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Phase 2a > ICS - microbiolgy > Flashcards

ICS - microbiolgy Flashcards

1
Q

define pathogen

A

Pathogen
Organism that causes or is capable of causing disease

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2
Q

Define Commensal

A

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

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3
Q

Define Opportunist Pathogen

A

Opportunist Pathogen
Microbe that only causes disease if host defences are compromised

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4
Q

Define Virulence/Pathogenicity

A

Virulence/Pathogenicity
The degree to which a given organism is pathogenic

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5
Q

Define Asymptomatic carriage

A

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

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6
Q

what areas are open to bacterial colonistation

A

muscoal surfaces
The GI tract, lungs, bladder, kidnyes, urter, urethrer, gallbladder
out of thses, teh lungs and bladder should try and be bacterial free

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7
Q

what dhape is a cocus

A

spherical

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8
Q

what shap is a bacillus

A

rod

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9
Q

what colour is gram positive

A

purple

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10
Q

what color is gram negaitve

A

pink

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11
Q

what is a curved rod shaped bacteria

A

vibrio

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12
Q

what is teh name for spiral rod

A

spirochaete (sounds like a type of pasta)

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13
Q

what stain is for microbactrium

A

ziehl-neelsen stain (acid fast stain)

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14
Q

what are the differences between gram positive and gram negative bacteria

A

gram posiitve bacteria have a thick peptidoglygan layer and gram negative dont, they have a large lipoplysachoride (also known as endotoxin) layer instead

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15
Q

what are the two types of bacterial toxins

A

ENDOTOXIN
Component of the outer membrane of bacteria, eg lipopolysaccharide in Gram negative bacteria
EXOTOXIN
Secreted proteins of Gram positive and Gram negative bacteria

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16
Q

what is a toxoid

A

Toxoid is a toxin treated (usually with formaldehyde) so that it loses its toxicity but retains its antigenicity

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17
Q

what are teh features of an exotoxin

A

protien, specific action, strong antingencity, produced by gram + and - bacteria, and convertable into a toxoid

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18
Q

what are teh features of endotoxins

A

liposaccoride, non specific, produced only by gram negative, not convertable to a toxoid

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19
Q

in what 3 modes can bacteria gain new genetic information

A

conjugation - via a sex pilus
transformation - sent over in a plasmid
transduction - via phage (infected by a virus)

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20
Q

what are the three ways a bacterias DNAs can change

A

base substitution, deletion, insertation

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21
Q

what is obligate intracellular bacteria

A

bacteria that cannot be grown on an artifical media, only in human cells and tissues

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22
Q

what are the three tpes of obligate intracellular bacteria

A

rickettsia, chlamydia, coxiella

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23
Q

what are teh cypes of bacteria that can grwo on an artifical media and have no cell wall

A

mollicutes

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24
Q

what are the cocci, gram negative, anaerobic bacteria

A

veillonella

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25
Q

what are teh cocci, which are gram negative and aerobic

A

neisseria and moraxella

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26
Q

what are the cocci, gram positive, aerobic, bacteria

A

staphylococcus, streptococcus

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27
Q

what test is done to distuinguish between streptococccus and what are the three outcomes

A

Macconkey
beta heamolytic, alpha heamolytic, non heamolytic

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28
Q

what are the cocci, anerobic, gram posiitve bacteria

A

peptostrepococcus

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29
Q

how does staphylococcus often grow and how does streptococcus grow

A

in clusters, streptococcus grows in chains

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30
Q

what does coagulase mean

A

Coagulase: enzyme produced
by bacteria that clots blood plasma.

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31
Q

what are teh three most important staphylococcus, and are therse coagulase positive or negative

A

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

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32
Q

what is the information about Staphylococcus aureus

A

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

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33
Q

what is S.epidermidis

A

S.epidermidis
Infections are ‘opportunistic’
immunocompromised,
prostheses
Main virulence factor - ability to form persistent biofilms

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34
Q

S.saprophyticus

A

S.saprophyticus
Acute cystitis
haemagglutinin for adhesion
urease

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35
Q

what is heamolysis

A

destruction of red blood cells (in thsi case by bacteria to access teh nutrienst)

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36
Q

what test is done after teh alpha heamolytic and what are teh bacteria found?

A

optochin test

resistant - viridans strep
sentitive - s. pneumoniae

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37
Q

what are the beta and gamma heaolysis bacteria, and what lancefield group are they?

A

beta - complete lysis
e.g. S.pyogenes
(ABCG)

gamma - no lysis
S.Boris and Enterococcus (not a streptococcus)
(D)

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38
Q

what is Antigenic sero-grouping and 2 exmaples

A

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

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39
Q

what is teh Lancefield microbead agglutination test

A

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

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40
Q

what are the Infections caused by S.pyogenes

A

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

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41
Q

what are virulance factors

A

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.`

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42
Q

what are the S.pneumoniae virulence factors

A

Capsule
polysaccharide (84 types), antiphagocytic
polysaccharide vaccine ‘PPV’ 23 types
conjugate vaccine ‘PCV’ 13 types

Inflammatory wall constituents
teichoic acid (choline)
peptidoglycan

Cytotoxin
pneumolysin

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43
Q

describe teh Viridans group streptococci

A

- 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

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44
Q

what are the S.pyogenes virulence factors

A

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

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45
Q

what are three aerobic gram posiitve bascilli

A

Listeria monocytogenes

Bacillus anthracis

Corynebacterium diphtheriae

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46
Q

what are three anerobic gram posiitve bacteria

A

all from teh clostridia species

C. tetani - causes tetnus

C. botulinum - causes botulism

C. difficile - causes antibiotic assocaited diarrhea, pseudomembranous colitus

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47
Q

what makes a gram negative bacteria so special

A

it has two membranes, a phospholipd and a lipopolysacchoride

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48
Q

what are teh two types of virulence factors

A

coloinsation factors - adhesions, invasins, nuterin aquesition, defence against teh host
toxins - secreted protiens that daeg

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49
Q

what does peritrichous flagella mean

A

the entire surface is coverd by flagella

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50
Q

what are proteobacteria

A

They come from the enterobacteria family
they are rods are noramlly are motile with pertrichous flagella
some specied colonise in teh intestinal tract

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51
Q

what is a MacConkey-lactose agar, how does it work, and what is an example of a lac positve and a lac negitive

A

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.

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52
Q

what is a serotype

A

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.

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53
Q

what are teh most commn infections cased by pathogenic Escherichia coli strains

A

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

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54
Q

what is an example of how ecoli cause diohrea

A

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

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55
Q

what is dysantry

A

bloody dihoreah containg pus, blood and mucus

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56
Q

what is shigella

A

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.

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57
Q

how does shigella invade the colonic mucosa

A

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

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58
Q

what are teh two types of samonella

A

S. enterica - responsible for salmonellosis

>2,500 serovars*

S. bongori - rare (contact with reptiles)

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59
Q

what are the three forms of salmonellosis caused by S. enterica:

A
  1. 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
  2. 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)
  3. Bacteraemia (serovars Cholerasuis and Dublin)Uncommon
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60
Q

what is the process of pathogensis of salmonellosis

A

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

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61
Q

what is heamophilius influenza

A

a human parasite that is carried in the nasopharyngeal of many people,

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62
Q

what are 5 oportunistic infections

A

meningitus, bronchopneumonia, pneumonia in CF, COPD and HIV patients

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63
Q

what is blood agar and choclate gar

A

blood - agar jelly mixed with horse blood
choclate agar - blood agar heated to lysis teh RBCs

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64
Q

what does the capsule of H.influenza do

A

penatrates the nasopharyngea epithelium
resistance to phagocytosis and teh complenent system

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65
Q

what does fastidiuos bacteria mean

A

Microorganisms that are difficult to grow in the laboratory because they have complex or restricted nutritional and/or environmental requirements.

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66
Q

what bacteria is responibe for most of teh food poinsengiins in teh UK

A

camplobacter

67
Q

what is mycobacteria and what is an example of it

A

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

68
Q

what is teh structure of a mycobacteria

A

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

69
Q

how do macrophage fight off mycobacteria

A

phagocytosed by macrophage
the bactuerim has evolved to escape into teh cytosol
CD4T cells genreate interferon gamma to activate intracellular killing

70
Q

how does a granulomma form

A

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

71
Q

what are two reasons that granuomas can become unstable

A

CD4 depletion (can be caused by HIV)
TNFa depletion by anti tumour necrosis factor drugs

Ths causes teh bacteria to escape into teh body

72
Q

what are teh two types of leprosy

A

tuberculoid leprosy - tissue hypersensitivity and granulomma, tissue damage to neerves

lepromatous leprosy - lesions but poorly formed granulomas, skin lesion, TH2 based

73
Q

how is TB diagnosed in clininc

A

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

74
Q

how is TB diagnosed in clininc

A

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

75
Q

what is a virus

A

an infections obligate intracellular parasite comprising of genetic materieral surronded by a proten coat and membrane

76
Q

what are teh three shapes of a virus

A

helical
isosahedreal
complex

77
Q

what 5 ways can virus3s cause disease

A

-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
78
Q

what are the 5 types of vaccine makers and an example for each

A

inactivated - polio
attenueated - MMR BCG
secreted products - tetanus
contituents of cell walls - Hep B
recombiant components - experinmental

79
Q

what is prophylacxis

A

prevenging teh disease from developing via using vaccine and so on

80
Q

what are teh 5 major classificatoin of protozoa

A

Flaggelates - have a flagelum to propel them
Amoebae -
Sporozoan
Cilliates - lots of little hairs to move them
Microsporidia

81
Q

what is sleeping skiness

A

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,

82
Q

what is myalgia

A

pain in muslces

83
Q

what is teh most fatal type of malaria

A

plasmodium falciparum

84
Q

what are the syptoms of malaria

A

FEVER!!! chills, headache, mylagia, fatuigue, Diarrhoa, vomiting, abdominal pain

85
Q

what are some signs of malaria

A

aneamia, jaundice, heaptoslpenomegally blac water fever (black urine)

86
Q

what is teh malerial life cycle

A

three cycles

exoerythrocytic cycle
erethrocytic cycle
sporogenuic cycle

87
Q

what is teh sporogenuic cycle of maleria

A

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

88
Q

what is the exoerythrocytic cycle of maleria

A

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

89
Q

what s the erethryocytic cycle of malaria

A

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

90
Q

how does complicated malaria form and what areteh consequences

A

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

91
Q

what are teh treatments for malaria

A

IV artesunate for complicated

treat each organ affected - oxygen, fluids, antibiotics, blood products

92
Q

defien host pathogen interactions

A

how pathogens sustain themseles withi teh host

93
Q

defien host pathogen interactions

A

how pathogens sustain themseles withi teh host

94
Q

what are the 4 stages of pathogenesis

A

exposure (contact),
adhesion (colonization),
invasion,
infection.

95
Q

what are commensal microorganisms

A

Commensal microorganisms are the resident flora and usually nonpathogenic

96
Q

what is the humoral resoponse to viruses

A

antibodies - G, A, block binding, block virus host cell opsionation

IgM - Agglutinates particals

coplemetn factors - opsonation, lysis

97
Q

what is teh cell mediated response to viruses

A

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

98
Q

define antigenic drift and antigenic shift

A

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.

99
Q

how is a gram stain completed

A

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

100
Q

what are the gram positive rods?

A

Gram +ve rods = Corneybacteria, Mycobacteria, Listeria, Bacillus, Nocardia

101
Q

what is teh ost response to a bacterial infection

A

IgA(s) Block attachment to host cells

Ab C3b Opsonisation, Prevents proliferation

Complement Cell lysis, Prevents proliferation

Ab Neutralise toxins

102
Q

what are symptoms of meningitus

A

stiffness of the neck, photophobia + severe headache
Infective: fever, malaise
Petechial rash associated with meningococcal meningitis

103
Q

what are teh tow most common bacterial causes of meningitus

A

Neisseria meningitidis, Streptococcus pneumoniae

these are both diplococci

104
Q

What would be present in the blood if meningitus was presant for bacteria, viral, TB

A

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

105
Q

what are the treatment for viral and then bacterial meningitus

A

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

106
Q

what are teh catogries of antibiotics that inhibit cell wall synthesis

A

glycopeptides - vancomycin

beta lactams - peniclins (flucoxacillin), cephalosporins (cephalein) carbapenems (imipenem)

107
Q

what test is done after teh alpha heamolytic and what are teh bacteria found?

A

optochin test

resistant - viridans strep
sentitive - s. pneumoniae

108
Q

what are the gram positive aerobic bacilli

A

bacillus anthratics
corynebactera diptherria
listeria monocytogenes

109
Q

what are the gram negative positive mcConcey bacteria

A

E.coli
Klebsiella

110
Q

what are teh gram negative, negative McConkey, oxidase positive bacteria

A

pseudomonas
campylobacter

111
Q

what are the gram negative, McConkey positive, oxidase negative, bacteria

A

shigella
salmonella
protwas

112
Q

what are teh three catogries of beta lactams and an an examle of each

A

penicillins - fluccloxicillin

cephalosporins - cefotaxime, cefriaxone, cefuroxime

carbapenems - meropenem

113
Q

when would glycopeptide antibiotics be given

A

for gram positive only
for penicilllin allergys
if resistant to teh beta lactams

114
Q

what are two glycopeptide antibiotics

A

vancomycin
teicoplanin

115
Q

what are teh 4 drug catogires of protien synthesis inhibitors and when is each one used

A

lincosamides - clindamycin (G+, cellulitus, nectosinf fasciitus)

macolides - clarithromycin (penicillin allergys)

tetracyclines - doxycycline (cellulitus, pneumonia)

aminoglycosids - genatamicin (G- nd staphs, UTIs, Endocarditus)

116
Q

what are teh folate synthesis blocker antibiotics

A

sulphonamides - trimothroprim and co-trioxazole

117
Q

which antibiotic should never be giver to a pregnant woman

A

Folate synthesis blockers - no sulphonamides

sulphemthoazole, trimethoprin

118
Q

what is the broadest antobiotic and which catogry is it in

A

Meropenem

carbopenem group

119
Q

what are teh RNA synthesis blocker antibiotics

A

metronidazole
ciprofloxacin

120
Q

what are the folate blocker antibiotics and what are they used for

A

trimethoprim and co-trimxazole

UTIs and mainly gor G-

121
Q

what antibiotic would be given for staph infections

A

Flucloxacillin

122
Q

what antibiotic would you give to treat a UTU

A

Trimethoprim

123
Q

what antibiotic would you give for MRSA

A

Vancomyocin

124
Q

what are two examples of mycobacteria diseases

A

TB and leprosy

125
Q

what is myobacteria

A

Aerobic, non-spore forming, non-mobile bacilli
Slow-growing causes gradual onset of disease
Requires multi-antibiotic treatment for a prolonged period

126
Q

what type of stain will show myobacteria

A

Ziehl- Neelson - its an acid fast

127
Q

how do viruses cause disease

A

Can cause disease via direct destruction (polio), modification (rotavirus), over-reactivity (hepatitis B), damage through cell proliferation (HPV)

128
Q

how are viral infections diagnosed

A

PCR + nucleic acid amplification tests (NAAT) used, can also do serology (look for antibodies in response to virus

129
Q

what are teh antibodies for a viral infection

A

IgM within 1 week of onset, IgG appears later

130
Q

what drug is teh main one given for viral infections

A

Acyclovir

131
Q

what are protozoa

A

Microscopic unicellular eukaryotes

132
Q

what are the 4 classification of protozoa

A

ameoboids, ciliates, sporozoan, flagellates

133
Q

what are 4 examples of protozoa `

A

malaria, giardia lamblia, toxoplasmiosis, trichomonas vaginalis

134
Q

what sjould a high fever and recent travel indicate

A

MALARIA!

135
Q

what are fungi

A

Eukaryote
Have a cell wall - chitin + glucans (polysaccharides)
Move by growing across or through structures or by dispersion in air/ water

136
Q

what are the 2 forms of fungi

A

Yeast - single cell that divide via budding
Moulds - form multicellular hyphae or spores

137
Q

what are some examples of diseases caused by fungi

A

candida, athlete’s foot, nappy rash

138
Q

what do anti fungal drugs normally end in

A

-azole

139
Q

what are the three classifications of worms

A

nematodes (roundworms), trematodes (flatworms), ceratodes (tapeworms

140
Q

how do worms reproduce

A

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

141
Q

what are teh antibodies response to worm infections

A

Mainly IgG + IgE mediated

142
Q

what are two exampes of worm caused diseases

A

hookworm, schistosomiasis

143
Q

what are teh layers of teh HIV envelope

A

RNA + Capsid + RNA transcriptase

144
Q

what are three diseases that heamophilus influenzea cause

A

meningitus in pre school children
pharyngitus
otisis media
Exaubation of COPD

145
Q

what are fungi

A

Eukaryotic
Chitinous cell wall
Heterotrophic
“Move” by means of growth or through the generation of spores (conidia), which are carried through air or water

146
Q

what is teh difference between yeast and mould

A

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

147
Q

what are some invasive fungi conditions taht can affect: imounocm[armised hosts, post surgical patients, and healthy hosts

A

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

148
Q

how are fungal infections diagnosed

A

radiology, microscopy, cultur, molecular (PCR and antigen)

149
Q

why are fungo harder to treat than bacteria

A

they are eukaryotic, so more similar ot humans

150
Q

what is one of teh best drug tyoes against fungi

A

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

151
Q

what is the broadests types of antifungal

A

amphotericin B

152
Q

what is a bad CD4 level in HIV+ patients

A

anything below 200

if they have a normal Cd4 of above 500 it means that they can effectivly be treated as a normal patient

153
Q

what are some fungal drug interactions

A

they react with cytochrome p450 enzymes and can inhibit them, thsi means that it shouldbe be taken with some drugs such as warfrin

154
Q

what was teh target for 2020 in teh world for HIV

A

90-90-90

90% diagnosed
90% treated
90% to an undetectable level

155
Q

what are teh three HIV transmission routes

A

Sexual
Vertical (mother to child)
Blood (needles - reduced due to teh needle exchange and also blood transfusoins screened)

156
Q

what is prep, what is PEP

A

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

157
Q

what are the original symptoms of HIV

A

Generalised lymphadenopathy
Acute generalised rash
Glandular fever/ flu-like illnesses
Think about seroconversion

HIV rash it ofther on teh paksm of teh hands!

158
Q

what else can be confused with HIV wit teh first, flu and rash like sympotms

A

Syphyliss
hand foot and mouth disease

159
Q

what are teh later sympotms of HIV

A

Unexplained weight loss or night sweats
Persistent diarrhoea
Gradually increasing shortness of breath and dry cough
Recurrent bacterial infections including pneumococcal pneumonia

160
Q

how does HIV affect teh CD4 receptors

A

HIV fuses to teh receptors and passes on its content

161
Q

what are 4 drug targets for anti HIV

A
  • entry point
    reverse transcriptase inhibitors
    Protease inhibitors
  • intergrase inhibitors
162
Q

how does teh immune system respond to HIV

A

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

163
Q

what makes HIV avoident of the immune system

A

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

164
Q

what is teh difference between gram pos and neg cell walls

A

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

Phase 2a (18 decks)

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