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MicroB > Gram Positive Bacteria > Flashcards

Gram Positive Bacteria Flashcards

1
Q

Streptococci Spp. is

A

GPC in Chains
Catalase Negative

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2
Q

Outline Streptococcus pyogenes

A

Gp A BHS
MESH + Capsule

Suppurative disease:
Pharyngitis (1/3 of all cases in kids), tonsillitis, quinsy
Post-influenza pneumonia
Erysipelas / Cellulitis (also often streptococcal) *
Streptococcal Toxic Shock Syndrome (IVIG, Clindamycin)
Impetigo (also caused by staphylococcus aureus)
Necrotising fasciitis

Non-suppurative (post-infectious):
Acute Glomerulonephritis
ARF (JONES criteria) -> RHD that can occur years later

Diagnosed with clinical picture, culture, gram stain, serology particularly for post-infectious sequelae (Anti-streptomycin O, ASO, antibody made by immune system)

Treated with penicillin V / cephalosporins
NO VACCINE - Fear of autoimmunity and RHD

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3
Q

Outline Streptococcus agalactiae

A

Gp B BHS

EOD: <7 days from vaginal flora (if mother positive, give prophylactic penicillin)
LOD: >7 days from randos

Sepsis, Meningitis, Arthritis

Targets Elderly, DM. Commonly nosocomial especially in SSTI, chronic wounds, bedbound pts

LEADING CAUSE of neonatal sepsis*****

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4
Q

Outline Gp C and Gp G BHS

A

Just pharyngitis and SSTIs. Rare to see toxic shock or post-infectious complications

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5
Q

Outline streptococcus bovis

A

Associated with endocarditis, bowel cancer, hepatobiliary infection

Newly categorised into streptococcus gallolytics, pasteurianus, infantarius

Treated with pens*

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6
Q

Outline Enterococcus spp.

A

Every single Enterococcus spp. is Gp D Lancefield
GPC in chains, catalase negative

BENVU:
Biliary infection*
Endocarditis
Nosocomial
Vancomycin-Resistant Enterococcus
UTI

Some spp. resist Vancomycin and pens, give ampicillin and gentamicin*

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7
Q

Outline streptococcus pneumoniae

A

ALPHA HS*
Sensitive to optochin (Viridans spp.)*
Capsulated*

Characteristic draughtsman colonies***

Disease is invasive:
Pneumonia
MOST COMMON CAUSE OF BACTERIAL MENINGITIS
Septicaemia / Bacteraemia

Also non-invasive:
Otitis
Sinusitis
Conjunctivitis

Age, crowding, alcohol, TYPE of capsule (>90 antigenically different types) increase risk - Think of the photo of babies! (ACACA - Age, Crowding, Alcohol, Capsule, Asplenic)

Be worried about asplenic patients (functional / anatomical). They are at a higher risk especially because the spleen deals with capsulated bacteria.

Different capsule antigens offer different AMR

Two vaccine types:
- Polysaccharide (older / TC-independent so not good in kids)
- Conjugated (newer / polysaccharide + protein / good for kids, those at risk)

Pneumonia - Pens and Ceftriaxones, VANCOMYCIN FOR MENINGITIS
However, these cannot cross BBB to help meningitis. Hence vancomycin also given for meningitis. Recall the tutorial on different bugs that cause meningitis and how you cover all bases until the labs return

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8
Q

Outline Viridans group

A

AHS + NHS
Found on normal mucous membranes :. cause dental caries / polymicrobial abscesses

Attacks previously damaged heart***:
Congenital defects like bicuspid aorta
Acquired defects like IE, RHD from prior GAS, Prosthetic valves

Pens given for GAS pharyngitis to prevent later infection caused by Viridans

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9
Q

Treatment for enterococcus?

A

Ampicillin and gentamicin because it is resistant to some pens

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10
Q

What do you think of when you see enterococcus?

A

BENVU
Biliary
Endocarditis
Nosocomial
Vancomycin-Resistant
UTI

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11
Q

What do you think of when you see S. agalactiae?

A

EOD (prophylactic pens for mom) / LOD

Sepsis
Meningitis
Arthritis

DM, Elderly, Nosocomial*****

2015 SG Yusheng outbreak

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12
Q

What do you think of when you see S. bovis?

A

Hepatobiliary
BOWEL CANCER
Endocarditis

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13
Q

Colonies of S. pneumoniae appear as…

A

Draughtsman colonies

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14
Q

Disease caused by S. pneumoniae?
Hint - Invasive and non-invasive

Treatment?

A

Pneumonia / Meningitis / Septicaemia
.
Sinusitis / Otitis / Conjunctivitis

Pens, Ceftriaxones, Vancomycin
Treat with pens and ceftriaxones but won’t cross BBB so not very useful for meningitis (vancomycin!)

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15
Q

Main concern in Viridans is…

A

Endocarditis in pts with prior heart damage

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16
Q

What drug is given to penicillin-allergic patients?

A

Macrolides

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17
Q

Enterococci are resistant to…

A

Cephalosporins, vancomycin

Hence given ampicillin and gentamicin combination therapy

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18
Q

Outline staphylococcus spp.

A

GPC in clusters, coagulase +_
Catalase negative

If coagulase +, staph aureus
If negative, can be epidermidis, saprophyticus, lugdunensis

Coagulase is a virulence factor!

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19
Q

Outline Staphylococcus aureus

A

30% of general px carries it in anterior nares

Coagulase and other enzymes + toxins cause tissue damage
Protein A allows for adhesion

Toxins - Alpha toxin (haemolytic), Enterotoxin, Toxic Shock Syndrome Toxin 1 (TSST-1 superantigen), Epidermolytic toxin

SSTI - Folliculitis, Impetigo, Boils, Furuncles, Carbuncles, Cellulitis! (Differentiate from the erysipelas caused by streptococcus pyogenes), Infection at surgical sites

Deep tissue - Bone and joint, Pneumonia (following influenza), DT INFECTIONS COMMONLY THROUGH LINES, and most importantly endocarditis which, if staphylococcal in cause, can be rapidly fatal. S. aureus in general kills you in days once it invades the bloodstream and without treatment

Treatment - Cloxacillin / BL + Erythromycin, Vancomycin, Others if needed **
Topical mupirocin ***

Abscesses are common and if superficial must be drained because it could cause further infection

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20
Q

Why is MRSA resistant ? 1

A
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21
Q

Why is MRSA resistant?

A

mecA gene causing PBP mutation that confers resistance to BLs

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22
Q

Treatment for MRSA?

A

Empirical treatment is vancomycin if MRSA suspected in HAI

Further ceftriaxone / ceftobiprole can be given**

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23
Q

Give 3 spp. of CNS and treatment

A

S. epidermidis is common
S. saprophyticus is a common cause of UTI in sexually active young women
S. lugdunensis is normal in perineal flora but if infected, common cause of endocarditis and can cause UTI

Susceptible to vancomycin but many strains resistant to antibiotics***

Line-related sepsis is very important to note for staphylococcus, both CNS and SA***

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24
Q

Outline Corynebacterium diphtheriae

A

Gram Positive Bacillus, Chinese character appearance under LM
MANDATORY TO GIVE KIDS 5 DOSES OF DIPHTHERIA (TOXOID VACCINE)

Diphtheriae toxin => Alpha subunit for activity (blocks protein synthesis) and Beta subunit for binding:
Myocarditis (arrhythmia, HF) **
Neuropathy (Lower limb paralysis, Dysphagia because of palatal paralysis, Visual deficit) **

Pseudomembrane that later turns black and obstructs airway
Bull neck, very heavy breathing with accessory muscles

Can also present as nasal diphtheria (small red sores around the nose), which is more infectious but less severe.

Diagnosed with PCR* or Culture (TINSDALE’S MEDIUM*, selective indicator agar) using a throat swab

Do not wait for a diagnostic result, just start treatment: Antiserum // Antitoxin because the disease is primarily caused by the toxin. Eryhtromycin / penicillins can be given***

Mnemonic: GPB, Chinese character on Tinsdale’s though PCR is preferred, M, N, Pseudomembrane that darkens, Chest collapse, Nasal diphtheria, Diphtheria toxin (A and B subunits, A blocks protein synthesis), Eryhtromycin + Penicillin + Antiserum + ALL KIDS MUST GET 5 DOSES OF THE TOXOID VACCINE

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25
Q

Outline non-diphteriae spp. Of corynebacterium

A

Known as diphtheroids because they have similar appearance under LM
C.Ulcerans produce the same toxin so there can anything from a throat infection to full-blown diphtheria

Some species of corynebacteria exist in the skin and can cause line-infections and bacteaemia

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26
Q

What is the bacillus species

A

Gram positive rods that produce SPORES in aerobic growth!!!

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27
Q

Outline bacillus anthracis

A

GP Bacillus that secretes toxins and has capsule, produces highly resistant spores (lasts decades in soil and animal hides). Recall that the bacillus spp. produces spores in aerobic growth! The bacteria affects many animals

Capsule - Gives it virulence by resisting phagocytosis and complement activation
Toxin - Tripartite toxin that comprises the oedema toxin and a lethal toxin
Also causes pneumonia if inhaled, but consider where the inhalation is from i.e. most likely to be animal-hide related

Cutaneous anthrax in 95% of cases. Fatality is 1%, but very poor prognosis if bacteraemia occurs
Forms eschars, oedema is prominent in the face (Recall that super swollen baby face!)

Diagnosis via culture from vesicle, fluid, blood, sputum

Treat with ciprofloxacin / penicillin. Generally BA is susceptible to BLs but give ciprofloxacin if concerned about BLase inhibitors

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28
Q

Why is bacillus anthracis used as a weapon?

A

Cheap and easy to make, allows for quick pneumonia with high mortality if the bacteria is aerosolised. A strain that is multi-resistant can be used

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29
Q

Outline Bacillus cereus

A

Food poisoning is very typical of cereus. Other bacillus species can contaminate blood too
Associated with fried rice

Rapid onset - Preformed toxin that results in vomiting
Late onset - Toxin formed in GIT that results in diarrhoea and abdominal pain

Chance of infecting the cornea

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30
Q

Outline Listeria monocytogenes

A

Gram positive bacillus, ubiquitous in the environment.
Notably, grows at fridge temperatures of 4C. Spread by animal produce, salads

Hacks the cell’s actin mechanism to travel intracellularly, allowing it to evade the immmune response

Causes gastroenteritis, but also bacteraemia leading to meningitis and encephalitis
Listeriosis is one of the top 3 causes of gastroenteritis that leads to hospital admission

Hits immunocompromised (particularly TNF inhibitors, cancer pts, DM, alcoholic) and elderly (>65 y/o = 4x)
Pregnant women are at VERY high risk (100x!!!) -> Abortion, stillbirth, sepsis

RESIST cephalosporins but susceptible to ampicillin, amoxicillin

Empirical therapy must cover bacteria like streptococcus pneumoniae (MOST COMMON cause of meningitis), Neisseria meningitidis because meningitis in general is likely to be bacterial in nature. As such, give a triple therapy of ceftriaxones, ampicillin, vancomycin EMPIRICALLY. However, after lab confirmation, ampicillin +_ gentamicin works fine for listeria specifically.

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31
Q

How is listeriosis treated?

A

RESIST cephalosporins but susceptible to ampicillin, amoxicillin

Empirical therapy must cover bacteria like streptococcus pneumoniae (MOST COMMON cause of meningitis), Neisseria meningitidis because meningitis in general is likely to be bacterial in nature. As such, give a triple therapy of ceftriaxones, ampicillin, vancomycin EMPIRICALLY. However, after lab confirmation, ampicillin +_ gentamicin works fine for listeria specifically.

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32
Q

Outline nocardia asteroides

A

Gram positive bacillus
Affects mainly the immunocompromised
Enters via inhalation or can be inoculated in wounds

Causes a disseminated infection that could develop into brain abscess.
More pertinently, it can cause madura foot (mycetoma). Madura foot can also be caused by actinomyces

*Poor staining in culture, easy to mistake for other bacteria
Forms aerial hyphae (Very pretty appearance)

Treated with co-trimoxazole that can take months or even longer
Co-trimoxazole = Trimethoprim and sulfamethoxazole combination!

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33
Q

What is madura foot?

A

An infection from bacteria in soil that usually affects farmers who don’t wear shoes. Cuased by a variety of bacteria such as nocardia asteroides and actinomyces. Can also be caused by fungi!

There can be gross osteomyelitis and draining sinuses that form. The foot just looks really grossly swollen and infected and pus-y

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34
Q

What are lactobacilli?

A

Gram positive bacilli that are common in normal vaginal, oral, gut flora! Indicates healthy vaginal flora. Plays a role in dental caries

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35
Q

Incidence of TB in Singapore? What programme helped quell TB infection rates in SG?

A

35/100,000
1/3-1/4 of the world has TB in the latent form, 5-10% will go on to develop active TB
STEP - SG TB Elimination Programme (Contact tracing + Immediate treatment + Medical leave)

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36
Q

Name the different ways to diagnose TB

A

Tuberculin skin test
IGRA
T-SPOT / ELISPOT
Sputum smears / Microscopy with Ziehl Neelson
MGIT

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37
Q

Outline a TST / Mantoux skin test. Also give benefits and disadvantages

A

Give 100uL intraderml injection of purified protein derivative (glycerol extract of the tubercle bacillus). A small bump appears on the skin, to measure after 72h (>5mm is positive)

Disadvantages - Takes 72h.
Can also give a false positive if:
Received the Bacillus Calmette-Guerin (BCG) vaccine, Poorly administered, inaccurate interpretation, infection with NTM!

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38
Q

Outline IGRA

A

IFN-y ae produced by TC. QuantiFERON-TB Gold (QFT-G) is a test that quantitates the amount of IFN-y in response to the TB antigens ESAT-6 and CPF-10

Good because 24h objective result, single visit. TB-specific and doesn’t matter if you have the BCG vaccine because these are not the antigens used in making the vaccine

However, it takes 16 hours and doesn’t work very well at kids. Doesn’t determine who is at risk

39
Q

Outline T-SPOT / ELISPOT

A

Isolate the PBMC (peripheral blood mononuclear cells) and then stimulate a known number of cells with TB antigens for 24h. The Anti-IFN-y antibody detects the number of IFN-y + cells

Gives an indication of the response against TB

40
Q

What is the sensitivity of sputum smears / microscopy in TB testing?

A

Ziehl-Neelson // Acid-fast staining has a sensitivity of 53%. VERY poor.This is improved by using a fluorescent microscope. Note that this is not growing culture, rather looking at a sample from the patient as-is.

41
Q

Outline TB Culture

A

Takes 1-8 weeks to grow and expensive but has a sensitivity of 82%
Grows on a special medium called Lowenstein-Jensen (LJ)

A false negative may occur in HIV+ pts / immunocompromised. This causes TB to become very diffused all over the lung instead of being localised in a large granuloma, which is what a good immune system should do. Consequently TB doesn’t leak into the airway and CAN’T be detected in the sputum, marking the test as negative

42
Q

What is MGIT?

A

Mycobacteria Growth Indicator Tube

Contains fluorophore that is sensitive to oxygen. Bacteria use the oxygen, and a signal is produced. Results are read every hour for 42-60 days, though it is expensive at $80 a tube

43
Q

When are you considered negative for TB?

A

3 consecutive negative sputum samples

44
Q

What is the application of molecular diagnostics in TB?a

A

We can identify whether the strain is MDR / Rifampicin-resistant as we know where on the gene the mutation occurs that confers resistance. Line-probe assay / Gene Xpert can be used

45
Q

Why is streptomycin less commonly used as a TB drug?

A

ADR, Less effective

46
Q

Outline TB treatment

A

First 2 months - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Streptomycin
Next 4 months - Isoniazid, Rifampicin

Streptomycin not included in WHO guidelines but still used

47
Q

What is used if TB unresponsive to first-line treatments?

A

Rely on a fluoroquinolone alone and something from group 5 like rifapentine, delamanid, etc.

48
Q

Rifampicin side effects?

A

Body fluids are turned purple-red like tears and urine. GI discomfort, hepatotoxicity

49
Q

Rifapentine may shorten the TB treatment to _

A

4 months

50
Q

What drugs are in the rifamycin class?

A

Rifampicin // Rifampin
Rifapentine
Rifabutyn

51
Q

Why don’t we use second-line drugs very often for TB?

A

Significant ADR and often they are less potent

52
Q

Outline the types of TB resistance

A

MR-TB = Monoresistance (only one first-line drug)

PR-TB = Polyresistance (Resistance to >1 first line, other than rifampicin or isoniazid)

MDR-TB = Resistance to at least BOTH rifampicin and isoniazid

XDR-TB = Any fluoroquinolone, minimally 1 out of 3 second-line injectable drugs (capreomycin, kanamycin, amikacin). This is IN ADDITION to MDR

RR-TB = Rifampicin Resistant (a subset of many other resistance types)

TDR-TB = Totally drug resistant; 4th + 5th. Treatment can take up to 2 years and you need to use drugs that are less effective and more toxic and more expensive

53
Q

What is Telacebec (Q203)

A

A new antiTB drug currently in development

54
Q

What groups are particularly at risk for TB?

A

Malnourished, Immunocompromised, Very young / Elderly, TB Close contacts

55
Q

A gram stain can be done for TB detection. True or false?

A

FALSE
These are acid-fast aerobic bacilli. They need a ZN, not a gram stain

56
Q

Can sputum be used for TB testing?

A

Yes

57
Q

What is an AFB smear?

A

Detecting for AFB, but unable to differentiate TB and NTM

58
Q

What does it mean to be AFB negative but culture positive for TB?

A

You do have TB, but you’re less infectious

AFB smear positive means you are HIGHLY INFECTIOUS BECAUSE TB IS LITERALLY COMING OUT IN YOUR SPUTUM IN SIGNIFICANT QUANTITIES

59
Q

Outline primary stages of TB infection

A

TB inhaled via respiratory droplets and enter the lungs

MTB multiplies in lungs. They start as a singular focus but can be multiple in high doses

Alveolar macrophages are attracted to the site

As macrophages try to engulf the bacteria, some die in the process. Inflammation occurs at the focus and cellular debris begins to accumulate; Leads to pneumonitis.

This goes on for 3-9 weeks before we develop antibodies and a tuberculin skin test can be shown positive. This is a type IV hypersensitivity because the response is TC mediated

60
Q

Where in the lungs does TB classically infect?

A

Apex

61
Q

Outline the good ending for a TB infection

A

There is a small load of TB and a high hypersensitivity reaction (BC, TC, Macrophages, Langhans giant cells, fibroblasts)

Healing occurs with fibrosis and scarring

TB is non-progressive and well-contained inside a well-formed granuloma.

The infection is quiescent, though latent TB are still viable and may cause reinfection if:
Neonates, 15-25, old age
HIV / Immunocompromised
Poorly controlled DM

62
Q

Outline the bad ending for TB

A

High TB load AND high hypersensitivity

Poorly organised granuloma that cannot contain the infection. This leads to a caseating granuloma as the bacteria liquifies and escapes the granuloma.

It then starts spreading around the bronchial tree.

63
Q

What cells transport TB to the apex of the lung?

A

Infected macrophages!

64
Q

What is the worst case scenario for TB called?
What happens in this state and who is primarily affected by it?

A

Miliary TB, whereby TB circulates in the blood - Disseminated haematogenous tuberculosis.

Symptoms like fever (IL-1), weight loss due to TNF and anorexia, chronic cough, bronchial erosion, lymphadenopathy, malaise

65
Q

Can TST / IGRA differentiate LTBI vs. ATBI?

A

No

ATBI is diagnosed by symptoms, scans, lab tests, physical exam

66
Q

What is an AFB test?

A

Looks for AFB in sputum

AFB smear is just smearing the sample on a glass slide and looking at microscope

AFB culture is growing the bacteria in the lab to get a more conclusive test

67
Q

How can you confirm that TB has spread to different parts of the body?

A

Take samples from there and send for AFB smear

This is also helpful to confirm that there is a casseating granuloma

68
Q

TB vaccine?

A

Live Bacillus Calmette-Guerin vaccine

Prevents progression to ATBI and miliary TB in young children

LIVE VACCINE SO NOT FOR HIV PTS!

69
Q

Name the two prominent NTM

A

Mycobacterium leprae
Leprosy

Mycobacterium avium complex
Not spread from person to person so not usually caught but very difficult to treat

70
Q

Certain parameters must be assessed before giving a particular TB drug.

What are the parameters and what is the drug?

A

Ethambutol: Visual acuity, colour vision, baseline liver enzyme levels, weight

This is why ethambutol is hard to give kids - Their visual acuity is difficult to assess

71
Q

Outline TB treatment

A

2 months intensive RIPE (kills majority of TB)

4 month continuation of daily OR 3/week R+I (ensures cure)

72
Q

TB drugs side effects?

A

RIPE+S => Itchy skin (pruritis) with / without rash. TEN may occur in rare cases

RIP => GI symptoms like anorexia, nausea, abdominal discomfort

73
Q

How does rifampicin work?
How does resistance develop?
When is it used?

A

Bactericidal!

Blocks DNA-dependant RNA polymerase (blocks transcription and hence protein synthesis, killing cell)

Resistance can occur because of mutation in gene coding for RNA polymerase enzyme

Used in ATBI, LTBI, LEPROSY too!

74
Q

PK of Rifampicin

A

Oral, absorbed well on empty stomach

Hepatic metabolism and rapidly removed in bile (hepatic impairment is important)

CNS concentration is 10-20% of serum, but increases in meningitis

Category C - Can be given with pregnancy as no risk of teratogenesis but increased risk of thrombocytopenia so give the mom Vit K to avoid post-partum haemorrhage. During breastfeeding, small concentrations can pass into infant (monitor infant for jaundice!)

75
Q

Contraindications to Rifampicin?

A

Renal impairment is fine
Hepatic impairment is fine too, but BE CAREFUL with the dose and monitor liver function. Using isoniazid with rifampicin increases the potential for hepatotoxicity

DO NOT GIVE PATIENTS with hypersensitivity to Rifamycin

It is also a CYP450 inducer, so be careful when giving warfarin, corticosteroids, contraceptives

76
Q

Rifampicin ADR?

A

Cutaneous - Flushing and pruritis with or without rash

Fever, chills, malaise, body aches

Respiratory - Shortness of breath

Hepatitis

CYP450 inducer

Orange discolouration of body fluids, incl. tears, sweat, urine!

If things like thrombocytopenia, purpura, haemolytic anemia, acute renal failure start happening, STOP rifampicin and never give again

77
Q

Isoniazid MOA?

Resistance?

A

Prodrug activated by MTB. Active form produces oxygen free radicals that inhibit formation of mycolic acids of cell wall and damages DNA

Used in ATBI and prophylactically in LTBI

Resistance can occur if mutation in the catalase peroxidase enzyme of MTB. This enzyme activates the prodrug

78
Q

PK of Isoniazid?

A

Orally given and taken well on an empty stomach. In fact, taking with food esp carbs can decrease the absorption by 57%. Taking with foods rich in tyramine and histamine (tuna, cheese, red wine) because can cause flushing, headachex. Antacids, by increasing the gastric pH, also slow absorption.

Isoniazid is a CYP450 inhibitor!!!!!!!

Metabolised by liver

There is genetic polymorphism (variance) when it comes to the acetylation rate (rapid vs. slow acetylator phenotypes, rapid gives an isoniazid T1/2 of 1h and slow gives 2-5h)

79
Q

Isoniazid during pregnancy - Think of?

A

Pyridoxine for mom and baby!!! So as to prevent Vit. B6 deficiency for those at risk of peripheral neuropathy

80
Q

Rifampicin and isoniazid need dose adjustments / monitoring in renal impaired pts?

A

NO. Liver impaired!

81
Q

Isoniazid and pyridoxine relationship?

A

Isoniazid inhibits the formation of active form of Vit B6, resulting in peripheral neuropathy

Need to take Pyridoxine supplements!

It is the naturally occurring form of Vit B6 in the body, ESSNETIAL for CNS function

82
Q

Isoniazid ADR?

A

Hepatotoxicity

Peripheral neuropathy due to drop in Vit. B6

INHIBITS CYP450!!!!

83
Q

Effect of pyrazinamide?

A

Prodrug activated by MTB enzyme called pyrazinamidase. Active form enters the bacteria and lowers the pH, killing the bacteria

It is a potent steriliser and is very effective in eliminating bacteria. It reduces treatment time from 9 to 6months.

Resistance develops in a pyrazinamidase mutation

Safe for pregnanacy! Monitor breastfed baby for jaundice because of hepatic clearnace

84
Q

Pyrazinamide in liver / kidney?

A

Hepatotoxic drug and generally avoided for those with liver disease

In kidney failure, dose will have to be decreased because the drug tends to accumulate

85
Q

Pyrazinamide ADR?

A

GI nausea vomiting

Photosensitivity

Hepatotoxicity (discontinue or even replace! Riss of pyrazinamide is even higher when combined with isoniazid)

Hyperuricemia because the metabolite of pyrazinamide inhibits the tubular secretion of uric acid

Arthralgia

Exanthema and pruritis
Exanthema is widespread rashes

86
Q

Ethambutol MOA?

A

Bacteriostatic

Inhibits arabinosyltransferase enzyme that interferes with cell wall formation.

87
Q

Ethambutol PK?

A

75-80% absorption orally

Does not cross BBB in healthy cases, but does so in meningitis and achieves healthy concentrations

Cleared renally so careful with renal impairmenst

88
Q

Ethambutol ADR?

A

High risk in renal impairment and elderly individuals and in prolonged treatment of >2 months

Visual toxicity - RGcb, Blurring
Dose-dependent toxicity

Cautioned in kids because visual acuity is hard to assess

Hyperuricemia aka GOUT because of drop in uric acid excretion by kidney

Safe in pregnancy and EVEN IF RENAL IMPAIRMENT!

WARNING - Reduce dose in kidney failure because metabolites can accumulate

Antacids can reduce concentration. Separate antacids and general RIPE by 2h

89
Q

Streptomycin MOA/

A

Binds MTB ribosomes and distorts them -> Misreading codons and inhibit translocation (moving the mRNA out of the nucleus)

In SG, may be used in place of ethambutol

90
Q

Streptomycin PK / ADR?

A

IM injection
Poor BBB crossing

Vertigo and ataxia because of ototoxicity (risk increases with age, is bad for the fetus)

Neurotoxicity - Circumoral PARESTHESIA, tingling for a bit after injection (avoid in myasthenia gravis)

Nephrotoxicity

91
Q

When do you suspect drug-resistant TB?

A

Previously treated TB pts

Pts that failed TB treatment

Close contacts of MDR-TB pts

Pts from countries that have lots of MDR-TB like India,Philippines, Russia, South Africa

92
Q

What is BCG?

A

Bacille Calmette-Guerin! Vaccine against tuberculosis

93
Q

What is the most common bacterial cause of meningitis?

A

Streptococcus pneumoniae!!!!!!!

MicroB (4 decks)

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