ICS - microbiolgy Flashcards
define pathogen
Pathogen
Organism that causes or is capable of causing disease
Define Commensal
Commensal
Organism which colonises the host but causes no disease in normal circumstances
Define Opportunist Pathogen
Opportunist Pathogen
Microbe that only causes disease if host defences are compromised
Define Virulence/Pathogenicity
Virulence/Pathogenicity
The degree to which a given organism is pathogenic
Define Asymptomatic carriage
Asymptomatic carriage
When a pathogen is carried harmlessly at a tissue site where it causes no disease
what areas are open to bacterial colonistation
muscoal surfaces
The GI tract, lungs, bladder, kidnyes, urter, urethrer, gallbladder
out of thses, teh lungs and bladder should try and be bacterial free
what dhape is a cocus
spherical
what shap is a bacillus
rod
what colour is gram positive
purple
what color is gram negaitve
pink
what is a curved rod shaped bacteria
vibrio
what is teh name for spiral rod
spirochaete (sounds like a type of pasta)
what stain is for microbactrium
ziehl-neelsen stain (acid fast stain)
what are the differences between gram positive and gram negative bacteria
gram posiitve bacteria have a thick peptidoglygan layer and gram negative dont, they have a large lipoplysachoride (also known as endotoxin) layer instead
what are the two types of bacterial toxins
ENDOTOXIN
Component of the outer membrane of bacteria, eg lipopolysaccharide in Gram negative bacteria
EXOTOXIN
Secreted proteins of Gram positive and Gram negative bacteria
what is a toxoid
Toxoid is a toxin treated (usually with formaldehyde) so that it loses its toxicity but retains its antigenicity
what are teh features of an exotoxin
protien, specific action, strong antingencity, produced by gram + and - bacteria, and convertable into a toxoid
what are teh features of endotoxins
liposaccoride, non specific, produced only by gram negative, not convertable to a toxoid
in what 3 modes can bacteria gain new genetic information
conjugation - via a sex pilus
transformation - sent over in a plasmid
transduction - via phage (infected by a virus)
what are the three ways a bacterias DNAs can change
base substitution, deletion, insertation
what is obligate intracellular bacteria
bacteria that cannot be grown on an artifical media, only in human cells and tissues
what are the three tpes of obligate intracellular bacteria
rickettsia, chlamydia, coxiella
what are teh cypes of bacteria that can grwo on an artifical media and have no cell wall
mollicutes
what are the cocci, gram negative, anaerobic bacteria
veillonella
what are teh cocci, which are gram negative and aerobic
neisseria and moraxella
what are the cocci, gram positive, aerobic, bacteria
staphylococcus, streptococcus
what test is done to distuinguish between streptococccus and what are the three outcomes
Macconkey
beta heamolytic, alpha heamolytic, non heamolytic
what are the cocci, anerobic, gram posiitve bacteria
peptostrepococcus
how does staphylococcus often grow and how does streptococcus grow
in clusters, streptococcus grows in chains
what does coagulase mean
Coagulase: enzyme produced
by bacteria that clots blood plasma.
what are teh three most important staphylococcus, and are therse coagulase positive or negative
s. aureus (because it looks gold) is coagulase positive
s. epidermis is coagulase negative
s. saphrophyticus - negative
Staphylococcus’ normal habitiat is the nose and skin
what is the information about Staphylococcus aureus
Spread by aerosol and touch
carriers & shedders
Virulence factors
Pore-forming toxins (some strains)
a - haemolysin
Panton-Valentine Leucocidin ‘PVL’
Proteases
Exfoliatin
Toxic Shock Syndrome toxin
(stimulates cytokine release)
Protein A
(surface protein which binds antibodies in wrong orientation)
It causes wound infections on the skin (pyogenic)
impertigo, pneumonia, sceptacemia
it is also sotin mediated and can causes toxic shock and food poisnening
what is S.epidermidis
S.epidermidis
Infections are ‘opportunistic’
immunocompromised,
prostheses
Main virulence factor - ability to form persistent biofilms
S.saprophyticus
S.saprophyticus
Acute cystitis
haemagglutinin for adhesion
urease
what is heamolysis
destruction of red blood cells (in thsi case by bacteria to access teh nutrienst)
what test is done after teh alpha heamolytic and what are teh bacteria found?
optochin test
resistant - viridans strep
sentitive - s. pneumoniae
what are the beta and gamma heaolysis bacteria, and what lancefield group are they?
beta - complete lysis
e.g. S.pyogenes
(ABCG)
gamma - no lysis
S.Boris and Enterococcus (not a streptococcus)
(D)
what is Antigenic sero-grouping and 2 exmaples
Antigenic sero-grouping (for Beta haemolytic strep only)
It is done by using teh lancefiels micobead agglutination test, to put them into groups
Group A - S.pyogenes
thraot, skin, post partum
Group B - S.agalactiae neonatal infections
what is teh Lancefield microbead agglutination test
Antiserum (antibodies) made that recognise each group
Tagged to tiny plastic beads
added to a suspension of bacteria
Antibodies bind bacteria and beads clump together
Visible to naked eye
what are the Infections caused by S.pyogenes
Respiratory
Tonsillitis & pharyngitis
Otitis media
Skin and Soft tissue
Wound infections
Impetigo
cellulitis
puerperal fever
Scarlet fever
SPeA and M type
Complications
rheumatic fever
glomerulonephritis
what are virulance factors
Virulence is described as an ability of an organism to infect the host and cause a disease. Virulence factors are the molecules that assist the bacterium colonize the host at the cellular level. These factors are either secretory, membrane associated or cytosolic in nature.`
what are the S.pneumoniae virulence factors
Capsule
polysaccharide (84 types), antiphagocytic
polysaccharide vaccine ‘PPV’ 23 types
conjugate vaccine ‘PCV’ 13 types
Inflammatory wall constituents
teichoic acid (choline)
peptidoglycan
Cytotoxin
pneumolysin
describe teh Viridans group streptococci
- haemolytic (or non-haemolytic)
Optochin resistant
Some cause dental caries & abscesses
Important in infective endocarditits
S. sanguinis, S. oralis
Cause deep organ abscesses (e.g. brain, liver)
Most virulent are the “milleri group”
S.intermedius, S.anginosus, S.constellatus
what are the S.pyogenes virulence factors
Exported factors
Enzymes
Hyaluronidase
- spreading
Streptokinase
- breaks down clots
C5a peptidase
- reduces chemotaxis
Toxins
Streptolysins O&S
-binds cholesterol
Erythrogenic toxin
-Streptococcal pyrogenic toxin e.g. SPeA – exaggerated response
Surface factors
Capsule - hyaluronic acid
M protein – surface protein
(encourages complement degradation
what are three aerobic gram posiitve bascilli
Listeria monocytogenes
Bacillus anthracis
Corynebacterium diphtheriae
what are three anerobic gram posiitve bacteria
all from teh clostridia species
C. tetani - causes tetnus
C. botulinum - causes botulism
C. difficile - causes antibiotic assocaited diarrhea, pseudomembranous colitus
what makes a gram negative bacteria so special
it has two membranes, a phospholipd and a lipopolysacchoride
what are teh two types of virulence factors
coloinsation factors - adhesions, invasins, nuterin aquesition, defence against teh host
toxins - secreted protiens that daeg
what does peritrichous flagella mean
the entire surface is coverd by flagella
what are proteobacteria
They come from the enterobacteria family
they are rods are noramlly are motile with pertrichous flagella
some specied colonise in teh intestinal tract
what is a MacConkey-lactose agar, how does it work, and what is an example of a lac positve and a lac negitive
this is a tye of agar that is pH senstiive and will turn red when the bacteria used lactose as theri food as it will make lactic acid, whihc has a low pH. Therefore if it is lac positive such as E Coli, it will be red and if it Lac negative, such as samonella or shigella, it will not show up red.
what is a serotype
it is a way of catogrinsing bacteria based on teh aino a cids and carbohydrates in teh cell surface.
therre can be variation inbetween varietns of a single specied and different strains of teh same species
Antigenically distinct variants of a single species are referred to as
‘serovars’, i.e. E. coli O157:H7 (an enterohaemorrhagic E. coli; EHEC) and E. coli
O45:K1:H7 (a neonatal meningitis-associated E. coli, NMEC) are different serovars.
what are teh most commn infections cased by pathogenic Escherichia coli strains
Wound infections (surgical)
(ii) UTIs (cystitis; 75-80% of ♀ UTIs - faecal source or sexual activity;
catheterisation - most common type of nosocomial infection)
(iii) Gastroenteritis
(iv) Travellers’ diarrhoea
(v) Bacteraemia (sometimes leading to sepsis syndrome)
(vi) Meningitis (infants) - rare in UK
what is an example of how ecoli cause diohrea
teh toxin secreted causes teh pump in teh intestinal cells to be turned on and Cl- ions to be pumped out en mass
thsi causes water to follow via osmosis whihc causes diorhea
what is dysantry
bloody dihoreah containg pus, blood and mucus
what is shigella
Very closely related to Escherichia (= “E. coli + virulence plasmid”)
Four species: S. dysenteriae, S. flexneri, S. boydii, S. sonnei
Shigellosis: severe bloody diarrhoea (bacillary dysentery)
S. dysenteriae causes most severe form.
S. sonnei most prevalent in developed world.
how does shigella invade the colonic mucosa
it is incredibly acid tolerant
it enters though eh M cells - antigen sampling cells
it then moves laterally though all of ghe gap junstions between cells and kills te enterocytes
It also produces shiga toxin, which can traget teh kidneys and causes heamolutic uraemic kidneys
this causes microvascular thromobosis in teh kidneys and causes kidney faliure
what are teh two types of samonella
S. enterica - responsible for salmonellosis
>2,500 serovars*
S. bongori - rare (contact with reptiles)
what are the three forms of salmonellosis caused by S. enterica:
- Gastroenteritis/enterocolitis (serovars Enteritidis and Typhimurium)Frequent cause of food poisoning (milk, poultry meat & eggs)
Second highest no. of food-related hospitalisations/deaths (UK)
6-36 hr incubation period, resolves (~7 days)
Localised infection, only occasionally systemic - Enteric fever - typhoid/paratyphoid fever (serovars Typhi and Paratyphi)Poor quality drinking water/poor sanitation
Systemic disease
~20 million cases, ~200,000 deaths/year (globally) - Bacteraemia (serovars Cholerasuis and Dublin)Uncommon
what is the process of pathogensis of salmonellosis
Ingestion of contaminated food/water - high I.D. (~106) (‘faecal-oral route’)
Invasion of gut epithelium (small intestine)
Transcytosed to basolateral membrane
Enters submucosal macrophages
Intracellular survival/replication
what is heamophilius influenza
a human parasite that is carried in the nasopharyngeal of many people,
what are 5 oportunistic infections
meningitus, bronchopneumonia, pneumonia in CF, COPD and HIV patients
what is blood agar and choclate gar
blood - agar jelly mixed with horse blood
choclate agar - blood agar heated to lysis teh RBCs
what does the capsule of H.influenza do
penatrates the nasopharyngea epithelium
resistance to phagocytosis and teh complenent system
what does fastidiuos bacteria mean
Microorganisms that are difficult to grow in the laboratory because they have complex or restricted nutritional and/or environmental requirements.
what bacteria is responibe for most of teh food poinsengiins in teh UK
camplobacter
what is mycobacteria and what is an example of it
the are a weakly gram positive but not classafied as it, acid fast staining bacteria. Thye have a thicker cell wall, with no capsule and dont form endospores.
An example is Mycobacterium tuberculosis and mycobacterium leprae
what is teh structure of a mycobacteria
high lipid contnt with mycolic acids in there
slightly curved bacilli
rewact to teh zhiel neelson stain so are classified as acid fast
they can survive in low pH enviroments and even inside of macrophages
how do macrophage fight off mycobacteria
phagocytosed by macrophage
the bactuerim has evolved to escape into teh cytosol
CD4T cells genreate interferon gamma to activate intracellular killing
how does a granulomma form
alveolar macrophages digest pathogens
they then become more epithelioid and can fuse together to become langahan giant cells
it get surronded by lymphocytes creasing a small pocked of ingfected macrophages
fibroblasts are lad aroung it to wall it off
teh central tissue necrosis
If it works thenteh bacteria turn dorment, and if it doesnt there is just a cavidty of live bacteria that can causes condumption disease 9disseminated disease) later on
what are two reasons that granuomas can become unstable
CD4 depletion (can be caused by HIV)
TNFa depletion by anti tumour necrosis factor drugs
Ths causes teh bacteria to escape into teh body
what are teh two types of leprosy
tuberculoid leprosy - tissue hypersensitivity and granulomma, tissue damage to neerves
lepromatous leprosy - lesions but poorly formed granulomas, skin lesion, TH2 based
how is TB diagnosed in clininc
The mantoux skin test
The person is injected wth tuberculin and 2-3 days later comes back to see teh doctor
if there is a reaised red bump they are TB posiitve - either latent or active
how is TB diagnosed in clininc
The mantoux skin test
The person is injected wth tuberculin and 2-3 days later comes back to see teh doctor
if there is a reaised red bump they are TB posiitve - either latent or active
what is a virus
an infections obligate intracellular parasite comprising of genetic materieral surronded by a proten coat and membrane
what are teh three shapes of a virus
helical
isosahedreal
complex
what 5 ways can virus3s cause disease
-direct destruction of host cell
poliovirus - infects nerve cells and cuases lysis of teh cells cusing paralysis
- modification of teh most cell
rotavirus atrophies villi and causes flat epithelium cells whihc decreases surface area, causing sugar not to be absorbed and water to be draw out f teh cells cuaing dihorreha - over reactivity of teh immune system
hepatitus B cuases teh cytotoxix T lymphocyte destory all infected cells causeing fanduc and destruction of hepatocytes - damage through cell proliferation
HPV, cuases cervical cancer by putting its own DNA into host chromosomes causing oncoprotien to be made whihc causes cell mutations - Evasion of host defences leading to dormancy and later reinfection
On a cellular level - Herpes virus goes latent in teh cells but never goes away, its teh same with chickenpoc and shingles later on
On a moleculr level - the viruss mutates so its not recognized
what are the 5 types of vaccine makers and an example for each
inactivated - polio
attenueated - MMR BCG
secreted products - tetanus
contituents of cell walls - Hep B
recombiant components - experinmental
what is prophylacxis
prevenging teh disease from developing via using vaccine and so on
what are teh 5 major classificatoin of protozoa
Flaggelates - have a flagelum to propel them
Amoebae -
Sporozoan
Cilliates - lots of little hairs to move them
Microsporidia
what is sleeping skiness
sleeping skiness - caused by the tsetse fly bight whihc passes on teh protozoa
causes a chancre, CNS changes and then coma and death, there are two types of this,
what is myalgia
pain in muslces
what is teh most fatal type of malaria
plasmodium falciparum
what are the syptoms of malaria
FEVER!!! chills, headache, mylagia, fatuigue, Diarrhoa, vomiting, abdominal pain
what are some signs of malaria
aneamia, jaundice, heaptoslpenomegally blac water fever (black urine)
what is teh malerial life cycle
three cycles
exoerythrocytic cycle
erethrocytic cycle
sporogenuic cycle
what is teh sporogenuic cycle of maleria
how teh mosquito itself gets infected
it feeds on blood from an infected human
it creates an oocyte
this bursts and frees lots of sporozoites
what is the exoerythrocytic cycle of maleria
teh parasite gets into teh hepatic cell
reproduces by forming a schizont
teh schizont bursts and spreads the protozoa
THis cuses an inflamed liver and am=bdminal pain
what s the erethryocytic cycle of malaria
the parasite enters teh erethrocyte
mature trophozoite turns into a schizont
this ruptures and reeases more malaria into teh body
thsi cuases aneamia, jaundice, haemoglobinuria
how does complicated malaria form and what areteh consequences
the infected red blood cells turn stick and adhere to eachother and the epithelium
thsi causes mini blockedges in small blood vessles called microinfarcts
cereberal - hypoglycemia causing coma and drowsyness
renal - dehydration, hypotension, heamobloburina - fatuigue, things in urine
ARDs - vascular occulsion, aneamia, acidosis, casuing hypoxia, pulmonary oedema
what are teh treatments for malaria
IV artesunate for complicated
treat each organ affected - oxygen, fluids, antibiotics, blood products
defien host pathogen interactions
how pathogens sustain themseles withi teh host
defien host pathogen interactions
how pathogens sustain themseles withi teh host
what are the 4 stages of pathogenesis
exposure (contact),
adhesion (colonization),
invasion,
infection.
what are commensal microorganisms
Commensal microorganisms are the resident flora and usually nonpathogenic
what is the humoral resoponse to viruses
antibodies - G, A, block binding, block virus host cell opsionation
IgM - Agglutinates particals
coplemetn factors - opsonation, lysis
what is teh cell mediated response to viruses
IFN from Th (CD4+) or Cytotoxic T lymphocytes (CTL)/Tc (CD8+) – has direct antiviral action
CTL can kill infected cells
NK cells and macrophages are involved in antibody-dependent cellular cytotoxicity(ADCC) killing
IFN induces anti viral proteins for bystander cells
define antigenic drift and antigenic shift
Antigenic Drift - spontaneous mutations, occur gradually giving minor changes in HA (haemagglutinin) and NA (neuraminidase). Epidemics.
Antigenic Shift - sudden emergence of new subtype different to that of preceding virus. Pandemics.
how is a gram stain completed
Fixation of clinical materials to microscope slide (heat/methanol)
Application of primary stain: crystal violet (all cells turn purple)
Application of mordant (iodine): crystal violet-iodine complex formed
Decolourisation step: distinguishes gram +ve and gram -ve, use acetone or ethanol
Application of counterstain: safranin to stain gram -ve pink
the mnumonic for this is
Come in and stain
crystal violet, iodene, alcohol, safranin
what are the gram positive rods?
Gram +ve rods = Corneybacteria, Mycobacteria, Listeria, Bacillus, Nocardia
what is teh ost response to a bacterial infection
IgA(s) Block attachment to host cells
Ab C3b Opsonisation, Prevents proliferation
Complement Cell lysis, Prevents proliferation
Ab Neutralise toxins
what are symptoms of meningitus
stiffness of the neck, photophobia + severe headache
Infective: fever, malaise
Petechial rash associated with meningococcal meningitis
what are teh tow most common bacterial causes of meningitus
Neisseria meningitidis, Streptococcus pneumoniae
these are both diplococci
What would be present in the blood if meningitus was presant for bacteria, viral, TB
What would be present in the blood if
SF sample (lumbar puncture at L4) for microscopy + sensitivity testing
Bacteria: turbid yellow colour, neutrophil polymorphs, raised protein, low glucose
Viral: lymphocytes, normal protein, normal glucose
Tb: lymphocytes, raised protein, low/normal glucose
Nose + throat swabs for viral
what are the treatment for viral and then bacterial meningitus
Bacterial: start antibiotics before tests come back if suspected
Cephalosporins: IV cefotaxime/ IV ceftriaxone
If over 50/immunocompromised add IV amoxicillin to cover listeria
One dose oral ciprofloxacin - prophylaxis for contacts
Meningococcal septicaemia: immediate IM benzylpenicillin in community/ IV cefotaxime in hospital
Viral: supportive treatment, self-limiting in 4-10 days, acyclovir for HSV meningitis
what are teh catogries of antibiotics that inhibit cell wall synthesis
glycopeptides - vancomycin
beta lactams - peniclins (flucoxacillin), cephalosporins (cephalein) carbapenems (imipenem)
what test is done after teh alpha heamolytic and what are teh bacteria found?
optochin test
resistant - viridans strep
sentitive - s. pneumoniae
what are the gram positive aerobic bacilli
bacillus anthratics
corynebactera diptherria
listeria monocytogenes
what are the gram negative positive mcConcey bacteria
E.coli
Klebsiella
what are teh gram negative, negative McConkey, oxidase positive bacteria
pseudomonas
campylobacter
what are the gram negative, McConkey positive, oxidase negative, bacteria
shigella
salmonella
protwas
what are teh three catogries of beta lactams and an an examle of each
penicillins - fluccloxicillin
cephalosporins - cefotaxime, cefriaxone, cefuroxime
carbapenems - meropenem
when would glycopeptide antibiotics be given
for gram positive only
for penicilllin allergys
if resistant to teh beta lactams
what are two glycopeptide antibiotics
vancomycin
teicoplanin
what are teh 4 drug catogires of protien synthesis inhibitors and when is each one used
lincosamides - clindamycin (G+, cellulitus, nectosinf fasciitus)
macolides - clarithromycin (penicillin allergys)
tetracyclines - doxycycline (cellulitus, pneumonia)
aminoglycosids - genatamicin (G- nd staphs, UTIs, Endocarditus)
what are teh folate synthesis blocker antibiotics
sulphonamides - trimothroprim and co-trioxazole
which antibiotic should never be giver to a pregnant woman
Folate synthesis blockers - no sulphonamides
sulphemthoazole, trimethoprin
what is the broadest antobiotic and which catogry is it in
Meropenem
carbopenem group
what are teh RNA synthesis blocker antibiotics
metronidazole
ciprofloxacin
what are the folate blocker antibiotics and what are they used for
trimethoprim and co-trimxazole
UTIs and mainly gor G-
what antibiotic would be given for staph infections
Flucloxacillin
what antibiotic would you give to treat a UTU
Trimethoprim
what antibiotic would you give for MRSA
Vancomyocin
what are two examples of mycobacteria diseases
TB and leprosy
what is myobacteria
Aerobic, non-spore forming, non-mobile bacilli
Slow-growing causes gradual onset of disease
Requires multi-antibiotic treatment for a prolonged period
what type of stain will show myobacteria
Ziehl- Neelson - its an acid fast
how do viruses cause disease
Can cause disease via direct destruction (polio), modification (rotavirus), over-reactivity (hepatitis B), damage through cell proliferation (HPV)
how are viral infections diagnosed
PCR + nucleic acid amplification tests (NAAT) used, can also do serology (look for antibodies in response to virus
what are teh antibodies for a viral infection
IgM within 1 week of onset, IgG appears later
what drug is teh main one given for viral infections
Acyclovir
what are protozoa
Microscopic unicellular eukaryotes
what are the 4 classification of protozoa
ameoboids, ciliates, sporozoan, flagellates
what are 4 examples of protozoa `
malaria, giardia lamblia, toxoplasmiosis, trichomonas vaginalis
what sjould a high fever and recent travel indicate
MALARIA!
what are fungi
Eukaryote
Have a cell wall - chitin + glucans (polysaccharides)
Move by growing across or through structures or by dispersion in air/ water
what are the 2 forms of fungi
Yeast - single cell that divide via budding
Moulds - form multicellular hyphae or spores
what are some examples of diseases caused by fungi
candida, athlete’s foot, nappy rash
what do anti fungal drugs normally end in
-azole
what are the three classifications of worms
nematodes (roundworms), trematodes (flatworms), ceratodes (tapeworms
how do worms reproduce
Adult worms cannot replicate inside body without a period of development outside the body
Pre-patent period = interval between infection + appearance of eggs/ larvae in stool
what are teh antibodies response to worm infections
Mainly IgG + IgE mediated
what are two exampes of worm caused diseases
hookworm, schistosomiasis
what are teh layers of teh HIV envelope
RNA + Capsid + RNA transcriptase
what are three diseases that heamophilus influenzea cause
meningitus in pre school children
pharyngitus
otisis media
Exaubation of COPD
what are fungi
Eukaryotic
Chitinous cell wall
Heterotrophic
“Move” by means of growth or through the generation of spores (conidia), which are carried through air or water
what is teh difference between yeast and 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
what are some invasive fungi conditions taht can affect: imounocm[armised hosts, post surgical patients, and healthy hosts
Immunocompromised hosts:
Candida line infections
Invasive aspergillosis
Pneumocystis
Cryptococcosis
Mucormycosis
Post-surgical patients:
Intra-abdominal infection
Healthy hosts:
Fungal asthma
Travel associated fungal infections
Dimorphic fungi
Post-influenza aspergillosis
how are fungal infections diagnosed
radiology, microscopy, cultur, molecular (PCR and antigen)
why are fungo harder to treat than bacteria
they are eukaryotic, so more similar ot humans
what is one of teh best drug tyoes against fungi
attacking teh cell wall as humans dont have one
or attacking teh cell membrane as teh humna one cntians cholesterol ad teh fungal one contains ergsterol
what is the broadests types of antifungal
amphotericin B
what is a bad CD4 level in HIV+ patients
anything below 200
if they have a normal Cd4 of above 500 it means that they can effectivly be treated as a normal patient
what are some fungal drug interactions
they react with cytochrome p450 enzymes and can inhibit them, thsi means that it shouldbe be taken with some drugs such as warfrin
what was teh target for 2020 in teh world for HIV
90-90-90
90% diagnosed
90% treated
90% to an undetectable level
what are teh three HIV transmission routes
Sexual
Vertical (mother to child)
Blood (needles - reduced due to teh needle exchange and also blood transfusoins screened)
what is prep, what is PEP
pre-exposure prothylaxis
take it before exposure to stop yourself from being able to get it
PEP:
Post exposure prophylaxis, you take it after you are exposed
what are the original symptoms of HIV
Generalised lymphadenopathy
Acute generalised rash
Glandular fever/ flu-like illnesses
Think about seroconversion
HIV rash it ofther on teh paksm of teh hands!
what else can be confused with HIV wit teh first, flu and rash like sympotms
Syphyliss
hand foot and mouth disease
what are teh later sympotms of HIV
Unexplained weight loss or night sweats
Persistent diarrhoea
Gradually increasing shortness of breath and dry cough
Recurrent bacterial infections including pneumococcal pneumonia
how does HIV affect teh CD4 receptors
HIV fuses to teh receptors and passes on its content
what are 4 drug targets for anti HIV
- entry point
reverse transcriptase inhibitors
Protease inhibitors - intergrase inhibitors
how does teh immune system respond to HIV
One of the key immune responses to HIV-1, from CD4+ T-helper cells, is lost from very early in infection, because these are the cells HIV infects first
There is a very vigorous response from cytotoxic CD8+ T-cells, which provides the major force controlling viral replication but ultimately fail when “immune exhaustion” sets in
what makes HIV avoident of the immune system
it onlt contains a few envelops strikes
tey antigens are highly glycosaeted whihc makes it haed for teh Antibodies to bind
The envelope (gp120/41) proteins can change substantially without affecting virus function
what is teh difference between gram pos and neg cell walls
pos - have a thick layer of peptidoglycan
neg - have a thin latyer of peptidoglycan and an outer mebrane called lipopolysaccoride, which is also called endotoxin
