and interactions)
