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Microbiology Flashcards

1
Q

Infective endocarditis (IE)

  1. def
  2. types

I. Native valve IE

  • RF? 4
  • common pathogen?

II. Prosthetic valve endocarditis
- common pathogen?

III. IVDU-associated IE

  • age group?
  • which side affected most?
  • common pathogen

IV. Nosocomial infective endocarditis

  • age group
  • RF?
  1. 3 culture negative causes of IE?
A
  1. bacterial (or fungal) infection of heart valves or endocardium

2.
I. Native valve IE
- increased risk with congenital heart diseases, rheumatic fever, mitral valve prolapse, degenerative
- viridans streptococi (oral flora, α-haemolytic)

II. Prosthetic valve endocarditis
- coagulase negative staphylococi

III. IVDU-associated IE

  • median age 30 (M>F)
  • Rights sided more common (tricuspid 50%, aortic and mitral 25 each)
  • staphylococus aureus

IV. Nosocomial infective endocarditis

  • in elderly (>60)
  • ass with iv lines and invasive procedures (eg pulmonary artery catheterisation)

3.
I. Q fever- coxiella burnetti
- from contact with animals
- requires blood on admission of 4 weeks post-admission

II. Bartonella spp

  • cat scratch disease
  • Non-serological: requires 16s rRNA PCR on valve tissue to diagnose (sampled during surgery)

III. typheryma whipplei
- Non-serological: requires 16s rRNA PCR on valve tissue to diagnose (sampled during surgery)

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2
Q

Infective endocarditis (IE)

1. clinical symptoms?
I. general 
II. cardiac
III. vascular 4
IV. GI/GU
V. brain
  1. complications? 5
  2. treatment
    I. general
    II. Q fever
    III. chlamydia
  3. prevention
A 
1. 
I. malaise, pyrexia
II. cardiac murmer
III. Osler's node, Janeway lesion, splinter haemorrhages, Roths spot (flame shaped haemorrhage in opthalmoscopy)
IV. splenomegaly, haematouria
V. cerebral emboli
    • valvular destruction leading to heart failure
    • embolisation
    • acute renal failure
    • mycotic aneurysm
    • death
  2. I. appropriate Abx for different organisms
    II. tetracycline + hydroxychlorquine (>1 yr)
    III. tetracycline
  3. no prevention (abx prophylaxis no longer used)
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3
Q

Osteomyelitis

  1. def
  2. types 3
  3. Sx acute and chronic
  4. Ix 2
  5. Mx? duration??
  6. Pathogens age groups?
A 
1. progressive infectious disease
bone destruction (sequetrum) + new bone formation (involucrum)
  1. I. Haematogenous
    - following bacteraemia
    - esp in children (bone constantly remodelling)
    - metaphyseal areas of long bone
    II. contiguous
    - after trauma/surgery/overlying soft tissue infection
    - ass with prosthesis/plates and screws
    III. diabetic
    - reduced vascularity, skin ulcers, reduced local immunity
    - stick test: sterile swab on the ulcer, if hard, 99% means bone infection
  2. acute (10 days): painful swollen
    chronic (longer): sinus, scars, asymptomatic
    • blood: culture, FBC, CRP
    • deep tissue biopsy in theatre (dont start on Abx before this)
  4. 6-8 weeks abx for adults
    4 weeks abx for children
  5. Staphylococus aureus in adults and children (1-16yo)
    Group B streptococcus in babies
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4
Q

Septic arthritis

  1. pathogens
  2. treatment
A
    • staphylococcus aureus
    • haemophilis influenza if <3 yo (less common due to Hib vaccine)
    • Nieserria gonorrhoea
  2. 2-3 weeks Abx start immediately
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5
Q

Prosthetic joint infection (PJI)

  1. def
  2. pathogen
  3. Ix
  4. Mx? 4
A
  1. septic arthritis in prosthetic joint, normally starting with mild symptoms
  2. coagulase -ive staphylococci
  3. MC&S of joint aspirate
  4. I. debride and wash if within 10 days of surgery
    II. radical : 1 or 2 stage removal/replacement of joint
    III. lifelong suppressive abx (or 6-8 weeks)
    IV. do nothing
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6
Q

Health care associated infections (HCAI)

  1. hospital acquired infection def?
  2. mechanism of spread?
  3. Commonest sites?
A
  1. Infections that are neither present nor incubating when a patient enters hospital, but develop during hospital admission or are incubating when a patient leaves hospital
  2. I. Hands and contaminated equipment:
    MRSA and Group A Streptococcus (GAS)
    II. Faecal/oral spread and contaminated environment :
    Viral Gastroenteritis (VG) and C. difficile
    III. Airborne/Droplet:
    VG, Varicella zoster and GAS
  3. Urinary tract 23% (catheters)
    Lower respiratory 23 (ventilators, post op NG feeding)
    Blood stream 5%
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7
Q

Trachoma

  1. cause
  2. main complication
  3. transmission
  4. Mx
A
  1. Chlamydia serovars A-C
  2. Most common cause of preventable blindness worldwide
  3. Hand to eye contact
    Flies
    4.
    I. Prevention:
    - Clean water
    - Decrease fly populations
    II. Treatment
    - Systemic Erythromycin or Doxycycline
    - Trials of Azithromycin
    - Eyelid surgery
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8
Q

Prophylaxis of HIV peri/pre/post exposure?

A
  1. ASAP after exposure, preferably within 24 hours, but can be considered up to 72 hours
  2. 28 days Truvada and raltegravir
  3. STI testing, repeat at 2 weeks
  4. HIV testing at 8-12 weeks
  5. Hep B vaccine if clinically indicated
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9
Q

Hep B prophylaxis peri/pre/post exposure?

A

I. Vaccine
- 48 hours – up to 1 week
II. HBIG (hep B immunoglobulin) if high risk or vaccine non-responder
- 48 hours – up to 1 week

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10
Q

Hep C prophylaxis peri/pre/post exposure?

A

No effective post exposure prophylaxis

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11
Q

Polysaccharide and conjugated vaccines? (as opposed to live attenuated or dead pathogens)

Def?
Limitation? 2
Conjugation?

A
  • Polysac: are made of extracted and purified forms of the bacterial outer polysaccharide coat.
  • They do not stimulate the immune system as broadly
  • Protection is not long-lasting and response in infants and young children is poor.
  • Conjugation: Attachment of a carrier protein to a polysaccharide antigen. Conjugate vaccines generate a better immune response and are effective even in young children.
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12
Q

Pneumococcal conjugate vs pneumococcal polysaccharide?

A

I. Pneumococcal conjugate vaccine (PCV)

  • children <2 yo
  • 13 capsular types of pneumococcal bacteria.

II. Pneumococcal polysaccharide vaccine (PPV)

  • All adults who are over 65 years of age.
  • protection against 23 types of pneumococcal bacteria
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13
Q 
Routine Schedule in the UK
I. During 1st Year
II. During 2nd Year
III. Pre-school
IV. 2-17 years
V. 12-13 years (girls)
VI. 13-18 years
VII. 14-15 years
VIII. 70 years
A 
I. During 1st Year
- Dipth/Tet/Pertussis
/IPV
- Hib vaccine 
- Pneumo vaccine
- MenB
- MenC
- Rotavirus

II. During 2nd Year

  • MMR
  • Hib/MenC/MenB

III. Pre-school

  • Dipth/Tet/Pertussis /IPV (booster)
  • MMR (booster)

IV. 2-17 years
- Influenza

V. 12-13 years (girls)
- HPV (2 over 6 months)

VI. 13-18 years
- Dipth/Tet/IPV (Booster)

VII. 14-15 years
- MenACWY (Single dose)

VIII. 70 years
- Zostervax (Single dose)

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14
Q

Viral hepatitis classification?

A 
I. enteric pathogens
- eg HEP A &amp; E
- self-limiting acute infection
II. parenetal pathogens
- eg hep B, C, D
- could be self limiting or progress to chronic liver failure
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15
Q

Hep B:

  1. 4 phases of natural history
  2. age and chronicity?
  3. genotypes
    - which more likely to go chronic
    - which respond better to interferons
    - which have a higher rate of HCC
    - which is the most common
  4. Mx
A

1.
I. immune tolerance,
• normal alanine aminotransferase (ALT) levels,
• very high HBV DNA titres.
• This phase may last for up to 30 years.
II. an immune active phase,
• hepatocyte damage
• HBV DNA level remains elevated,
III. Inactive HBV phase,
• antibodies against the HBeAg (anti-HBe) are present,
• ALT is normal,
• little detectable HBV DNA .
IV. quiescent (cleared disease), or reactivation

  1. the younger the exposure, the more likely to be chronic
    • A&C
    • A&B
    • C
    • A
4. 
I. interferons
- peginterferon α 2a (1 yr course)
II. nucleotide analogue 
- eg:  lamivudine, telbivudine, adefovir, entecavir, and tenofovir
- inhibit HBV polymerase
- lifelong treatment
- risk of resistance
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16
Q

Hep D

  1. infection
  2. effect on the progression of HBV
  3. genotypes
A
  1. co-infection with hepB as requires hep b surface protein for lifecycle)
  2. increased rate of progression, fulminant hepatitis and HCC
  3. 8 genotypes:
    - 1 more severe
    - 2 less severe
    - 3 high risk of fulminant hepatitis
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17
Q

Hep C

  1. transmission
  2. chronicity
  3. genotypes
  4. Mx
A
  1. faeco-oral
  2. common in adults (85%)
  3. 6 genotypes (1-3 most common in europe)
  4. Tx: combination of DAAS (direct acting antivirals); highly effective
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18
Q

Hep A

  1. transmission
  2. chronicity
  3. Sx
  4. Tx
  5. prevention
A
  1. faeco-oral
  2. no chronocity
  3. mild to diarrhoea, vomiting, jaundice
  4. no Tx, just supporative care
  5. both pre-post-exposure vaccines
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19
Q

Hep E

  1. 4 genotypes
  2. Tx?
A 
1,2:
- account for epidemic outbreaks
3,4:
- sporadic cases, less severe
- similar to swine HEV
- ass with pig products
  1. Tx:
    ribavarin, pefinterferon alpha-2b
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20
Q

Salmonella

  1. common serotypes
  2. resulted from
  3. which time of the year most common
  4. what type of antigen
  5. what happens as a result of infection
  6. which part of GI wall is affected
  7. incubation
  8. Sx
  9. how quickly resolves?
  10. complications?
  11. MX
A
  1. Commonest S. enteritidis, S. typhimurium, and S. virchow
  2. Contaminated poultry/ dairy products common source
  3. summer (warm season)
  4. lipopolysaccharide O antigen, flagella is H antigen
  5. Excessive fluid secretion from ileum/jejunum, If transported through cells, leads to systemic infection
  6. Does not extend beyond basement membrane
  7. 12-72hours
    • Malaise, nausea, vomiting, fever ,watery brown diarrhoea
    • Typhoid and paratyphoid fevers
  9. several days (up to several weeks)
  10. I. Salmonella colitis
    Up to 10%, colic and bloody stools
    II. Bacteraemia
    Seeding to bones/ joints (sickle-cell), aneurysms
    III. Post-infectious reactive arthritis
    IV. Prolonged excretion
    Diverticulosis, IBD, HIV
  11. I. Rehydration
    II. Antibiotics if
    - no recovery after 48 hrs,
    - shock,
    - high risk (valve
    disease/prosthesis),
    - bacteraemic

Ciprofloxacin first line (alternative is cefotaxime)

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21
Q

Shigellosis

  1. transmission
  2. commonest pathogens
  3. which part of GI wall affected?
  4. S.dysenteriae type 1 toxin?
  5. incubation
  6. sx?
  7. mx
  8. microbiology
A
  1. Person to person spread and via contaminated food and water
  2. S.sonnei, others flexneri, boydii, dysenteriae
  3. Invade gut by destroying submucosa, infecting enterocytes, spread from cell to
    cell
  4. produces exotoxin (shiga toxin)
  5. Incubation 1-7 days
    • High fever, high WBC; fever resolves and diarrhoea and colic begin
    • sonnei and boydii mild, rarely colitis
    • flexneri and dysenteriae more severe,
    • mucus and blood in stools, marked colic
    • Asymptomatic excretion for days-weeks
    • Symptomatic: antispasmodics, rehydrate
    • ABx in severe cases, ciprofloxin (trimethoprim may be active,
      ceftriaxone also alternative)
  8. Non-lactose fermenters
    Non-motile
    Serotype on basis of O antigens
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22
Q

Campylobacter

  1. transmission
  2. common pathogens
  3. incubation
  4. Sx
  5. mx
A
  1. Mostly sporadic, undercooked poultry, bird pecked milk
    Large food/waterborne outbreaks can occur
  2. C. jejuni, coli, fetus, lari
  3. Incubation period 2-5 days (up to 9)
  4. 24hr prodrome, fever, headache
    Watery diarrhoea, can be bloody, vomiting
    Pain significant, constant, not colicky
  5. Mild cases self-limiting
    Severe/ prolonged, use 3-4 day course oral erythromycin
    Ciprofloxacin active
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23
Q

Escherichia coli

  1. 2 types
  2. incubation
  3. sx
  4. complication
  5. mx
A
    • Enterotoxigenic E. coli (ETEC)
    • Verocytotoxic (VTEC) or Enterohaemorrhagic (EHEC)
  2. Incubation usually 1-5 days (up to 14)
  3. Abrupt onset vomiting and diarrhoea
    Later profuse watery diarrhoea only
    Mild fever, little pain
    Similar to viral gastroenteritis/salmonellosis
  4. Haemolytic Uraemic Syndrome
  5. Many E.coli resistant to broad spectrum penicillins, cephalosporins,trimethoprim
    - Ciprofloxacin 500mg BD, 3-5 days
    - Avoid antibiotics in HUS
    - Antimotility drugs probably increase chance of HUS through delayed clearance
    of toxin
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24
Q

ETEC vs VTEC

I.toxicity
II. transmission

A

I.
ETEC-produce 2 main types of toxin
- Polypeptide, like cholera toxin
- Stimulates hypersecretion
VTEC (or enterohaemorrhagic)-
- cytotoxin, kills cells, like Shigella toxin
- Haemorrhagic colitis and HUS (haemolytic uraemic syndrome)

II.
ETEC
- Commonest cause bacterial diarrhoea in children in areas of poor hygiene,
- important cause travellers’ diarrhoea.
- Reservoir-human GI tract
VTEC
- Several types, commonest O157, now common cause of acute renal
failure in Western countries
- Reservoir-GI tract of healthy cattle
- Contaminated food/ animal carcasses (hamburgers), unpasteurised milk,
farms, paddling pools, person to person rare e,g nurseries

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25
Q

Haemolytic Uraemic Syndrome

A
  • May accompany colitis as a complication
    10% children in outbreaks
  • Rising urea and creatinine, haemolytic anaemia and thrombocytopenia
    Raised BP, fitting
  • More than half need haemodialysis, almost all cases recover (most
    deaths in elderly, fatal <5%)
  • Preceding GI illness may be unrecognised
  • Mucosal damage and microangiopathic haemolytic anaemia and renal
    vascular disease
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26
Q

Clostridium difficile

  1. why common cause of hospital acquired diarhoea
  2. sx
  3. complications
  4. risk groups?
  5. mx
A
  1. Some antibiotics disturb balance of microbial flora -> rapid multiplication ->
    toxin production -> mucosal injury & inflammation -> diarrhoea
  2. Antibiotic-associated diarrhoea
    Antibiotic-associated colitis
  3. Acute abdominal syndrome/toxic megacolon, colonic perforation, pseudomembranous colitis, recurrence (in 20%)
  4. > 65 yrs
    Antibiotic treatment (esp. clindamycin, cephalosporins, penicilins)
    GI surgery/manipulation
    Long stay in hospital/residential care
    Immunosuppression
    • Stop or change antibiotics if possible
    • Fluid/electrolyte replacement
    • Avoid antiperistaltics
    • If above not possible or unsuccessful, treat with metronidazole (2nd line
      vancomycin)
    • Infection control
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27
Q

Viral Gastroenteritis

  1. Ix
  2. commonest caues
  3. incubation
  4. sx
  5. prevention
A
  1. I. Stool electron microscopy, ‘catch all’
    II. Stool enzyme immunoassays (e.g. rotavirus)
    III. Molecular diagnosis: Stool PCR
    NOte: cant do cell culture
  2. rotavirus
  3. Incubation around 1 day
    • Abrupt onset D and V (D>V)
    • Mild fever, short-lived
    • Recovery in 48 hrs usual (D for up to a week)
    • live attenuated vaccines (Rotarix and RotaTeq) highly effective against
      severe disease
    • Protection against severe disease, not necessarily against infection
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28
Q

Norovirus Gastroenteritis

  1. incubation
  2. sx
  3. lasts for
  4. where does it occur most
  5. transmission
  6. season
A 
1. Incubation 10-50 hrs
2.
- Asymptomatic to explosive vomiting and diarrhoea
- Headache and abdominal cramps
3.  Lasts 24-48 hrs
  1. closed communities / hospitals/ cruise ships
  2. Breathe in aerosolised vomit/faeces and swallow
  3. winter vomit
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29
Q

Enteric Adenoviruses

  1. incubation
  2. sx
A
  • Second most common cause of infantile diarrhoea in temperate climates
  1. Incubation period up to 10 days,
  2. watery diarrhoea, mild fever, illness may
    last longer in general (3-11 days)
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30
Q

Astroviruses

  1. who does it affect most
  2. co-infection with
  3. season
A
  1. Infants and elderly exhibit significant illness
  2. Often co-infection with rotavirus/ norovirus
  3. Winter time
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31
Q

HIV

  1. transmission
  2. biggest reduction in risk of transmission
  3. clinical stages
  4. monitoring
  5. which T cell does it affect?
  6. Complication
A
  1. sexual contact, needlestick
  2. Biggest reduction due to circumsision (if sex not safe)
  3. Stage I: Acute seroconversion
    Stage II, III: Asymptomatic and PGL (progressive glandular lymphadenopathy)
    Symptomatic infection (ARC although should be Stage IVC2)
    Stage IV: AIDS
  4. T cells:
    - >500 normal
    - 200 to 500 asymptomaticHIV, but may start highly active retroviral therapy
    - <200 AIDS
    - <50 High risk of death in next 12 months
  5. CD4
  6. opportunistic infection
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32
Q

Adaptive vs innate immune

A 
Innate : NO MEMORY
- mucosal barriers
-bone marrow derived phagocytes
- alternative complement pathway
- acute phase response
- cytokines / chemokines
- interferons
Adaptive: SPECIFICITY + MEMORY
- Lymphocyte mediated - T + B cell
- Specific receptors for Ag
- TCR / sIg
- Specific recognition for activation
- Delay in primary response
- Memory gives more effective subsequent response
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33
Q

Helper” T cells

2 types and what they each produce

A 
Produce cytokines
I. Th 1 T cells
- produce IFNγ, IL-2, IL-12
- Involved in cell mediated immunity
- macrophage activation
II. Th 2 T cells
- produce IL-4, IL-13
- Involved in humoral immunity (Ab production)
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34
Q

AIDS criteria

1. Infective
I. fungal 
II. protozoal
III. bacterial 
IV. viral
2. malignancy
3. other
A

The infections that occur with any T Cell deficiency

1.
I. 
Oesophageal candidiasis
II.
Toxoplasmosis
Cryptosporidiosis, chronic
Pneumocystis cariini pneumonia
III.
Mycobacterium tuberculosis, any site
Atypical mycobacteria
Salmonella
Recurrent bacterial pneumonia 
IV. 
CMV retinitis
Other site CMV disease
2. 
Kaposi’s sarcoma
Lymphoma’s (NHL)
  1. HIV dementia
    HIV wasting syndrome (loses at least 10 percent of her body weight and has at least 30 days of either diarrhea or weakness and fever)
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35
Q

Hairy leukoplakia

A

White plaques on lateral aspect of tongue
EBV driven
AIDS defining disease

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36
Q

3 viral rashes?

A 
I. Measles (Rubeola)
Florid maculopapular rash
Conjunctivitis
Koplik’s spots
Almost always symptomatic

II. Rubella (German measles)
Less florid red-pink skin rash made up of small spots
Swollen glands behind ears
Aching and painful joints– more common in adults
May be subclinical

III. Parvovirus B19 (Erythema infectiosum)
Rash maculopapular typically more florid on face (children)
Moves to trunk, limbs
Central clearing leads to reticular, lace-like appearance
Re-appears with heat
Aching/ painful joints
May be subclinical

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37
Q

Antiviral therapy

A
  1. Antiviral Nucleosides
    - Act as competitive inhibitors and DNA chain terminators
  2. inhibition of viral DNA polymerase
    - eg Aciclovir:
  3. Neuraminidase Inhibitors
    - eg Oseltamivir (Tamiflu) and Zanamivir (Relenza)
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38
Q

Aciclovir

  1. how is it selective
  2. mech of action
  3. used against
  4. dosing
A
  1. activated only by the virus
  2. Competitive inhibitor of viral DNA polymerase, Leading to viral DNA chain termination
  3. Effective against HSV types 1 & 2, and VZV infections
  4. requires to be given 5x daily for 5-7 days. Treatment needs to start within 24-72 hours
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39
Q

Neuraminidase Inhibitors

I. Relenza (Zanamivir)

  1. use?
  2. delivery
  3. dose?

II. Tamiflu (Oseltamivir)

  1. method of delivery
  2. used for
  3. dose?

III. mech of action

IV. when to be taken

A

I.

  • Treatment and prevention of influenza A (inc avian) & B
  • Delivery as an aerosol of powder from blister pack inhaled as 10mg x b.d. for 5 days

II.

  1. Oral formulation
  2. for the treatment of influenza A & B (and prevention- o.d. regimen)
  3. (75 mg capsule) b.d for 5 days and oral suspension

III.

  • Removes sialic acid from cell surface and new viruses, preventing virus slip through mucous reaching the respiratory cell epithelium

IV.
- Needs to be taken within 48 hours of first symptoms for maximum benefit but should be given later if severely unwell/ high risk group

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40
Q

Neisseria meningitidis

  1. source
  2. what group of pathogens does it belong to?
  3. causes what diseases?
  4. capsular groups?
  5. abx
A
  1. Lives in the nose. normal commensals
  2. G neg diplococci.
  3. Cause meningitis and septicaemia.
  4. Several capsular groups B C W…
  5. meningitis sensitive
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41
Q

Haemophilus influenzae

  1. source
  2. what group of pathogens does it belong to?
  3. causes what diseases?
  4. capsulated?
  5. vaccine
A
  1. Live in the nose.
  2. G neg cocco-bacilli.
    • Cause otitis media (children) and pneumonia (adults).
    • Type b (“Hib”)– (capsulated) causes invasive disease in children including
      meningitis
  4. polysaccharide capsule,
  5. a protein incorporated in the capsule, which allows the immune system produce a bigger reaction
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42
Q

Strep pneumoniae

  1. source
  2. what group of pathogens does it belong to?
  3. causes what diseases?
A

“Pneumococcus”

  1. Live in nose.
  2. G pos (diplo)cocci.
    • Cause otitis media (children)
    • pneumonia (children and elderly adults)
    • invasive disease including meningitis.
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43
Q

Moraxella (Branhamella) catarrhalis

  1. source
  2. what group of pathogens does it belong to?
  3. causes what diseases?
A
  1. Live in nose.
  2. G neg diplococci (kidney bean shaped).
  3. Causes otitis media in children and sinusitis and Chronic Obstructive Airway Disease in adults.
44
Q

Cefotaxamine

  1. what type of abx
  2. used for what types of bacteria?
  3. route of administration
  4. CSF penetration?
A
  1. 3rd generation cephalosporins,
  2. Broad spectrum
    I. especially good for Gram negatives (Neisseria, Haemophilus),
    II. good for some Gram positives (Most Streptococci incl pneumococci, not Staph). 3. Given IV.
  3. Good CSF penetration.
45
Q

Kids bugs

I. meningitis

  1. causative organisms
  2. Abx

II. otitis

  1. causative organism
  2. Abx
A 
I. 
1. 
N. meningitidis,
S. pneumoniae, 
Hib
2. Cefotaxime 
II.
1. 
S. pneumoniae,
H. flu, 
Moraxella Viruses
2. Amoxycillin
46
Q

Amoxycillin

  1. what type of abx
  2. used for what types of bacteria?
  3. route of administration
  4. co-administrated with?
  5. resistance?
A
  1. Broad spectrum penicillins.
  2. broad spectrum, activity against Gram negatives as well as positives.
  3. Can be given orally.
  4. Can be given with betalactamase inhibitors (Clavulanic acid) to impede resistance: Coamoxyclav/Augmentin
  5. But resistance (usually via beta
    lactamases) is frequent (e.g. among Gram positives) (Staph) and Gram negatives (Haemophilus, Moraxella).
47
Q

Bugs shapes?

A

cocci- round

Bacilli- rods

48
Q

Gram stain

A

stain all purple
decolourise with a solvent
positive retains the die

49
Q

Dehydration

A
  • measured in % body weight

- loss more than 10% is clinically significance

50
Q

Old vs new defs:

  1. old sepsis def?
  2. New sepsis def?
  3. New way of assessing sepsis severity?
A
  1. Clinical evidence of infection, plus evidence of a systemic response to infection
  2. life threatening organ dysfunction caused by a disregulatory immune respond to the infection
  3. Quick SOFA score:
  • tachypnoea
  • Low mental status
  • low Systolic BP
  • (acute) impairment of any 2 of above suggests sepsis
51
Q

Spectrum of severity of sepsis?

A
  1. Sepsis
    – Clinical evidence of infection, plus evidence of a systemic response to infection.
  2. Severe sepsis
    – Sepsis with organ dysfunction, hypoperfusion or hypotension
  3. Septic shock
    – Sepsis with hypotension unresponsive to fluid resuscitation
  4. Multiple Organ Failure
52
Q

Sepsis pathogenesis:

I. 3 vascular changes in microvasculature in sepsis?
II. overall outcome of these vascular changes for the tissue?
III. cardiac changes?
IV. immune changes

A

I.

  1. PAF (platelet activating factor): causes increased platelet aggregation and adhesion
  2. TNFα & C5a: cause increased vascular permeability
  3. Nitric oxide: causes loss of contractility of vascular smooth muscle

II.
Occlusion of microcirculation causing hypoperfusion then organ failure

III. 
1. Initial high cardiac output
– Classic ‘bounding pulse’ of sepsis
2. As cardiac muscle becomes affected
by organ hypoperfusion and toxic
products, cardiac output falls
3. Patient becomes cold, clammy,
resembling patient with cardiogenic
shock

IV.

  1. increased immune response initially due to TNF, IL-1, IL-6 release
  2. with time, immunesuppression due to anti inflammatory cytokines, eg. IL-10
53
Q

Sepsis risk factors?

A
  1. Immunosupression
  2. Comorbidity
  3. Age
  4. Invasive devises
    – Vascular
    – Surgical
    – ventilatory
  5. Use of antimicrobials
54
Q

Signs and symptoms of sepsis

A
  1. Signs and symptoms of underlying focus of infection
  2. Symptoms and signs of SIRS
  3. Signs and symptoms of shock
  4. Signs and symptoms of organ hypoperfusion
55
Q

Systemic inflammatory response syndrome

  1. 4 criteria
  2. other markers
  3. future marker
A 
4 criteria
– Temp >38 °C or <36°C
– Tachycardia
– Tachypnoea
– (WCC > 12 or <4)
Other markers
– increased CRP
– decreased platelets
• Future markers
– Procalcitonin
-----Differentiates response to bacterial infection from response to other pathogens
56
Q

Early and late signs of hypoperfusion

A 
• Early signs
– Respiratory alkalosis
– Oliguria
• Later signs
– increased lactate (metabolic acidosis)
– Decreased capillary refill
57
Q

Management of sepsis?

4 steps?
Sepsis 6?
Adjunctive therapy?

A 
I. 
1 Resuscitation
2 Antibiotics
3 Treat focus of infection
4 Monitor and minimise organ damage
- Look for and treat DIC
-------Heparin
-------Replace clotting factors and platelets
where appropriate
- Correct severe acidosis

II. Sepsis 6:
Give 3: 
I. O2
II. fluid challenge
III. Abx
Take 3: 
I. lactate 
II. blood culture 
III. Urine output

III. Adjunctive therapy
• Steroids
– High dose: no benefit
– Low dose: most say no benefit
• Intravenous immunoglobulin
– Evidence of survival benefit in specific infections, eg streptococcal toxic shock
• Activated protein C
– Significant bleeding risk
58
Q

Acute bronchitis

Most likely due to what pathogens?

A

Acute viral infection causing a cough/sore throat, etc

Viral:

  • Influenza
  • RSV
  • rhinovirus
  • adenovirus
  • parainfluenza virus
  • human metapneumovirus

Bacterial:
- pertussis (whooping cough)

59
Q

Chronic obstructive airway disease

  • def?
  • vs chronic bronchitis?
A

Clinical Definition :

  • Productive cough for more than 3 months per year for at least 2 years
  • Wheezing
  • Dyspnoea (shortness of breath)

COPD = Chronic bronchitis with airflow limitation
- Most chronic bronchitis develop COPD over time.

60
Q

Infective exacerbation of COPD

I. Anthonisen criteria for abx for infective exacerbation of COPD?
II. most likely pathogens?
III. which abx?

A

I. Antibiotic therapy indicated if two of:

  • Increased breathlessness
  • Increased sputum volume
  • Increased sputum purulence

II.

  • 40% of acute exacerbations are viral!
  • Patients with COPD may have colonisation of the LRT with organisms normally found in the URT such as H. influenzae, M. cattarhalis.

III. Give amoxicillin or a tetracycline

61
Q

Influenza caused bronchitis treatment

A
  • Amantidine, rimantidine (interfere with virus uncoating and assembly)
  • Neuranimidase inhibitors: inhaled zanamivir (Relenza) & oral oseltamivir (Tamiflu) relieves symptoms, reduces complications
62
Q

Pneumonia

  1. Community acquired vs hospital acquired?
    - duration in hospital
    - pathogens
    - treatment
  2. general clinical features
  3. localised clinical features
A 
1. 
I. Community Acquired
- < 48 hours in hospital
- Due to S. pneumoniae and sometimes other organisms
- Narrow spectrum therapy

II. Hospital Acquired

  • ≥ 48 hours in hospital
  • Due to multi-resistant “hospital flora”
  • Need to treat with broad spectrum agents
  1. General
    - Fever/rigors/sweats
    - Headache
    - Confusion (esp. elderly)
    - Vomiting/ Diarrhoea
  2. Localised
    - Breathlessness
    - Cough (may be productive)
    - Haemoptysis
    - Pleuritic chest pains
63
Q

Microbiological investigations for lower respiratory tract infection? 6

A

I. Serum
- stored; use retrospectively to diagnose
II. Blood cultures
- +ve in 15% of severe cases
III. Sputum
- shown to be of no clinical value except for TB or Legionella
IV. Throat swab
- Influenza PCR (dependant on time of year)
V. BAL
- Bronchio-alveolar lavage; optimal sample but only in severe cases since invasive
VI. Urine
antigen for Legionella/ S.pneumoniae

64
Q

Assessing severity of CAP

A 
1.
CURB65
- Confusion (AMT of 8 or less)
- Urea raised  >7 mmol/l
- Respiratory rate > 30 / min
- Blood pressure   Systolic <90 mmHg
        		\+/- diastolic <60 mmHg
- 65  and over
  1. Additional adverse features :
    - Hypoxaemia PaO2 < 8 kPa , SaO2 , 92 %
    - Bilateral or multilobar involvement on CXR
  2. I. CURB-65 scores :
    ≥3
    - Severe pneumonia (mortality 22%, admit to hospital)
    = 2
    - Non-severe , (mortality 9.2%, consider admission)
    0 or 1
    - Non-severe (mortality 1.5%, treat at home)

II. In the community assessment based on CRB-65 scores
≥ 3 Urgent Hospital admission
1 or 2 Hospital referral & assessment
0 Treat in community

65
Q

Typical and Atypical Pathogens causing pneumonia?

  1. degree of spread
  2. common causative pathogens
  3. treatment
  4. age
A

I. Typical

  • Often lobar
  • Streptococcus pneumoniae
  • Amoxicillin sensitive, Sometimes macrolide sensitive

II. Atypical (different cell wall structures, mostly in young people)

  • Often multisystem, multilobar
  • Mycoplasma, Chlamydia, Coxiella, Legionella
  • Amoxicillin resistant, Macrolide sensitive
66
Q

Treatment difference in pneumonia treatment depending on curb65 score?

A
  1. CURB-65 = 0 or 1 or CRB-65 = 0
  • Offer a 5-day course of a single antibiotic
  • Consider amoxicillin in preference to a macrolide or a tetracycline for patients with low-severity community-acquired pneumonia.
  • Consider a macrolide or a tetracycline for patients who are allergic to penicillin
  1. CURB-65 ≥ 2 or CRB-65 ≥ 1
  • a 7- to 10-day course of antibiotic therapy
  • Consider dual antibiotic therapy with amoxicillin and a macrolide for patients with moderate-severity community-acquired pneumonia.
  • Consider dual antibiotic therapy with a beta-lactamase stable beta-lactam and a macrolide for patients with high-severity community-acquired pneumonia.
67
Q

Aspiration pneumonia?

  1. cause
  2. which parts of lung does it affect?
  3. complication
  4. Mx
A
  1. Inhalation of material (eg food); about 10% of community cases, Usually neurological problem predisposing
  2. Commonly affects posterior segment of right upper lobe
  3. Can lead to abscess formation
  4. Treat with antibiotics to cover URT flora e.g. penicillin or cephalosporin plus metronidazole
68
Q

Nosocomial pneumonia

  1. def
  2. mx
A
  1. hospital acquired pneumonia
  2. I. If early onset infection (less than 5 days post admission) and no abx already:
    - co-amoxiclav or cefuroxime

II. If early onset, but alrady had some abx or has some RFs:

  • a third generation cephalosporin (cefotaxime or ceftriaxone),
  • a fluroquinolone or piperacallin/tazobactum
69
Q

Cystic fibrosis and bronchiectasis

  1. defs
  2. pathogens
  3. complications
A
    • Bronchiectasis is due to abnormal structure of bronchi leading to inflammation and obstruction
    • Cystic fibrosis leads to abnormal and tenacious mucus in bronchial tree
  2. Staphylococcus aureus, Haemophilus influenzae, Moraxella catarrhalis and Pseudomonas aeruginosa
  3. I. Pleural effusion
    - Diagnosis made by diagnostic tap

II. Parapneumonic effusion

  • reactive, Not infected
  • pH>7.2
  • Manage conservatively

III. Empyema

  • Infected
  • pH<7.2
  • Needs drainage ±Surgery (to remove infective material)

IV. Lung abscess
- Haemotogenous abscess usually due to Staphylococcus aureus

70
Q

RFs for TB activation?

A 
I. HIV
- at all CD4 counts
- more extrapulmonary disease 
II. Immunosuppressive drugs:
- High dose steroids
- Infliximab
III. Age: very young; very old
IV. Poor nutrition
V. Homelessness/ alcohol/ IVDA/ poverty
71
Q

Diagnosis of TB

A 
1. Specimens:
I. sputum, gastric washings, broncho-alveolar lavage
II. early morning urines
III. biopsies
2. Procedures:
I. Microscopy (result within 24h; not all AFBs are TB)
- Ziehl-Neelsen
- Auramine
II. Culture (crucially important, but often negative)
- Solid phase: Lowenstein-Jensen medium
- Liquid phase: 
- Drug sensitivities
III. Histology
Granulomata with central caseous necrosis
IV. M.Tuberculosis PCR
Smear positive – sensitivity 98%
Smear negative – sensitivity ~60%
Can indicate rifampicin resistance
72
Q

Mantoux test

  1. used instead of which test?
  2. procedure?
  3. interpretation?
  4. limitation
A
  1. used instead of heaf test (not used anymore)
  2. killed MTB, mash it up, inject into skin
  3. if negative, no reaction in skin
    - if positive, after 3 days you get a rash in the injected area/necrosis
  4. I. Poor specificity:
    - if you had BCG vaccine or present in the environment, you may get false positive results

II. Poor sensitivity:
- 75-90% in active disease (lower in disseminated TB and HIV infection; unknown for latent infection)

73
Q

Interferon Gamma Release Assay, IGRA test for latent TB

  1. advantage over tuberculin skin tests
  2. 2 types?
  3. limitation
A

I. Dont show a false positive if the person had a BCG vaccine

2.
I. Quantiferon gold InTubeTest
- 3 tubes: 
----- +/- controls, 
----- ESAT6 and CFP10 genes added to blood and and see how much interferon gamma they produce

II. T-spot

  1. ESAT6 and CFP10 genes also present in non tuberculosis mycobacteria
  • In low prevalance low incidence, a + result indicates a non tuberculosis mycrobacterium infection or exposure
  • In high prevalance, high incidence population, most people will have a positive result
74
Q

NICE guidelines for management of latent and active TB

A

I. Positive Mantoux or IGRA
- Assess for active infection

II. If no active infection and
and high risk
(
- those with HIV,
- aged younger than 65years with evidence of latent TB who have been in close contact with people who have suspected infectious
- confirmed active pulmonary or laryngeal drug‑sensitive TB )

  • –> Offer either of the following drug treatments:
  • 3months of isoniazid (with pyridoxine) and rifampicin or
  • 6months of isoniazid (with pyridoxine).
75
Q

MDR-TB vs XDR-TB definitions?

A

MDR-TB (Multidrug Resistant TB) describes strains of tuberculosis that are resistant to at least the two main first-line TB drugs - isoniazid and rifampicin.

XDR-TB, or Extensive Drug Resistant TB (also referred to as Extreme Drug Resistance) is MDR-TB that is also resistant to three or more of the six classes of second-line drugs.

76
Q
  1. Erysipelas
  2. Erysipeloid
  3. Erythrasma
  4. Cellulits
  5. Which part of body mostly affected?
  6. RFs?
  7. how common bacteraemia ?
  8. appears like?
A
  1. Erysipelas
    – Group A Streptococci or Streptococcus pyogenes
  2. Erysipeloid
    – Erysipelothrix rhusiopathiae
    _ carried by pigs and fish (more in vets and farmers)
    _ different abx sensitivity to erysipelas
  3. Erythrasma
    – Corynebacterium minutissimum
    _ rare, mainly in children
  4. Cellulitis
    – numerous organisms from Streptococci to Vibrios (seagull shape organisme eg vibrio cholera)
    _ deeper
  5. 70-80% of cases of erysipelas affect the lower extremities, 20% the face.
  6. Predisposing factors – lymphoedema, venous staisis, obesity, diabetes, EOH.
  7. Streptococcal bacteraemia occurs in ~ 5% of cases.
  8. Painful, bright red, oedematous, peau d’orange.
77
Q

Scarlet Fever Syndromes

  1. common pathogen?
  2. when does desquamation occur?
  3. what is the rash due to?
  4. what other complications caused by the pathogen?
A
  1. Most commonly due to S. pyogenes rarely similar with S. aureus.
  2. Desquamation occurs 2-5 days after the scarlatiniform rash.
  3. Due to organisms producing toxins.
  4. I. Scalded Skin Syndrome
    – exfoliative toxin: Intradermal cleavage at the granular layer.
    _ looks like someone was dumped in a bath of scalding water (caused by toxins released by the bacteria)
    _ skin easily comes off: increased risk of infection, increased dehydration
    II. Toxic Shock Syndrome
    – TSST-1.
    _ causes septic similar shock
    _ Exotoxins act as super antigens.
78
Q

Cellulitis

  1. def
  2. caused by?
  3. RFs?
  4. Mx?
A
  1. An acute spreading infection of the skin extending deeper than erysipelas and involves the subcutaneous tissues. Blood cultures positive in 2-4%.
  2. S. aureus and Group A Streptococci
    (but other beta haemolytic Streptococci eg Groups C and G are implicated.)
  3. eg
    - occupation for Erysipeloid,
    - immunocompromised,
    - disasters/earthquakes/hurricanes.
    • should include antibiotics active against the most common isolates.
      Eg. Flucloxacillin, Benzyl-penicillin.
79
Q

Necrotising Fasciitis

  1. def
  2. rate of progression
  3. Pathogens for type 1 and 2
  4. RFs for type 1 and 2
  5. sx?
  6. Diagnosis
A
  1. An uncommon severe infection involving the subcutaneous soft tissues, particularly the superficial and often deep fascia.
  2. Usually an acute rapidly progressing process.
3. 
Type I 
- polymicrobial, 
- deep infections, if on foot, more likely to be skin, if around abdomen, more likely to be abdomenal flora
Type II = Streptococcus pyogenes
    • For Type I, pre-exisiting conditions such as IDDM, EOH, elderly, male;
    • For Type II, IVDU.
    • very tender in the early stages,
    • erythematous and swollen,
    • rapidly progressing to skin breakdown and bullae formation within 3-5 days.
    • Frank cutaneous gangrene,
    • area becomes anaesthetic secondary to thrombosis of small blood vessels and destruction of superficial nerves.
  3. I. Aspiration of pus or fluid
    II. Biopsy of tissues
    III. Serology eg ASO (anti-streptolysin O) titres (only in type II)
    IV. Culture and antibiotic sensitivities of organisms grown
  4. I. High dose benzyl-penicilin PLUS flucloxacillin PLUS metronidazole
    II. Cephalosporins PLUS metronidazole
    III. Meropenem PLUS vancomycin (MRSA) or imepenem PLUS vancomycin
    IV. Addition of high dose clindamycin for Type II, (Streptococcus pyogenes)

High dose IVIG

80
Q

Gas Gangrene

  1. caused by?
  2. def? pathogen?
  3. mx?
A
  1. Usually the result of trauma, May also occur after bowel surgery
  2. Contamination of wound with spores of Clostridia (they multiply producing gas), usually Clostridium perfringens
  3. Depends on culture results
    - Until known broad spectrum antibiotics eg. Benzyl-penicillin plus gentamicin plus metronidazole or piperacillin/tazobactam (also affects anaerobic) or meropenem
    - Essential to include anaerobic cover
    - Surgery
    - Hyperbaric oxygen
81
Q

Anthrax

  1. causative organism
  2. RFs?
  3. cutaneous vs pulmonary
  4. Mx?
A
  1. Bacillus anthracis
  2. Those at risk – Tanners, wool workers, vets, farmers
  3. Cutaneous anthrax = malignant pustule
    Pulmonary anthrax = due to inhalation of spores, biological warfare – high mortality
  4. Treatment = penicillin
82
Q

Infections of skin?

A
  1. Impetigo – most commonly affects children, highly infectious, outbreaks common.
  2. Folliculitis
    _ base of follicules
    – outbreaks can occur particularly in poorly maintained hottubs, swimming pools etc.
  3. Faruncles and carbuncles (multiple follicles) .
    - larger infections at base of follicules
  4. Ecthyma
    – penetrate the epidermis often secondary to insect bites.
    - with time they become very necrotic in the centre leaving you with a scar
  5. Paronychia (nail bed)
  6. Erysipelas
83
Q

Streptococci

Staphylococci

A
  • long chains of

- chains of grapes

84
Q

Alpha and beta haemolytics

A

Beta->

  • breaks down blood, complete breaking
  • mainly streptococci (A,C,G)

Alpha->

  • partial haemolysis (green colony, bilirubin leaking out)
  • less destructive
85
Q

Staphylococci

A

Arues: golden, causes haemolysis, very pathogenic, co-agulase +ive (clots the blood when mixed with rabbit blood)

Co-agulase -ive: not aureus , not as pathogenic

86
Q

Impetigo

A
  • most commonly affects children, highly infectious, outbreaks common.

Staphylococcus aureus

Other organisms include Group A Beta haemolyitic streptococci

  • golden lesions spreading around beacause of poor hand hygiene

Bullous:
- get boulae formation (blisters filled with fluid)

87
Q

pasteurella multocida

spread by?
causes?

A

dog/animal bite

causes cellulits

88
Q

Fournier’s Gangrene

A

A horrendous infection of the genitalia that causes severe pain in the genital area (in the penis and scrotum or perineum) and progresses from erythema (redness) to necrosis (death) of tissue

89
Q

3 different types of infecting parasites?

A 
I. Single cell parasites 
- Protozoa eg malaria, giardia
- 
II. Multicellular parasites - Metazoa eg
helminths
III. Ectoparasites eg fleas and lice
90
Q

Malaria

  1. 4 types that affect humans?
  2. incubation period?
  3. Flu-like symptoms
  4. Respiratory Symptoms
  5. GI symptoms
  6. CNS symptoms
  7. Other Sx
  8. Ix?
A 
1. 
Plasmodium vivax
Plasmodium falciparum
Plasmodium ovale
Plasmodium malariae
  1. 7-30 days after mosquito bite depending on the species
    ((In P.vivax malaria incubation may rarely
    take up to 1 year.
    P.vivax and P.ovale can also exist as
    dormant forms (hypnozoites) that produce
    relapses months or years later))
  2. Fever, rigors, sweats, malaise, myalgia
  3. Cough, respiratory distress, pulmonary
    oedema
  4. Nausea, vomiting, diarrhoea, jaundice, liver failure
  5. Headaches, confusion, coma – cerebral
    malaria
  6. Other: Shock, Acidosis, Renal
    impairment, “Blackwater fever”,
    Anaemia, DIC, Hypoglycaemia,
    Splenic rupture
    • If you suspect VHF, do a malaria film only
    • Malaria antigen test
    • FBC – decreased platelets
91
Q

Viral Haemorrhagic Fevers

  1. causative viruses
  2. RFs?
A
    • Lassa
    • Marburg
    • Ebola
    • CCHF
    • Travel to high risk area in the
      last 21 days
    • Contact with human or
      animal with suspected VHF
      (body fluids/tissues)
    • Ingestion of bush meat
92
Q

Malaria management?

A 
I. Antimalarials eg quinine, doxycycline,
fansidar, primaquine (see BNF, HTD)
II. Supportive therapy – correct shock ,
anaemia, bleeding abnormality, treat or
prevent convulsions, hypoglycaemia,
intercurrent infections)
III. Avoid overhydration
IV. Consider exchange transfusion
93
Q

Leishmaniasis

  1. types?
  2. transmission
  3. diagnosis?
  4. mx?
  5. prevention
A 
broadly categorised into:
1. 
I. Visceral leishmaniasis –
characterised by hepatosplenomegaly
II. Cutaneous leishmaniasis –
tropical sore
2. Transmission: Sandflies
3. Dx: Biopsy
4. Rx Antimonials, pentamidine,
amphotericin
5. Prevention: impregnated bed nets,
elimination of animal vector eg
dog control
94
Q

Trypanosomiasis

  1. 2 types
  2. transmission of each types
  3. Sx?
  4. Mx?
A

I. Sleeping sickness,

  • encaphalopathy stops people functioning,
  • Africa
  • Tsetse fly transmits from wild animals to man
II. Chagas disease – S.America
- Rejuvid blood transmits to man causing
megaoesophagus, megacolon and
cardiomyopathy
- Mx: arsenicals
95
Q

Transmission 2 Helminths (worms)

A
  1. Ingestion:
    i) Of eggs or larvae from the faeces of an infected host eg threadworm
    ii) Of soil or food contaminated by soil in which larvae have developed from eggs passed in the faeces of an infected host eg ascaris
    iii) Ingestion of larvae in the tissue of an intermediate host eg Taenia sp.
  2. Inoculation:
    i) By a blood sucking insect eg filariasis
    ii) By active penetration of the larvae eg
    Schistosomiasis, Hookworms
96
Q

Schistosomiasis (bilharzia)

  1. what is it?
  2. 3 forms
  3. Sx?
  4. diagnosis
  5. mx
A
  1. A trematode that infects man
  2. 3 forms infect humans:
    S. haematobium (bladder)
    S. mansonii (vessels around bowel)
    S. japonicum (vessels around bowel)
3. 
I. Swimmer’s itch
II. Katayama fever” – a seroconversion illness characterised by fever, arthralgia, urticarial rash
III. Haematuria
IV. Portal hypertension eg haematemesis
V. Malignancy
VI. Paraparesis
4. 
- Ova in urine, stool or biopsy
- Immunodiagnosis
- Eosinophilia
5. Praziquantel
97
Q

Examples of:
I. Soil transmitted helminths
II. Faecal-oral transmission of helminths
III. Arthropod borne helminth

A 
I.
1) Ascaris lumbricoides
2) Strongyloides (GI, immunosuppressed can get infected with E. coli
3) Hookworm (anaemia) 
II.

1) Enterobius, vermicularis
2. Taenia sp. (tapeworm)
3. Hydatid disease (Ecchinococcus)

III.
1. Filariasis

98
Q

Categories Of Immune Deficiency

A 
I. Phagocytic cells
neutropenia
phagocyte function
II. T cells and cell-mediated immunity
III. B cells and humoral immunity
99
Q

Neutropenia

  1. causes
  2. presentation
  3. common organisms causes bacteraemia
  4. Mx
  5. duration of abx
A 
1.
I. acquired
- drugs
- radiation
- cancer
- haematopoietic stem cell transplant (HSCT)
- autoimmune
II. congenital

2. 
Neutropenic sepsis: 
- neutrophil count ≤0.5 ×109/l plus
- either temperature >38°C
- or other signs/symptoms consistent with sepsis
3. 
I. Most infections are due to endogenous flora 
II. Damaged mucosa
- Escherichia coli and other coliforms
- Pseudomonas aeruginosa
- alpha-haemolytic streptococci
- anaerobic organisms
II. Intravascular catheters
- mostly skin organisms
e.g. coagulase-negative staphylococci

4. 
I. Monotherapy
------ anti-pseudomonal β-lactam
- piperacillin/tazobactam
- imipenem or meropenem
- ceftazidime
II. Combination therapy
----- anti-pseudomonal β-lactam
----- plus aminoglycoside
- gentamicin
- amikacin
- tobramycin
  1. Antibiotics may be stopped when patient has responded to treatment, irrespective of neutrophil count
100
Q

Prevention of infection in neutropenic patients

A
  1. Prophylactic antibiotics
    - ciprofloxacin for duration of neutropenia
  2. Granulocyte colony stimulating factor (G-CSF)
  3. Infection control
    - protective (reverse) isolation: single room isolation with HEPA-filtered air
101
Q

T cells And Cell-mediated Immunity deficiency

  1. causes
  2. pathogens
A 
1.
I. drugs (e.g. cytotoxic chemotherapy, steroids)
II. radiation
III. lymphoma
IV. HSCT
V. infections e.g. HIV
2. 
Pneumocystis jirovecii
Cryptococcus neoformans
herpesviruses (eg HSV, VZV, EBV, CMV)
102
Q

B Cells And Humoral Immunity

  1. causes
  2. common pathogens
  3. presentation?
    4.
A 
1. 
I. lymphoproliferative disorders
- e.g. chronic lymphocytic leukaemia, multiple myeloma
II. anti-cancer treatment 
- (cytotoxic chemotherapy, radiation, HSCT)
III. hypo/asplenism
- splenectomy
- sickle-cell disease

2. 
I. Encapsulated bacteria
- Streptococcus pneumoniae
- Neisseria meningitidis
- Haemophilus influenzae
II. Capnocytophaga canimorsus
III. Parasites
- Babesia spp.
- Plasmodium spp.

3. 
I. Congenital
recurrent respiratory infections
II. Acquired
sepsis in the asplenic patient
103
Q

Prevention Of Infection In Humoral Immune Deficiency

A 
I. Active immunisation
- Streptococcus pneumoniae
- Neisseria meningitidis
- Haemophilus influenzae
- influenza
II. Prophylactic antibiotics
- penicillin or macrolide
III. Immunoglobulin replacement
104
Q

Common Fungal Infections in immune deficient patient

A

Candida spp.

Dermatophytes

105
Q

Candidiasis in immune deficient

  1. common pathogens?
  2. sx
  3. common in which groups of ppl
  4. diagnosis
  5. tx
A
  1. Multiple species are pathogenic
    most commonly C. albicans and C. glabrata
    • thrush
    • commonly female genital tract or mucosa
      bloodstream infections
    • typically hospitalised patients
      related to broad-spectrum antibiotics,
    • intravenous catheters,
    • prosthetic devices,
    • parenteral nutrition
    • culture
    • fungal biomarkers
    • depends on disease
    • systemic agents include fluconazole, amphotericin B, and the echinocandins
106
Q

Dermatophyte Infection in immune deficient

  1. which body part infected?
  2. which pathogens
  3. diagnosis
  4. tx
A
  1. Infections of skin, hair or nails
  2. species belonging to the fungal genera
    - Trichophyton,
    - Microsporum and
    - Epidermophyton
  3. Diagnosis:
    microscopy and culture
  4. Treatment:
    - topical agents, but systemic agents used for some nail, hair and widespread infections

MS3 - general (6 decks)

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