Infective Flashcards
what are the 4 koch postulates. and why they aren’t true
- microbe must be present in all cases of disease but not in healthy people (BUT people can be asymptomatic)
- organisms must be isolated from a diseased and host and grown in pure culture (BUT some viruses and prions impossible to culture. And some infections are polymicrobial)
- Isolated organisms must cause disease when introduced in a suitable animal (BUT animal models may not be available or representative of human disease)
- the organism must be re-isolated from said infected animal
Modern Koch postulates
1-DNA sequence of a pathogen should be present in most cases of disease
2-Few/ no copies should be found in the host or tissues with no pathology
3-As the disease resolves, it should decrease & be undetectable
4-Sequence copy number should increase with severity of the disease
5-Proof of filterability (eg. viruses filtered out as smaller than bacteria)
6-Detection by immune system
is tonsillitis and cellulitis caused by primary or opportunistic pathogens. which are they caused by
-opportunisitve, causing infection in damaged host
Tonsilitis = streptococci =strep throat
Cellulitis=strep or staph
Give examples of disease transmitted via respiratory, sexual, blood, bites, feacal to oral, environmental and vector borne routes
-respiratory [HSV1, Influenza, measles, rhinovirus, TB]
-Sexually [HIV, syphilis, chlamydia, HPV, herpes, hep B & C]
-Blood [HIV, Hep B & C]
-Bites [anaerobic infection, Rabies, heb B]
-Feacal - oral [salmonella, norovirus]
-Environmental [C.difficile, enterovirus]
-Vector bourne through lice, ticks, fleas, sandfly, mosquitos & tsetse fly.
what are exotoxins and endotoxins
endotoxins = membrane compounds of gram negative. LPS released by gram negative when they die and activate inflammatory response
exotoxins = secreted locally by gram negative and positive
what is a virulence factors of leishmaniasis. what type of organisms are they
hides within macrophages, very motile,
Leishmania is a parasitic protozoan, a single-celled organism that are responsible for the disease leishmaniasis
difference between gram positive and negative (colour of microscopy, chemicals used to dye, membranes)
gram positive = purple, retain crystal violet, thick peptidoglycan cell wall, no outer lipid membrane
gram negative = pink, safranin stain, thinner peptidoglycan, LPS
how prokaryotes differ to eukaryotes
no internal membrane-bound organelles, single DNA strand, single chromosome, no histones, can transfer DNA, replicate by binary fusion, smaller, DNA in cytoplasm (not nucleus), peptidoglycan cell wall, appendages,
How viruses replicate. and their general structure
only replicate within the cytoplasm of cells of host organisms. Need host cells to survive - obligate intracellular parasites
-Attaches to the cell, enters it, synthesises its viral nucleic acids & proteins, and assembles new viruses.
-The host cell is destroyed and the new viruses are released via budding where it acquires a portion of the host’s virus-encoded glycoproteins to create an envelope
-RNA or DNA, double or single stranded
-capsid surrounds the DNA or RNA, some have envelopes too
fungus: are they eukaryotes or prokaryotes, what is in their cell walls, how do yeasts and moulds replicate
eukaryotes
cell walls contain chitin
yeast - mitosis (sexual)
moulds - meiosis (asexual)
name viruses that cause oral lesions. which viruses cause oral hairy leukoplakia and koplik’s spots
Herpes simplex = herpetic gingivostomatitis, herpetic ulcers
Herpangina (coxsackie virus) = white vesicles on soft palate
Epstein Barr virus (HHV4) = oral hairy leukoplakia
HIV= oral hairy leukoplakia, increased infections, Kaposi’s sarcoma
HPV = benign oral warts - cauliflower
Hand foot and mouth disease (coxsackie)
HHV3 reactivation = shingles and oral lesions
Measles virus= koplik’s spots (white surrounded by red patches on buccal mucosa)
HHV5 cytomegalovirus - palate ulceration
what surface proteins does influenza virus have
haemaglutinin (entry) and neurominidase (release). these allow attachment to respiratory tract of host
Name double stranded DNA, single RNA, single DNA, double RNA viruses
double DNA = herpes viruses, hep B, HPV
single RNA = influenza, measles, mumps, rubella, rhinovirus, hep C, HIV
single DNA - parvovirus
double RNA - rota virus
what is latency. examples of latent viruses
-Viruses can adopt a latent state where they are dormant. They are not replicating so cannot generate peptide for MHC class 1 and antigen presentation, so cannot be killed
-Hide from immunosurveillance
eg. Human herpes viruses and HIV
-reactivation causes by stress, fever, menstruation, cold, UV radiation, bacterial infection
what cells herpes simplex virus infects. and where it can become latent. how long cold sore vesicles last
-active viral replication in mucosal tissue and affects epithelial cells usually around the lips
-Virus spreads to sensory neurons of trigeminal ganglion and persists in a latent state so protected from immune system. no replication
-At times of stress or altered immune status the virus re-infects epithelial cells usually around the mouth causing cold sores, where vesicles last 5-12 days
Which HHV number is Epstein Barr virus. What disease it causes. what cells it infects and what cancer it is associated with
HHV4
-causes glandular fever (infectious mononucleosis), swollen glands, sore throat, headache, lots of little red spots on palate, cervical lymphadenopathy
-infects B cells, becoming latent in memory B cells. waits for them to be activated to reinfect.
-B cells can become malignant (Burkitt’s lymphoma) in immunocompromised
-can cause oral hairy leukoplakia - benign white striped lesion on tongue associated with HIV or immunosuppression
-tranmsision via saliva or sexual contact. Transfusions, transplants
symptoms of HSV 1 and 2
HSV1: disease above waist. Primary infection causes herpetic gingivostomatits, herpetic whitlow on fingers, meningitis, dermatitis, conjunctivitis. Later reactivation causes cold sores (herpes labialis), corneal ulcers, encephalitis.
-HSV2: disease below waist. mainly causes genital lesions, meningitis. Reactivation often symptomatic or can cause cold sores
Which HHV is varicella zoster virus. where it infects and what infection it causes. which ganglion it goes to. transmission
HHV3
-transmission via oral, sexual and respiratory route via aerosol droplets or through direct contact
-Primary infection - infects blood then liver and spleen, causing chicken pox (red raised spots and pus filled vesicles. Last 5 days in children until full crusting, more severe in adults)
- gains access to trigeminal and dorsal root ganglions and establishes latency.
-Reinfection causes shingles in the area depending on the nerve it infects. unilateral neuralgic pain and tingling then rash. it never crosses midline if in trigeminal nerve
Which viruses are associate with Kaposi’s carcinoma, cervical cancer and Burkitt’s lymphoma
kaposi’s = HHV8, HIV
cervical = HPV
Burkitt’s = HHV4
what is HHV5 virus called. what it causes
Human Cytomegalovirus (HHV5)
-infects WBCs
- glandular fever (infectious mononucleosis), palate ulceration
-severe disease in immunocompromised
how herpes viruses are transmitted. DNA or RNA? double or single stranded?
HSV1&2= oral or sexual
HHV3= respiratory, oral, sexual
HHV4=sexual, oral, transfusions, transplants, congenital
HHV5=saliva, urine, blood, breast milk
Enveloped
double stranded DNA
what is neonatal herpes simplex and how it is caused
life threatening. - HSV2 from the mothers birth canal is given to a baby. Babies have very poor immunity so prone to infection. Caesarian section avoids this, but neonatal disease does not outweigh risks of section
Or newborns can sometimes get HSV-1 from close contact with someone who is shedding HSV-1 virus in their saliva
how HHV is diagnosed
PCR for direct viral detection. do a lesion swab or cerebrospinal fluid sample. - molecular diagnostics
or clinical diagnosis
How acyclovir is used to treat human herpes virus. What is the topical drug called and the prodrug of it
it is activated/ phosphorylated by thymidine kinase (specific in infected patients) to the active triphosphate form. It inhibits DNA polymerase and causes DNA chain termination. It is a nucleoside analogue
-5x daily as poor oral bioavailability
-valaciclovir =prodrug (metabolised into acyclovir)
-Zovirax =topical form
Who can be given vaccines and post-exposure prophylaxis for the varicella zoster virus (HHV3)
-post-exposure prophylaxis: treatment only for those at increased risk - pregnant or immunocompromised. concentrated antibodies against HHV3 given intramuscular. Only effective if given within 10 days of contact
-vaccine: live attenuated vaccine given at childhood or healthcare workers who haven’t had chicken pox.
-shingles vaccine for 70+ year olds
what samples are sent to the lab to make a diagnosis. what coloured tubes are used for viral swabs and clotted blood
-specimens, not a swab as they hold tiny samples and anaerobes die
-submit tissue, fluid or aspirate
-viral = green
-blood for serology= yellow
what info is required when sending a specimen to the lab
-patient name, MRN, NHS no.DOB
-date/time/location of sample
-specimen type
-requestor name and contact details
-investigation required
-presenting complaint
-comorbitites
-allergies
-current and past treatment
how HIV and hep B is diagnosed. how long it takes
serology - antibody and antigen reactions
-antibodies take a long time to be produced by body so takes a few weeks for results, compared to PCR technique where you get results in 2-3 days
explain methicillin resistant staph aureus (MRSA) what antibiotics treat MRSA
methicillin is a narrow-spectrum Beta lactam antibiotic of the penicillin family. It targets the transpeptidase protein that is involved in the cross linking in peptidoglycan formation.
- S. aureus has mecA gene that encodes PBP2a (a transpeptidase involved in peptidoglycan formation and a protein that antibiotics bind to)
- Modification of the mecA gene and this protein reduces binding to B lactams, makes them resistant to methicillin.
- PBP2a has lower affinity for methicillin so is less sensitive to the action of methicillin.
-MRSA treated by vancomycin, teicoplanin, linezolid
strategies to improve effectiveness of antibiotics
-reduce infection and therefore need for antibiotics (immunisation, better infection control)
-change incentives that encourage antibiotic misuse and overuse
-finish a full course, correct dose and duration
-avoid over prescribing, only used when absolutely necessary to prevent resistance
-avoid use in agriculture
-educate public and healthcare workers on use
-no over the counter
-develop new antibiotics
antibiotic resistance mechanism. examples of natural and acquired resistance
-ability of a microbe to resist the effects of medication that could perviously eradicate it
- bacteria in biofilms mutate constantly and these mutant cells are more resistant than others. Biofilms also contain slow growing resistant persister cells that are also resistant.
- After a course of antibiotics, susceptible cells die, while these resistant cells can survive and continue to grow with less competition. Shift in population causes infection
- more microbials= increased chance of these resistant cells remaining and replicating, causing resistance and infection.
-Acquired: produce enzymes that degrade the drug, efflux pumps, alters drug’s metabolic pathway, alters drug target to affect binding,
-Natural: Have larger membranes, lack permeability so drug cannot enter, thick peptidoglycan so less affected by B lactam antibiotics
how pencillin work. how bacteria can become resistant, and how this can be combated. examples of other beta lactams
- Contains a beta lactam ring that inhibit peptidoglycan synthesis of gram positive bacteria which weakens the cell wall and causes it to swell and rupture.
- It inhibits transpeptidase enzyme, which is involved in the cross linking of NAG and NAM amino sugars into glycol chains
-bacterocidal - Bacteria can produce B lactamase which hydrolyses the Beta lactam ring in penicillin. Therefore the penicillin is ineffective at destroying peptidoglycan
- Beta lactamase can be inhibited by clavulanic acid. This can be given along side amoxicillin, in order to prevent resistance. (co-amoxiclav)
-carbapenems, cephalosporins, vancomycin
how macrolide and tetracycline work . examples of drugs
they target ribosomes and therefore inhibit protein synthesis
Tetracycline binds to 30S subunit which stops initiation of synthesis and elongation. (eg. doxycline)
-Macrolides bind to 50S to block translocation
(clarithromycin, erythromycin, clindamycin, chloramphenicol, rifampicin)
-bacterostatic
-useful in resp tract infections and skin’ soft tissue infections
how fluroquinolones work
DNA gyrase (a topoisomerase for preventing supercoiling) is inhibited by fluoroquinolone, so DNA replication is inhibited as knots are created
rarely used due to hypersensitivity and GI disturbances
-bacterocidal
how sulphonamides and trimethoprim work
inhibit folate metabolism so inhibit DNA synthesis. Sulphonamides: inhibit dihydropteroate synthetase
Trimethoprim: inhibits dihydrofolate reductase
-bacterostatic
cephalosporin action. when to give them
B lactam antibiotics, preventing cell wall synthesis
avoid if pt has penicillin allergy ad 3-9% patients are cross allergic to it
what are nitromidazoles. give an example
used if a pt has an anaerobic bacterial infection
eg. metranizadole
* Target imidazole ring to disrupt DNA, causing DNA to fragment and mutations
-prescribe if spreading infection with systemic signs
what are the 3 first line antibiotics for dental abscesses. what is 3rd line
-amoxicillin [500mg for 5days]
-metranidazole [400mg for 3 days] - if penicillin allergy
-erythromycin [500mg for 5 days]
-clindamycin [150-300mg for 5 days]
how to treat OAC, causing sinusiits
-immediate primary closure. consider Essex retainer if not possible
-antibiotics: 1st line amoxicillin and ephedrine hydrochloride nasal drops.
-2nd line doxycycline and nasal drops.
-3rd line co-amoxiclav
