Microbiology Flashcards

1
Q

Which patients are you more concerned about with UTIs

A

Children and pregnant women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is a midstream sample used for UTIs

A

The urethra isn’t sterile so midstream washes out any colonising bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a complicated urinary tract infection

A

UTI + functional or structural abnormalities in urinary tract - eg catheter and cauculi.
Men, pregnant women, children, patients in a healthcare setting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most common causative agent of UTIs

A

Single bacteria species. E.coli as its got many virulence factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 5 other causative agents of UTI and their associations
(Hint its not pseudomonas)

A

Proteus mirabilis - associated with patients who have kidney stones

Klebsiella aerogenes - resistance - often associated with catheter

Enterococcus faecalis - uncommon HAP and resistant

Staph saprophyticus - common in young women 2nd most common

Staph epidermis - Iatrogenic- catheter and surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the host defence against UTIs

A

Urine - pH, osmolality, urinary flow, urinary tract mucosa is bactericidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the route of infection in UTI

A

Urethra colonise often the vagina first ( from the GI tract due to proximity), sex increases this risk due to introduction.
Introduction can be done by a catheter.
Hematogenous - staph aureus abscess in the kidney (from bacteremia or endocarditis) - not a true UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of urinary outflow obstruction

A
mechanical
Extrarenal
 - valves, stenosis, bands, calculi, extrinsic urethral compression (BPH)
Internal 
-nephrocalcinosis, uric acid, analgesic, PCKD, hypokalemia, renal lesions of SCD
neurogenic - 
poliomuselitis
(Neurosyphilis) tabes dorsalis
diabetic neuropathy
spinal cord injuries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is vesicoureteric reflux?

A

Pooling of urine in the bladder after voiding. Can cause scarring of the kidneys`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the S&S of upper UTI?

A

fevers, rigours, flank pain, + all lower symptoms, frequency, pain- burning, small volume, turbid/ bloody tinge.

In elderly patients may be more atypical - abdo pain and change in mental state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the investigations for UTIs - low, upper, complicated.

A

Urine dip - leukcocytes (inflam) and nitrites (made by E.coli)
( not for diagnosis in >65s due to asymptomatic bacteria)
MSU - MC&S
Bloods - FBC, U&Es, CRP

Complicated

  • Renal USS
  • Intravenous urography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dx for UTI

A

Paeds - any other infection

Young men and women - Upper UTI, STI, prostatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the signs of a contaminated MSU sample

A

Mixed growth, squamous epithelial cells (more likely from the urethra).
Sterile pyuria - consider STI eg chlamydia, previous treatment, bladder neoplasm or nonculturable organisms eg TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

General treatment of UTI

A

Short course 3 dose standard does for lower UTI in women.
Everyone else needs longer, 7 days.
Remove the catheter +/- replace

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When would you image in pyelonephritis

A

Women after the second incidence

Men after the first more likely a structural cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do influenza pandemics arise?

A

An endemic avian influenza virus crosses over from an animal reservoir, most commonly ducks or birds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the issues associated with H5 and H7 flu?

A

H5 and H7 infect poultry and cause huge economic strain.
H5N1 multi basic cleavage allowing for cleavage anywhere in the body (no longer isolated to infect respiratory tract-> high fatality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the factors required of a virus for it to have pandemic capability?

A

Novel antigenicity
Ability to infect human airways
Efficient transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes antigenic changes?

A

When there is coinfection in a single cell by a human and avian virus.
RNA swapping, most commonly the capsid making the animal viruses able to infect humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What 3 factors affect influenza transmission (cellular)

A

Neuraminidase stalk length - longer =^virulence to go through the mucous barrier
Virion stability- stability in air droplets conveyed by HA
Receptor binding- bind to salic acid on cells via alpha-2,3 in avian, humans is 2,6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why did swine flu affect some people much worse than others?

A

Older people had experienced a similar type of flu before (1980 Spanish flu-> seasonal)
High respiratory dose
Mutant virus
Superimposed bacterial infection
Genetic predisposition - IFITM3
Co-morbid: Asthma, pregnancy, obesity, DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 3 classes of antiretrovirals for Influenza?

A
Polymerase inhibitors
  -Favipiravir, baloxavir
Neuraminidase inhibitors - - - 
  -Tamiflu (oseltamavir oral), Relenza (zanamivir (inhaled or IV), permavir (IV)-not used UK)
Amantadine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the MOA and resistance pattern of Amantadine?

A drug for dyskinaesia in parkinsonism and influenza A

A

targets M2 ion channel

One AA change in M2 = resistance (not effective against Influenza B or H3N2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What types are the flu vaccines?

A

Children - live attenuated nasal

Adult - Purified NA and HA proteins from inactive viruses + adjuvant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the potential target for a universal influenza vaccine?

A

Neuraminidase stalk as its invariant (whereas the head is highly variable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the different types of anti-virals?

A
Direct acting
Viral protein targets
- antiretrovirals
-nucleotide/side 
Immune modulation
-Interferons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What factors effect efficacy of anti-virals?

A
Host-immune response
-difficult in immunocompromised pts
Adherence
Antiviral drug resistance
Drug toxicity
Drug interactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the different herpes viruses

A
Alpha:
HSV1 & 2 (Cold sores and genital)
VZV (Chickenpox and Shingles)
Beta:
CMV (mononucleosis-like)
HHV6 (6th disease exanthemsubitum)
HHV7
Gamma- oncogenic
EBV- infective mononucleosis and Burkitt's
HHV8 - Kaposi's
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the first line agents for HSV1,2 and VZV?

2nd line, why second line?

A
(Val)Aciclovir
Famciclovir
2nd line- 
Foscarnet or Cidofovir if resistant
Ganciclovir used for co-  infection with CMV as toxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the MOA of aciclovir?

A

Guanosine analogue pro drug

Selectivity for HSV DNA pol 1>2>VZV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the treatment of HSV encephalitis

fever, confusion and new-onset seizures

A

Treat empirically (DO NOT WAIT)
IV aciclovir 10mg/kg tds
confirm and treat for 14-21 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the indications for treatment of VZV?

A
Pregnancy
neonates
Treat if risk of pneumonitis
Zoster in adults
Immunocompromised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are some complications of CMV (and typical histopathological appearance?)

A
Latency is in monocytes and dendritic cells so can cause :
Pneumonittis
Encephalitis
Heptatitis
Colitis
Retinitis
BM suppression 
(OWL's eye inclusions can be sign and highly specific for CMV in the infected tissue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the antivirals for CMV?

A
1st line Ganciclovir IV (Val is PO)
\+IVIG for pneumonitis
2nd Foscarnet (IV)
3rd Cidofovir (IV)
Letermovir new and high risk BMT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the MOA of ganciclovir

A

Guanosine analogue strong selectivity for CMV DNA pol (+ HSV, VZV, EBV and HHV6 but not used)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Why is val/ganciclovir not used in bone marrow transplant?

A

Bone marrow toxicity -> BM suppression

also renal and hepatic toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Foscarnet and Cidofovir have the same major SE what is it and how can it be mitigated?

A

Nephrotoxictiy
Hydration (and U&Es monitoring)
(+ probenicid for CIdofovir improves mobilisation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the management of CMV in transplant patients?

A

Treat - Ganciclovir/(Val), reduce immunosuppression
prophylaxis- GCV/vGCV (or ACV/vACV) - mainly for organ transplant
pre-emptive- monitor weekly CMV PCR. start Tx when +ve (HSCT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the MOA and use of letermovir?

A

CMV DNA terminase inhibitor specific to CMV

Nb - nil activity against other HSVs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the high-risk period after BMT?

A

<100 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the use of palivizumab?

A

IM Monoclonal antibody against RSV - used for prophylaxis in high-risk infants (eg prem, severe heart or lung disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the classes of drugs used in the treatment of SAR Cov2?

A

Antivirals
Remdesevir (broad-spectrum adenosine analogue IV), Molnupiravir (broadspectrum viral RNA mutagen), Palovid +ritonavir(PI)
Neutralising monoclonal antibodies - sotrovimab
Immunomodulators
- Dexamethasone
Tocilizumab and Sarilumab (IL-6 anta)
ANAKINRA (il1 ANTAG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the treatment of BK haemorrhagic cystitis? and BK nephropathy?

A

Bladder washout
v Immuno suppressants
Cidofovir (+probenicid)

nephropathy
v immunosuppression +IVIG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the criteria for CURB-65?

And score management

A
Confusion
Urea >7mmol/L
Respiratory rate>30
BP <90mmHg or <60mmHg
>65
2> admit
2-5- sever consider ITU
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the most common causative organisms of CAP?

A

Strep pneumonia, Haemophylis Influenza

(Staph A, Morazella catarrhalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the microscopic appearance of Strep pneumonia?

A

Gram +ve (Purple)
Cocci (alpha haemolytic and optochin sensitive)
Looks green on plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What does Hib look like on microscope

A
Gram negative (red), coci-bacilli.
On agar - look like mucus so on chocolate plate
48
Q

What are the most common causative organisms of CAP?

A

Strep pneumonia, Haemophylis Influenza

Staph A, Morazella catarrhalis, s aureus, Klebsiella Pneumoniae

49
Q
What organisms are prevalent 
0-1mnth
1-6mnth
6mnth-5y/o
16-30y/o
A

0-1mnth GBS, E.coli, listeria monocytogenes
1-6mnth Chlymydia Trochomatis , S.aureus RSV
6mnth-5y/o - Mycoplasma pneumoniae, influenza
16-30y/o - Strep p and mycoplasma pneumonae

50
Q

Which organisms can cause respiratory cavitation? (3)

A

Staph. aureus
Klebsiella pneumoniae
TB

51
Q

What are the RFs for hepatitis A?

A

Poor sanitation, endemic areas,

52
Q

What are the causative agents for HAP? (7)

A
Enterobacteria: E.coli, Klebsiella pneumonia
Staph a
Pseudomonas
Haemophilus influenza
Acintobacter baumanni
Fungal
53
Q

What are the reason why someone may fail antibiotics (6)?

A
Poor adherence
Empyema/ abscess
Resistance organisms
Poor absorption of ABX
Immunosuppression
Comorbidity : lung cancer, cryptogeni organism pneumonia
54
Q

What are the investigations for m TB?

A

CXR- cavitating lesion (upper)

Stain with auramine or Ziehl-Neelson shows red Acid fast bacilli

55
Q

What are the s&s of legionella?

A

Confusion, abdo pain, diarrhoea, lymphopenia, Hyponatraemia

56
Q

What are the stages of Hep B infection?

A
Immune tolerant
Immune reactive
Inactive HBV carrier state
HBe(envelope) negative = Chronic hep B
HBsAg negative
57
Q
What is the incubation period for hepatitis 
A
B
C
D
E?
A
A 2-6 weeks
B 2-6 mnths
C 2-8 weeks
D 3-6 weeks
E 2-8 weeks
58
Q

Which viruses belong to the Flavivirdae family?

A

Hep C, yellow fever, dengue , western nile, zika

59
Q

How does Hep C serology differ to Hep A and B?

A

In Hep C anti HCIgG is raised after ALT

60
Q

Is confection or superinfection with Hep D worse?

A

Superinfection is significantly worse and those with chronic HBV should be monitored for HDV

61
Q

What is the management of chronic Hep B

A

Anti-virals
Inf A
Tenofovir, Entecavir, Emtricitabine and Lamivudine
Liver failure: Liver transplant+ immunosuppression (do not use interferons)

62
Q

What are the different types of drugs used in the management of Hep C

A

Protease inhibitors
NS5A inhibitors
NS5B inhibitors

63
Q

Is confection or superinfection with Hep D worse?

A

Confection can cause a nasty acute hepatitis
Superinfection has a significantly worse associated risk of cirrhosis and those with chronic HBV should be monitored for HDV (as antivirals for HBV are not effective against HDV)

64
Q

What is the PC of HAV?

A

Fever, Malaise, anorexia, nausea, abdominal discomfort, diarrhoea, jaundice, 99% resolution

65
Q

What is the pre and post exposure prophylaxis for HAV?

A

Pre- Vaccination of at risk people

Post- exposure - HAV vaccine +/- HNIG for at risk

66
Q

What is the pre and post-exposure prophylaxis for HAV?

A

Pre- Vaccination of at-risk people

Post-exposure - HAV vaccine +/- HNIG for at risk

67
Q

What type of Virus is Hepatitis

ABCDE?

A

A- quasi enveloped SS positive sense RNA
B- dsDNA with reverse transcriptase, enveloped virion
C- SS positive sense RNA
E - SS positive sense RNA

68
Q

What are the pre and post-exposure prophylaxis for HBV?

A

Pre- routine vaccination in children 2017, at risk population
Post- Neonates (HBV+ mother) Sexual partner - HBV vaccine +/- HBIG (<7 days from contact)
Needlestick

69
Q

Why doesn’t penicillin work against atypical pneumonias?

What would you use instead?

A

Penicillin affects the cell wall and atypical agents do not have cell walls
Use agents that interfere with protein synthesis Macrolide or Tetracyclines

70
Q

What are the exam buzz word RF for coxiella burnetti and Chlamydia psittaci?

A

Coxiella burnetti - domesticated farms (aerosol / milk) - give macrolides
Chlamydia psittaci - birds - inhalations (macrolides)

71
Q

What is the investigation finding and management for pneumocystis jirovecii?

A

Investigate with BAL, vSat on exertion, CXR - BAT wing shadow
Co-trimoxazole (same for prophylaxis)

72
Q

What diseases are associated with aspergillus

A

Aspergilloma (often preexisting cavity eg TB)
Allergic bronchopulmonary aspergillosis
Invasive aspergillosis (immuno comp and needs amphotericin B)

73
Q
What LRTI infection are associated with
HIV
Neutropenia
BMT
splenectomy?
A

HIV - PCP, TB, atypicals
Neutropenia - aspergillus
BMT - CMV
Splenectomy - encapsulated viruses eg S. pneumoniae, H. Influenzae, malaria

74
Q

What are the investigations of LRTI?

A

Sputum culture (can be induced)
BAL
Pleural fluid
CXR
FBC, U&Es
Antigens - urine Legionalla and S. pneumoniae (severe CAP)
Antibody tests - needs paired acutely unwell and getting better - Chlamydia and legionella as difficult to culture
Immunoflurescence - PCP (+silver stain in cytology)
PCR

75
Q

What is the empirical treatment for CAP? And allergy

A

Mild - Amoxicillin or Erythromycin/ Clarithromycin

Moderate/ severe - Co-amox and clarithomycin

Allergy cefuroxime + Clari

76
Q

What is the empirical treatment for HAP?

A

1st - Cipro +/- Vancomycin
2nd (/ITU)- Piptazobactam + Vancomycin

If MRSA - Vancomycin
Pseudomonas - piptazobactam or ciprofloxacin +/- gentamicin

77
Q

What is the MOA of Foscarnet

A

Non competitive inhibitor of vDNA pol - no phosphorylation

78
Q

What is the MOA of cidofovir

A

Nucleoside (cytidine) analogue (not a prodrug)

79
Q

How do you diagnose PTLD and treat?

A

Post-transplant lymphoproliferative disease
>10^5 c/ml viral load
reduce immunosuppression
Rituximab (anti CD20)

80
Q

What antiviral drugs are used for COVID

A

Resmdesevir (broad spectrum adenosine nucleotide analogue pro drug)
Molnupiravir - vRNA mutagen
Paxlovid PI (so + ritonavir)

81
Q

What immune moduation is used for COVID

A

Dexamethasone
Tocilizumab (anti IL-6)
Sarilumab (anti IL-6
Anakarin (anti IL-1)

82
Q

What neutralising monoclonal antibodies are used for COVID

A

Ronapreve
Sotrovimab
(targets S protein to prevent entering cell via ACE2)

83
Q

What and when would you treat adenovirus?

A

paeds, transplant or sever multi-organ involvement

cidofovir + IVIG

84
Q

How does most ACV resistance occur in HSV?

A

Viral thymidine kinase mutations (>95%)

DNA pol is rare

85
Q

How does most CMV drug resistance occur?

A

Protein kinase gene (DNA pol is rare)

86
Q

What are the mechanisms of antiobitic resistance?

A

Altered target
Decreased concentration - ^efflux or v uptake
Abx destruction/ neutralisation

87
Q

What is the order of narrow to broad spectrum of penicillins?

A
penicillin
amoxicillin
co-amoxicillin
pipperacillin
tozoacin
88
Q

Why is co-amox not helpful in MRSA?

A

MRSA is not due to beta-lactamases, it is a change in the penicillin binding protein
so Clauvonic acid as an beta-lactamase inhibitor doesn’t help

89
Q

What is the difference between the different generation cephalosporins? (name examples)

A

Increasing G- coverage
1st gen- cephalexin
2nd gen- Cefruoxime
3rd gen- cefutaxime, ceftriaxone, ceftazidime

90
Q

What is the use of glycopetides - give examples?

A

Vancomycin
Teicoplanin
Oral for c.diff
IV for MRSA

91
Q

Which antibiotics are affective against pseudomonas (5 groups)

A
Aminoglycosides - gentomycin, amikacin, atreptomycin
Colistin
Fluroquinolones (not moxifloxacin) - 
Pipperacillin
3rd gen cephlosporins - ceftazidime
92
Q

Which antibiotic is helpful in necrotising fascitis and why?

A

Clindamycin as it is bacteriostatic and prevents toxin production which is the main pathological factor

93
Q

Why is Linozolid only used if recommended by micro or ID?

What is an alternative abx

A

thrombocytopenia and optic neuritis and very expensive - is effective against MRSA and VRE

Daptomycin

94
Q

What antibiotic has the side effect of orange urine?

A

Rifampicin - must check LFTs and watch out for DDIs

95
Q

Why is nitrofurantoin used in UTIs

A

Urinary excretion means it builds up in the bladder

96
Q

What is co-trimoxazole and why is it useful?

A

Sulphonylurea + dihydropyridine
(Sulfamethoxazole + trimethoprim)
Both are anti-folate but act of sequential parts of the metabolism so have a synergistic effect

97
Q

What is the management of c.diff

A

stop abx most likely Ceftriaxone (cephalosporines)

Start PO vancomycin or metronidazole

98
Q

What are the different patterns of antibiotic dosing action - give examples

A

T1 - peak (max dose dependent - aminoglycosides, daptomycin, fluroquinolones -

T2- time dependent - penicillins, carbepenems, cephalosporins , erythomycin, linezolid

T3- AUC (combo of both) Glycopeptides - vancomycin, tetracycline, clindamycin, oxazolidones, azithromycin

99
Q

What are the common reasons for misuse of antibiotics

A
No infection
Wrong drug
Wrong treatment length
Not needed - would self resolve
Wrong pharmacokinetics for the infection
100
Q

What should you take into account before starting antibiotics?

A

Take cultures before empiracle treatment.
Start broad> culture and sensitivity > narrow spectrum (bacteriocidal)
CHAOS
Host - pregnancy, neonates, immunosuppression,
Antimicrobialy susceptibility
Organism
Site of infection

Pharmacokinetics - if septic pure GI perfusion, ^GI transit, cannot tolerate oral intake - think IV. Necrotic tissue - topical will not work without debrinement

101
Q

What antibiotic treatment should be given for

a. simple UTI
b. HAP uti
c. strep A
d. CAP
e. Meningitis - adults and children

A

a. 3 days trimethoprim or nitrofurintoin
b. cefatriaxone +/- gentamicin if catheter
c. 10 days to prevent Rheumatic fever and glomerulonephritis
d. mild - amoxicillin or clindamycin moderate to severe co-amox + clindamycin
e. cefrtiaxone or high dose benpen, neonates <3months cefuroxime

102
Q

What are the side effects of antibiotics

A

Gi upset
Rash
Anaphylaxsis

103
Q

Give examples of DNA viruses

A
HSV
EBV
VZV
CMV
HBV
HHV8
Pox virus (eg Molluscum contangiosum, HPV)

Uneveloped
JCV and BK, adeno, parvovirus B19

104
Q

Give examples of RNA viruses

Positive and negative sense

A

Positive sense
Rubella, Zika, HAV (une), HCV (enveloped), HEV

Negative sense
Influenza, HDV, morbillivirus (measles)

105
Q

What are the prophylaxis and treatment of PCP

A

Co-trimoxazole

106
Q

What is the causative agent of meningenitis specific to HIV

A

Cryptocoides

107
Q

What is the causative agent of

a. cat scratch fever
b. hookworm
c. tape worm
d. Chagas disease
e. sleeping sickness
f. Schistomiasis - bladder and liver

A

a. Typhi gondii
b. nematodes
c. Tapes solnium
d. amoeba bordella
e. amoeba 2
f. Schitoma

108
Q

What is the treatment for schistomiasis?

A

Steroids and anti protazonas

109
Q

Define pyrexia of unknown origin

A

Pyrexia >3 weeks without diagnosis despite intensive investigation
Hospital >3 days in hospital
Neutropenic - PUO + v neutrophils

110
Q

What should be considered in PUO

A
Normal infections
HAP - lines, surgery, c.diff, VRE, MRSA
STIs 
HIV seroconversion
Vasculitides - cANCA, pANCA
MAlignancy
Rheumatoid
111
Q

What causes neutropenic PUO

A

Chemo therapy

Clozapine, Clopramide

112
Q

Describe the PC of

a. Typhoid
b. Dengue
c. falciparum
d. non-falciparum malaria

A

a. enteric fever - rose spots, constipation 1-2 weeks, incubation, hepatosplenomegaly (G-ve bacili)
b. mild pyrexia, myalgia onset days self limiting (reinfection = dengue hemorrhagic fever)
c. 48hr recurrent fever, myalgia, anaemia hepatosplenomegaly.
d. Same but milder (except malariae which is 72hrs)

113
Q

What is the treatment for

a. Typhoid
b. Dengue
c. falciparum
d. non-falciparum malaria

A

a. Typhoid - IV ceftriaxone > PO azithromycin
b. Dengue - supportive
c. falciparum - Mild artemesin (artemether +lumefantrine) Severe - IV artesunate
d. non-falciparum malaria Chloquine + primaquine

114
Q

What are the causative agents fro

a. tinea (ringworm and athlete’s foot)
b. Pitariasis (sebhorreic dermatitis and vesiculor)
c. systemic fungal infections (3)

A

a. Tricophyton rubrum
b. Malassezia globosa/ FurFur
c. Candida, Cryptocoides, Aspergillus

115
Q

What is the treatment for

a. cryptococcosis encephalitis

A

IV amphotericin B +/- flucytosine