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M & D > Ch 22: Respiratory System Infections > Flashcards

Ch 22: Respiratory System Infections Flashcards

1
Q

Above the epiglottis

A

upper respiratory tract

most upper RTI are relatively mild

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2
Q

below the epiglottis

A

lower respiratory tract

lncludes the bronchi, bronchioles, and the alveoli

lower RTI are usually more severe, as they effect gas transfer

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3
Q

look at figures

A

22.3 and 22.2 pg 960 and 961

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4
Q

Normal microbiota of the respiratory system

A

some (but not all) organs and surfaces of the body are normally colonized by bacteria

called the resident microflora or commensals

the upper RT is heavly colonized while the lower RT is generally sterile or has a very low number of transient bacteria

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5
Q

microbiota of the nose

A

bacteria flora found just inside the nose resembles the skin

CNS (coagulase negative staphylococci)

virdians streptococci

staphylococcus aureus

coryneforms

neisseria spp

haemophilus spp

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6
Q

Staphylococcus in the nose

A

normal microbiota of the RT

colonizes the anterior nares primarily but also some in the phaynx (nose picking region)

coagulas positive

a major and serious pathogen of the skin, soft tissue, RT and other parts of the body

found in about 30% of the population

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7
Q

coryniforms

A

gram +, aerobic, rod and pleiotrophic shaped

dessication resistant

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8
Q

Neisseria and haemophilus

A

fragile gram -ves, = gram + antibiotics work agaisnt them

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9
Q

are strep penicillin resitant

A

nope

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10
Q

what do we use in North america instead of methicillin

A

oxicillin

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11
Q

Different types of carriers of nasal staphylococci

A

persistnet carriers (20%) that carry a specific strain

non-carriers (20%) that almost never carry SA

intermittent carriers (60%) acquire and lose different strains of staph. aureus

SA tends to be disseminated from nares to other body parth and other people

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12
Q

nasal viridians streptococci

A

alpha haemolytic streptococci other than strep. pneumoniae

strep. salivarius, milleri, gordonii

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13
Q

Nasal neisseria spp

A

gram negative cocci, often in pairs

catalase and oxidase positive

microaerophillic, grow best in higher CO2 conc.

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14
Q

Nasal Haemophilus spp

A

non-motile, gram negative rods

fastidious

grow best in elevated CO2 conc

capsulated

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15
Q

Nasopharyx

A

aerobic region with high bacterial population

mucus covered epithelial cells

therefore, bacterial colonizationis either inteh mucus or to underlying cells

most epithelial cells have about 10-50 cells attached to them (quite a small amount)= sparse colonization

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16
Q

co2 incubate

A

5% co2 rich atmosphere

dats a lot

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17
Q

normal microbiota of the nasopharynx

A

staph aureus (20% of pop)

a-haemolytic strep, gamma-haemolytic strep

strep pneumonaie (6%)

neisseria spp
=> N. meningitidis, N. subflava, N. sicca

Haemophilus spp.
=> H. influenzae, H. parainfluenzae

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18
Q

Obligate anaerobic gram negatives of the nasopharynx

A

fusobacterium
preotella
prophyromonas

biofilms on teeth
and inflammation of the gums
=> these implies that these bacteria could enter the bloodstream through the capillaries in the gums

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19
Q

Obligately anaerobic gram positives int eh nasopharynx

A

peptostreptococcus

mouth full of air does have strict anerobe living in anerobic pockets and sub-structures

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20
Q

Moracella catarrhalis in the nasopharynx

A

aerobic, gram-negative cocci usually in pairs

catalse positive, oxidase positive

children generally colonized, frequent cause of sinusitis and otitis media, not common in adults

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21
Q

The mouth, a complex enviroment for bacteria

A

hard surfaces, 20% of the area of the mouth is the surface of the teeth

keratinized mucosa= skin
non-keratinized mucosa

regions which can become anaerobic

gingivial crevice

saliva

neutral pH

contains proteins, glycoproteins, mucins, carbs, organic nitrogen compounds

basically, non-extreme environment provides a good growing area for many bacteria

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22
Q

What must resident bacteria of the mouth do

A

attach to solid support or reproduce faster than alive removal rate

epithelial cells subject to desquamation

teeth subject to mechanical forces

protected areas around teeth and tongue

formation of biofilms on hard surfaces

over 200 species of bacteria have been isolated from teh mouth, over 500 other species have been detected by moleuclar techniques

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23
Q

Oral streptococci

A

gram positive, aerotolerant, fermentative in diploids or chains
streptococci in general =>divided into 4 major groups

mitis group, found mostly in the dental plaque including strep mitis, sanguis, parasanguis

mutand group, also in plaque, strep mutans, sobrinus

salivarius group, found mainly on mucosal membranes

angiosus group, strep anginosus, intermedius

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24
Q

Actinomyces of the mouth

A

non-motile, non-spore-forming, gram + pleomorphic (bumpy and lumpy even y shaped) or branching rods

facultatively anaerobic, ferment sugars to acid

opportunisitc pathogens and associated with dental caries
=>dental biofilms
=> ferment acid in biofilms, phosphate is mobalized out of the bones of teeth (mineralization) = cavities

antimyces naeslundii
=> nasty pathogen, opportunistic
=> cavities that can cause absesses that may end up degrading the jaw bone

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25
Q

Veillonella spp of the mouth

A

anaerobic gram negative cocci arranged in pair, chains and clumps

co-aggrefate with other oral bacteria to initiate biofillm formation

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26
Q

Fusobacterium of the mouth

A

fusiform morpology = cigar shaped, with tapered ends

bridging species, attach to first colonizers of teeth then to late colonizers

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27
Q

Porphyromonas

A

proteolytic, ferment aa = > stricland ferementation (one aa ox another is red)

second biofilm colonizer of teeth (fusobacterium is the first)

por. gingivalis is major cause of periodontitis
por. endodontalis can degrade bone, cause endodontic infections

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28
Q

Streptococcal infections (strep throat)

A

streptococcal pharyngitis caused by streptococcus pyogenes

group A strep (GAS) by the lancefield system

symptoms include fever, pharynbgeal pain, inflammation and erythema, swollen tonsils with pus, petechiae

transmission by direct contact or airborne (droplets)

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29
Q

scarlet fever

A

strep throat

GAS

similar to pharyngitis with a diffuse bright red rash

rash due to the production of erythrogenic toxins by GAS

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30
Q

Treatment of strep thoat

A

Treatment - antibiotics - beta lactams like amoxicillin or a cephalosporin such as cefadroxil

if patient is allergic to or isolate is resistant to beta lactams then clindamycin, azithromycin or clarithromycin is used

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31
Q

Bad things that can happen after a sore throat

A

common with strep infections
=> sequelae of strep infections

Rheumatic fever

acute glomerulonephritis

sydenhams chorea

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32
Q

Rheumatic fever

A

an auto-immune disease where the immune system attacks heat tissue after a GAS infection

major reason why we use antiobiotics for GAS infections

fever, joint pains, polyarthritis which is migratory and involves multiple joints, abdominal and chest pain, erythema marginatum, nose bleeds and vomiting

Carditis, other damage to the mitral valve

heat murmurs, heart enlargement, congestive heart failure, cardiac arrect and death

2-3 months after GAS infection

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33
Q

Acute glomerulonephritis

A

inflammation of renal glomerulus with lesions

hematuria (blood in urine) and proteinuria (abnormally high levels or protein in urine)

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34
Q

Sydenhams chorea

A

muscle spasms, weakness, awkwardness and tendency to drop things

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35
Q

other sequelae that GAS can occur

A

wide range of different diseases in different organs

impetigo

puerperal sepsis (childbed fever)

toxic shock syndrome (toxins produced by bacteria [with strep] toxin diffuses across a mucus membrane, and is dissiminated throughout the circulatory system)

pneumonia (mostly strep pneumonia, but can be caused by other species like GAS, staph, gram neg, and atypical pneumoniae)

bacteria, septicaemia

septic arthritis, osteomylitis (bone infection)

endocarditis, pericarditis

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36
Q

bacterimia

A

the presence of bacteria in the blood stream

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37
Q

septicaemia

A

the presence of and reproduction of bacteria in the blood stream

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38
Q

GAS virulence factor

SpeB

A

streptococcal pyrogenic extoxin B
SpeB can degrade Ab into small fragments therefore, no neutralization or opsinization

complement protein C3b degraded therefore no opsinization

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39
Q

GAS virulence factor

SpeA

A

streptococcal pyrogenic exotocin A, erythrogenic toxin

found on a temperate phage of GAS, phage integrates into GAS, and the toxin is integrated.

attacks capillary endothelial cells and causes them to dialate (erythrogenic toxin)

Also the cause of streptococcal toxic shock syndrome (STSS)

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40
Q

GAS virulence factor

SpeA and STSS

A

simultaneously bind to MHCII moleucles and TcR
=> superantigen, activates T cell even if not cognate.

leads to the activation of a large number of T cells

increased secretion of cytokine such as TNFa, interlukin 1 and interferon g

activates the complement (complement doens’t work great against these floating toxins, attack your own cells), coagulation (clots to hide from immune cells, and dissemination from the body) and fibrolytic cascades resulting in hypotension and multiorgan failure

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41
Q

GAS virulence factors

The M proteins

A

probaby the most important virulence factor of the GAS

M protein is covalently attached to the peptidoglycan layer

antigenic - 83 serotypes

prevents complement activation and binding

can activate platelets for coagulation

redundancy in virulence factors

implicated in rheumatic heart disease
=> antibodies to M protiens are often cross reactive to cardiac tissue, big MAC attack of the heart

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42
Q

why does strep cause so many diseases

A

has a lot of virulence factors

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43
Q

How does the M protein works to cause virulence

A

binds kinigen and drabykinin is released with leads to inflammation

binds plasminogen which breaks down frigrinogen in local blood clots

M proteins interact receptor on monocytes resulting in production of inflammatory cytokines

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44
Q

Capsule in GAS

virulence factor

A

GAS capsule is composed of hyaluronic acid, a polymer of alternating N-acetylglucosamine and glucuronic acid
=> similar to stuff seen in body, poorly immunogenic and seen as self

poor immunogen, Abs to GAS hyaluronic acid not detected in humans

in mutant GAS which lose the ability to produce capsules resistance to phagocytic killing and mouse virulence decreased 100-fold

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45
Q

GAS virulence factors

streptolysin O

A

oxygen labile, pore-forming cytolysin

causes lysis => why it is called a lysin

toxic to a variety of cells including neutrophils

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46
Q

GAS virulence factors

Streptolysin S

A

produced by streptococci grwoing int he presence of serum

by weight one of the most potent cytotocins known

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47
Q

GAS virulence factors

DNase

A

serve to liquify pus and facilitate the spreading of streptococci through tissue

also release from neutrophil DNA nets in capillaries

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48
Q

GAS virulence factors

Hyaluronidase

A

degrades hyaluronic acid present in connective tissue

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49
Q

GAS virulence factors

streptokinase

A

dissolution of clots by catalysing the conversion of plasminogen to plasmin

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50
Q

GAS virulence factors

C5a peptidase

A

specifically cleaves the complement protein C5a

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51
Q

GAS virulence factors

Streptococcal inhibitor of complement (Sic)

A

inhibits lysis by MAC

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52
Q

STATS on GAS virulence

A

responsible for over 500 000 deaths each year

600 milliion new cases eaach year of S. pyogenes pharyngitis

30 million cases of rheuamatic fever every year

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53
Q

Cause of diphtheria

A

Corynebacterium diphtheriae

gram +, club-shaped bacterium

airborne transmission

colonization of the nasopharynx

production of an A-B toxin which binds to human EF-2 and inhibits protein translation = cell death
-> each toxin, inhibits many many elongation factors
=> toxin human lethal does estimated <0.1ug/kg

the gene encoding the toxin (dtx) is actually carried on a bacteriophage
=> strains are lysogenized with the phage

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54
Q

Other causes of Diptheria

A

Corynebacterium diphtheria (main)

occasionally C. ulceranc, C. pseudotuberculosis

C. ulcerans, and diptheriae can also cause skin leasions and infections

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55
Q

Symptoms of Diptheria

A

sore throat, low fever

formation of the pseudomembrane in the back of the throat
=> thick, grey membrane made up of dead cells, red blood cells, bacteria and fibrin
=> can expand to the nasal cavity and obstruct the pharynx or trachea leading to suffocation

toxin is absorbed into the bloodstream and ciculated causing heart damage and verve damage

irregular heartbeat, cardiac dilation from muscle weakening and thinning, shorness of breath

nerve damage leads to weakness, paralysis of tissue in the RT, eye, or total paralysis

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56
Q

Case fatality rate of diphtheria

A

5-10% with higher death reats up to 20% amoung persons younger than 5 and older than 40yrs

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57
Q

Treatment of diphtheria

A

b-lactam antibiotics such as amoxicillin, penicillin, or erythromycin

antiserum or antitoxin can be administered to prevent damage due to the toxin

=> emil adolph con bohring and shibasaburo kitasato developed an antitoxin based on immunization of horses in 1891

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58
Q

The history of diphtheria

A

see slide idk im lazy

dog sledding

Chapter 22 lecture 4

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59
Q

Diphtheria prevention

A

inactivated toxin (toxoid) vaccine

  • DTaP
  • DTaP-IPV-HPV (diphtheria, tetnaus, acellular pertussis, polio and haemophilus influenza type B) at 2, 4, 6 and 18 moths

-Tdap-IPV at school entry and Tdap at 15yrs

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60
Q

Prevalence of Diphtheria

A

in Canada, prevalence was about 80-100/100 000 in the 1920’s

in 1936, it was 20 in the 1964 pretty much 0

usually less that 100 cases per year, now about 0q

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61
Q

Bacteria pneumonia

A

pneumonia is inflammation in the lungs and fluid accumulation in the alveoli

pneumonia can be causes by bacteria viruses, fungi, or by non-biological events

most pneumonia is caussed by bacteria and most bacterial pneumonia is caused by streptococcu pneumoniae

the single largest infection cause of death in children worldwide
=> killed 800 000 under the age of 5 in 2017
=> 15% of all deaths of children are under 5 yrs old

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62
Q

Bacterial pneumonia in Canada

A

Together with influenza, pneumonia was the 7th leading cause of death in Canada in 2019

6893 deaths

20/100 000 / year in Canada

24 761 cases of community- aquired pneumonia in Canada that required hospitalization

63
Q

Pneumonococcal pneumonia

A

Streptococcus pneumoniae

humans are the only reservoir

droplet transmission, colonization of upper RT followed by aspiration into lungs

64
Q

Symptoms of pneumococcal pneumonia

A

abrupt onset

fever, chils

difficulty breathing

productive cough

rust coloured sputum

65
Q

What other diseases are pneumococcal pneumonia present as a co-infection in// opportunitic infection

A

influenza

chronic lung disease

smoking

aspiration due to intoxication

66
Q

Case-fatality rate of pneumococcal pneumonia

A

20-40% in hospitilized cases (in the past)

2-10% with antibiotics

20-40% with underlying disease

67
Q

Treatment of pneumococcal pneumonia

A

amoxicillin

azithromycin, clarithromycin

Cefpodoximie, cefuroxime

Doxycycline

Fluroquinolone such as levofloxacin, moxifloxacin or gemifloxixcin

penicillin G

68
Q

prevention of pneumococcal pneumonia

A

2 vaccines Pneumovax23 and Prevnar13

pneumovax23 protects against 23 different serotypes and prevnar protects against 13 serotypes

protects agaisnt the capsule of the bacteria

69
Q

List of different bacteria that cause atypical pneumonia

A 
Haemophilus influenzae
H. influenzae A HiB
Mycoplamsa pneumoniae
Klebsiella pneumoniae
Neisseria menigtidis
Staphylococcus aureus
Psuedomonas aeruginosa
chlamydia
70
Q

Atypical pneumoniae and Haemophilis influenza

A

small gram - coccobacilli, facultatively anaerobicx, fastidious
=> chocolate agar

nonencapsulated strains (non-typeable, NTHi) and HiB
commensals but also spreaad by aerosols
similar symptoms to pneumococcal pneumonia

71
Q

Atypical pneumoniae and Mycoplasma pneumoniae

A

small cell wall-less (no affected by beta lactams= selection method) organisms
actually gram + , small genome (<1 Mbp)
0.1-0.2 um diameter, 1 um length

usually mild and self-limiting disease
low fever, persistent non-productive cough
also pharyngitis, earache, headache, malaise
hard to isolate on agar, may require 30days incubation

airborne

damage to diliated epitheliad cells by tip organelles (from twictching motility) and H2O2 production leaads to an inhibtion of ciliary action, expultion of mucus inhibited

PCR, serological test is also used

treamtent with azithromycin or clarithromycin, doxycycline, fluoroquinolones

72
Q

Atypical pneumoniae

Chlamydial pneumoniae

A

parrot fever

cause by chlamydophia pneumoniae, psittica, trachomatis

obligate intracellular parasites, gram -
incubation period of 3-4 weeks

abrupt onset, headache, fever, myalgia, nausea and vomiting, cough all lasting 3-4 weeks

treatment: C. pneumoniae = azithromycin ort tetraculine
C. psittaci = tetracycline

73
Q

Klebsiella pneumoniae

atypical pnuemonia

A

gram negative, encapsulated, fermentative, facultatively anaerobic bacilus (releated to e.coli as it is in the enterobacteria)

humans are primary reservoir, about 3% carry K pneumoniae in their nasopharynx

fever, chest pain, cough with current jelly sputum

30-50% mortality, up to 100% with underlying complications

74
Q

Atypical pneumoniae

klebsiella pneumoniae treatment

A

treamtent with 3rd/ 4th generation cephalosporin, fluroquinolones, carbapenam if HAP

major problem with extened spectrum beta lactamase (ESBL) or carbapenam-resistant enterobacteria (CRE) or (KPC) strains

75
Q

Atypical pneumoniae

Pseudomonas aeruginosa

A

Gram negative, aerobic, non-spore forming, non fermentative bacillus

causes pneumonaia associated with cystic fibrosis and ventilator use in hospitals (VAP)

20% of all cases of VAP,m 15% mortality rate

76
Q

Treatment of pseudomonas aeruginosa atypical pnuemoniae

A

carbapenems (meropenem), cephalosporins (ceftaxidime, cefepime), aminoglycosides (gentamicin, tobramycin, and amikacin) and fluroquinolones (ciprofloxacin and levofloxacin)

77
Q

Atypical pneumonia

staphylococcus aurues

A

gram positive cocci found in clusters, catalase positive, oxidase negative, facultatively anaerobic, fermentative

produces bright yellow or golden coonies

20-30% of hospital-aquired pneumonias

typical bacterial symptoms except for nectrotizing pneumonia
(fever, rapid onset, chills, cough non-productive or productive (blood or not,m and apperance of the blood))

78
Q

Staph aurues atypical pneumonia symptoms

A

abrupt onset of fever, chest pain and a productive cough with purulent sputum, which can be blood-tinged

some S.aureus strains carry the panton-valentine leukocidin (PVL)

Kills macrophage and causes tissue necrosis and hemorrhaging.

79
Q

See slides for 2019 Tuberculosis stats

A

winnipeg manitoba

80
Q

Mycobacteirum tuberculosis is the most common human TB pathogen.

what are the others

A

Once was the most common human pathogen, now, might be heliobactor pylori (1/3) (1/4) people are infected by MTB

other species

mycobacterium africanum, M. micoti, bovis also cause human disease

Mycobactireum avium/ intracellulare complex causes TB in immunocompresised himans

Mucpbacterium Kansasii, fortunitum, canetti can cause TB or non-TB mycobacterial infections

81
Q

Mycobacterium tuberculosis

A

gram positive although not readily stainable by the gram strian
=> now use an acid fast stain for MTB

bacilli, 0.3 - 0.6um diameter, 1-4 um long
cells grow in serpentine, parallel bundles

aerobic (best growth with 5% CO2) but tolerates almost anaerobic conditions if adapted slowly

optimum growth temperature 37C, pH 6.5-7

considered to be a slow grower mycobacterium

82
Q

Lowebsteub-Jensen agar

A

for MTB

early methods to isolated MTB from agar media were not successful

better results were obtained by heating protein (from whole eggs) to solidify it in a solution containing potato flour, glycerol and salts

malachite green was added to make the medium selective by inhibiting sputum contaminants

still requires 18-24 days to detect micro-0colonies and 6-8 weeks for full growth of colonies

83
Q

Middlebrook Media

A

synthetic media developed in the 50’s

for MTB

defined salts, vitamins, oleic acid, albumin, catalase, glycerol, malachite green

7H10 contains glu
7H11 contains casein hydrolysate
both are solid media containing agar
7H9 is a similar compositionliquid medium

reduces the time to observe micro-colonies to 10 days

84
Q

BACTEC 460

A

MTB specimens are added to a 20mL glass bottle containing 7H9 broth plus BAS, catalase, antibiotics and 14C labelled palmitic acid

mycobacteria oxidize teh labelled palmitic acid to 4CO2

the headspace of the bottles is smapled and the gas passess to a scintillation counter

9-14 days for detection of growth

85
Q

Signs and symptoms of TB

A

can be a difficult diagnosis especially for non-pulmonary forms

productive cough for more than 3 weeks (streaked with blood) like Klebsellia (chunks) and then to full streaks from haemoraghing

fever (night sweats)

anorexia and weight loss

malaise

chest pain

86
Q

Lab test for TB AF

A

acid fast strain

70% sensitive

87
Q

Incidence rate and TB

A

most diseases have a U shaped curve,TB has the opposite. The incidence rate rises with increasing age, drops a little bit (cause they die), then spikes again

not very high in youger childern >5/10 like most infectious diseases

88
Q

Lab test fort TB

chest radiography

A

usually one or both upper lobes

consolidation, infiltration, cavitation and calcified nodules may be visible

not very sensitive, nodules need to be fairly large to detect

89
Q

Lab test for TB skin test = Mantoux

A

an injection of purified protein derivative (PPD) from a culture of mtb inhected under the skin

induration of greter than 10mm indicates at least exposure to mtb

90
Q

Tuberculosis Transmission

A

an airborne infection
=> dropletes of 2-4um can penetrate to the alveoli
=> droplets produced by infected person coughing and sneezing especially when they have active TB and a cavitation
=> mtb is a fairly resistant to desiccation

TB can also be transmitted though milk and food
=>pasteurization of milk and use of pasteurized milk in cheese-making, etc. has largely eliminated this route

91
Q

Trasmission rates of TB

A

only about 5-10% of newly infected people go on to develop TB immediately those who are latent have houts a 10% lifetime risk of developing TB

reactivation of latent TB as immunity waves

92
Q

Dissemination of TB

droplet to phagosome

A

mtb is taken into the lungs as a < 5mm droplet or droplet nuclei

penetrates to the alveoli

taken up by an alveolar macrophage or a lung DC by pasive phagocytosis
=> can reproduce in the macrophage but not DC

after phagocytosis, most bacteria should be killed but mtb survies and replicates inside the macrophage

93
Q

Dissemination of TB

Inside the infected macrophage

A

eventually the macrophage is killed, bacteria become extra-cellular and infect more macrophage.

mtb can also infect epithelium and other cell types

The infected macrophage returns from the alveoli to lung tissue, migrates to local lymph node
=> a local inflammation takes place
=> more macrophage are recuited to the site of infection
=> they surround the infected macrophage in ayers with tighly apposed membrane which interdigitate
=> macrophage becomes epitheliod cells

this is called a granuloma

94
Q

Dissemination of TB

Granuloma maturation

A

over time the individual macrophages fuse to become giant cells with multiple nuclei

macrophage inthe centre of the granuloma die and new macrophage are recuited to the periphery

granuloma exapmds

T cells become activated and home to the granuloma

granuloma now consists of a core of macrophage/ giant cells with live mtb and a periphery of T cells and fibroblasts

95
Q

Dissemination of TB

cytokines

A

activated T cells secrete IFNg and TNF
=> macrophage become activated adn more successful at killing mtb

fibroblasts secrete collagen and other material to form a fibrous shell to the granuloma

calcium may be deposited around the granuloma to seal it off

90% of infected people this is the end of the story

over time the mtb die off the and granulonas become sterile

96
Q

Dissemination of TB

the 5-10%

A

these ppl develop primary tuberculosis

also reactivation of latent TB with age or stress

mtb survives somewhere in the obdy

previously contained granulomas can enlarge

cells in the centre of the granuloma die, lyse and produce a ssheesy substance= caseous granulomas

granulomas expant by recruiting or reproduction of cells at the periphery and increasing necrotic core

97
Q

Dissemination of TB, errosion of the granuloma

A

may erode into a blood vessel and MTB spreads through the circulatory system

may erode into an alveoli and spill out caseous material
pulmonary cavitation

plenyy of oxygen in the cavity higher rate of replication of mtb
=> high numbers of cells in the cavity 10^10 cells

caseous material is very irritating
=coughing, sneezing and is highly infectious

98
Q

MTB treatment

A

streptomycin was the first antibiotic found to have any effect on mtb. (first random control done). 5 years later, the TB emerged with resistance. Before this you were sent to an sanitorium = you go into remission by relieving stress or ya die

Eventually pateitns developed streptomycin-resistant mtb

this lead to the idea of multiple antibiotic therapy

only when 3 different antibiotics were used simultaneously did patients recover were used simultaneously did the patient recover without re-emergence

2 years with SM alone
12 moths with combination therapy

99
Q

DOTS therapy

A

for mtb

directly observed treatment- short course

the current WHO recommended treatment

4 drugs for 8 weeks
= isoniazid, pyrazinamide, rifampicin, ethambutol

followed by 2 drugs for 18 weeks
= isonizid and rifampicin

100
Q

second line antibiotics for mtb

A

amikacin or kanamycin

capreomycin

cycloserine

ethinoamide

moxifloxacin or levofloxacin

101
Q

new anti-TB antibiotics

BPaL regime

A

bedaquiline

pretomanid

linezolid

clofazimine

102
Q

Bortadella Pertussis

A

whooping cough
=> peridoxal coughing, non-productive then the big inhale

Gram-negative cocco-bacillus. Doesn’t stain very well

aerobic, oxidase postive

motile, encapulated and humans are the only reservoir

7-10 day incubation

colonization of bronchi and trachea
=> different from pneumoniae and tuberculosis which colonize the alveoli

103
Q

Filamentous heamaglutin

A

causes rbc to agglutinate, on the surface of bacteria like pertusis (which has two types)

104
Q

fimbriae

A

10-12 nm in diameter

involved in specific adhesion

virulence factors for UTI e.coli infections

bind bacteria and mediate specific ahesion to certain cell types

105
Q

protractin

A

adhesion moleucle?

106
Q

pertussis toxin

A

A-B type toxin

one subunit binds, the other goes into the cell

exotoxin

causes cell death, and medation of inflammation

107
Q

Pertusis tracheal toxin

A

Prevents cillary motion

=> no mucus expultion in the trachea

108
Q

pertusis adenylate cyclase

A

targets immune cells

kill wbc

109
Q

Pertussis cataral stage

A

one of three stages of disease progression

moderate symptoms

runny nose, coughing sneezing, low fever

still highly infective during this stage for pertussis = before symptoms

110
Q

Pertussis paramoxamal stage

A

whooping sounds

can break your own ribs coughing, or brain damage

111
Q

final pertussis stage

A

convalence

declinign cough

100 day cough

112
Q

pertussis complicaitons

A

pneumonia

encephalopacy

113
Q

pertussis vacination

A

1930s heat killed, whole cell, inactivated vaccine
=> high effacacy, life long immunization

however later on, two infants died after vaccination

led to the acellular pertussis vaccine
=> aP, ap acellular pertussis
. against pertussis toxin, filamentous haemaglutin, and later, protectin and type 2/3 fibrian
=> processed to remove LPS

need a whole cell booster shot for the acellular vacccine

114
Q

legionares disease

A

relativly new, non-cultivatable

media has charcoal and cysteine

limited human to human tramsmission

grow better in macrophages than on a petri dish

115
Q

Influenza

A

ingle-stranded negative sense segmented RNA envaloped virus (8segments), 8 different genes
=> may lead to re-assortemented viruses

viral envelope contains 2 virus encoded protiens
h or hemagglutin
N or neuraminidase

4 species A, B, C, D

aerosol, direct and indirect contact transmission

116
Q

+ sense

A

protein synthesis

117
Q
  • sense
A

needs to be converted to + to make protein

=> replication intermediate is these doubled stranded intermediate to convert the two strands

118
Q

human glycolylation of protiens

A

siallic acid

=> leads to tethering of viruses from budding

neurimidase protein is important to cleave this

119
Q

heamaglutaninn

A

binds to siallic acid receptors on epitheial cells

sticky part of virus

trophisms?

virus is taken into epithelial cell

acidifies vesicle, then the heamagluttin changes in shape to mediate the fusion of the lysosome with the viral membrane, pops into the cytoplasm of cell

120
Q

Viral M proteins??

A

???

121
Q

figure 22.17

A

memorize

122
Q

signs and symptoms of flu

A

abbrupt onset

quick fever, then done

multiple hot cold hot cold events (fever, then chills)

non-productive cough (will NEVER cough up blood0

time of season is important

123
Q

Animal reservoirs of influenza A

A

Gulls, terns and shorebirds or waterfowl (ducks, geese and swans)

18 known H subtypes and 11 N in birds

almost every combination fo H and N occur

Pigs
=> though that flu is a zoonotic disease from birds maybe via pigs or other animals

124
Q

Epidemics and Pandemic with Influenza

A

flu starts every year in SE asia and moves to the southern hemisphere for our summer

Moves to the norhtern hemisphere in November, and ouriwndter in roughly November to April

125
Q

Inflenza Virus Genes

HA

A

HA binds to its receptor - sialic acid tipped galactose carbohydrates

NA cleaaves sialic acid form the end of the receptor to allow newly formed viruses to escape

126
Q

Influenza Virus genes

M1/2

A 
Matrix protein1 (M1), M2
M1 coats the inside of the envalope
M1 is the most important protein for the structure, assembly, and budding of the virus

M2 is found in small amounts in the envalope

127
Q

Influenza virus genes

nucleoprotein

A

nucleoprotein which associated with the RNA segments

Polymerase B1, B2, and A

RNA pol subunits which transcribe and replicate the viral genome are carried into the host cell along with the genome

non-structureal 1 and NS2

regulation of genome replication and export of RNA-protein from the nucleus (NEP)
figure 22-17

128
Q

Influenza symptoms

A

acute onset fever/ chills

headache, muscle aches

malaise

non-productive cough, shortness of breath

sore throat

lasting 3-7 days

129
Q

Influenza entry into the cell

A

The influenza hemagglutinin binds to sialic acid containing glycoprotein receptor on epithelial cells.

viral particles are taken up by receptor mediated enfdocytosis and fuse with a lysosome

the drop in pH in the virus containing endosome causes a conformational change in hemagglutinin

130
Q

Influenza entry into the cell

post pH drop in phagosome

A

after the conformational change of hemagglutinin, part fo the hemagglutinin is now exposed and can mediaate fusion between the viral envelope and the endosome mebrane

nucleocapsis are then liberated into the cytoplasm and move to the nucleus

Viral RNA is replicated in cell nucleus using viral encoded RNA-dependent RNA polymerase

10 transcripts produced, )+ sense mRNA)

131
Q

Influeza trascripts

A

10 transcripts produced, (+ sense mRNA)

viral mRNAs “steal” the 5’ cap and 3’ poly A tail from preformed cellular mRNAs

viral proteins are synthesized

nuclear repliction of the original 8 (-) strand RNAs

assembly of new virus nucleocapsids

migration to cell membrane

budding out through the membrane

132
Q

Influenza Antigenic shift

A

antigenic shift is caused by reassortment
=> two different types of flu viruses co-infect the same host

RNAs from both viruses are mixed together in a recombinant virus

the 957 pandemic virus (H2N2) was a recombinant of the previous human HN1
=> avian HA, NA, and Pb1. Other proteins are human flu viral

133
Q

Influenza antigenic drift

A

antigenic drift is the frequent change to influenza virus

RNA viruses mutate faster than DNA viruses or cells

estimated at 7x10^-3 substitutions/site/year for the HA gene in influenza A

a mutation may change the conformation of the HA enough that antibodies to the WT do not bind
=> no protective immunity

134
Q

Influenza strain nomenclature

A

a particular isolate is identified by type, host, species, geographical site of isolation, number and year

135
Q

Influenza vaccines (egg)

A

influenza virus is injected into chicken eggs and replicates

virus is separated from egg components and purifed

virus dissociated by detergent treatment

purified HA and NA protiens are used in the vaccine (split vaccine)
=> there are also quadrivalent (4 strain) vaccines

136
Q

Influenza vaccines (live attenuated)

A

live virus vaccines uses a cold-adapted strain

can be grown in culture at < 37C

replicated poorly in humans at body temperature but confers immunity

137
Q

Influenza vaccines (cell-culture)

A

since 2012

based on madin-daarby canine kidney (MDCK) cells and vero cells

since 2019 in canada FLUCELVAX QUAD form seqirus

138
Q

Influenza anti-virals

A

amantadine and rimantadine
=> only for flu A
=> no longer used (much) due to resistance

Oseltamivir, zanamivir, peramivir
=> for both A and B
=> neuaminidase inhibitors

Baxloxavir
=> inhibits RNA pol
=> inhibits “cap snatchin” of host mRNAs

139
Q

Serotypes of rhinovirus

A

also known as enterovirus

A, B, C

about 160 different serotypes

140
Q

virues that cause flu-like symptoms

A

corona viruses

6 other different types that cause symptoms

sars, mers, covid19

and 4 circulating corona viruses (seasonal)

rhinovirues

adenovirues

141
Q

Rhinovirus transmission

A

airborne and direct contact transmission

2day incubation
infection of URT, temperature optimun 32C

142
Q

Pertussis

A

also known as whooping cough

Bordetella pertussis

Gram-negative cocco bacillus

aerobic, oxidse positive, motile, encapsulated

humans or the only resivoir

143
Q

pertussis transmission

A

airborne

7-10 day incubation

attachment and colonization of the tracheal and bronchial epithelialcells

filamentous heamagglutinin
fimbriae, petractin

144
Q

pertussis exotoxins

A

produced at the site of infection
=> Pertussin toxin (PT), and A-B toxin kills cells and stimulates inflammation

tracheal cytotocin stops ciliary action of epithelial NK cells

145
Q

Stages of a pertussis infection

A

catarrhal
=> moderate symptoms, runny nose, low fever, cough or sneezing but patient is highly infective

paroxysmal
=> sever, spasmodia coughing lasting several minutes, whooping sound as air inhaled
=> can fracture ribs or cause brain damage (2-4 weeks duration)

Convalescent stage
=> one week to several months
=> decline in coughing

146
Q

complications of pertussis

A

bronchopneumonia

encephalopathy leading ot conulsions, brain damage and death

147
Q

pertussis vaccination

A

heat kille dwhole cell caccine was introduced in the 1940s

concern over fatal reactions in the 1970s lead to the development of acellular vaccines based on pertussis toxin and filamentous haemafflutinin

usually combined with pertactin and type 2 and type 3 fimbriae

may be less effective over the long term

new genetically modified whole cell vaccines

148
Q

Legionnaires disease

A

legionella pneumophila

aerobic, motile, Gram-negative coccobacillus

high fever, cough, shortness of breathg, myalgia, headaches

incubation 2-10 days

149
Q

Legionnaires disease transmission

A

inhalation of airborne droplets
=> often from contaminated water such as humidifiers, hot tubs, water cooling towers

case-fatality rate of 10% and up to 25% with underlaying respiratory conditions

amoeba-resistnace bacteria (ARB), a new disease?

150
Q

Human rhinovirus physiology

A

single-stranded positive sense TNA viruses (direct translation to proteins once in the cell)

genomes about 8000 nt in length

ath the 5’ end of the genome is a virus-encoded protein

3’ poly A tail

Virion about 30nm in diameter
=> smallest of ciruses, used to call them picornaviruses

151
Q

Human rhinovirus symptoms

A

sore throat

runny nose, nasal
congestion

muscle aches, headache

fatigue, malaise, muscle weakness

lasts one to two weeks

starve a cold, feed a fever => not true

152
Q

Temperature and Rhinoviruses

A

optimun temperature 32C

Many virues are much more sensitive to temperature that bacteria are

lowever temp in the extremities and upper respiratory tract
(note the temp of the lower RT is closer to 37 and thus they can really get down there)

Rhinovirus replicate in the nose, they get down the lower RT, but they dont replicate very well

temp a big factore

153
Q

Viral respiratory diseases causig skin rashes

A

Transmitted by aerosols, infect through the RT

sytemic infections

Red facial rash spreading to body and extremities

pustular (skin raised to lump that break open) rash in chickenpox

154
Q

Measles

A

RT infection that causes rash

long term immuno-suppression up to 4 months

can have case-fatality rates of up to 30% in cases with complications

used to the 4th highest cause of death in childern (infectious cause of disease) across the world. and this was in the 90’s when it was low (2million/ per in 80s) down form

long term immunosupression

M & D (18 decks)

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