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Year 5 Pathology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Characteristics of S Pneumonia

A

Rusty coloured sputum.
Usually lobar on CXR
Diplococci gram positive

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2
Q

Characteristics of H. Influenza

A 
Associated with smoking 
COPD
Kids 
Elderly 
Gram negative cocco-bacilli
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3
Q

Characteristics of Moraxella . Catarrhalis

A

Associated with smoking

Gram negative coccus

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4
Q

Characteristics of S. aureus

A

Associated with recent viral infection
Cavitation on CXR
ETOH, homeless, immunosupressed
Gram positive cocci (grape bunch clusters)

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5
Q

Characteristics of Klebsiella pneumonia

A

Alcoholism, elderly, haemoptysis
Gram negative rods
enterobacter

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6
Q

Characteristics of bordatella pertussis

A

Whooping cough in unvaccinated kids

Often in travelling community in EMQs

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7
Q

Characteristics of mycoplasma pneumonia

A 
Common 
Systemic symptoms 
Join pain
Cold agglutinin test
Erythema multiforme 
Risk of SJS and autoimmune haemolytic anaemia
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8
Q

Characteristics of chlamydia pneumonia

A

Hard to diagnose
Obligate intracellular pathogen
Doesn’t stain well

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9
Q

Common causes of pneumonia by age group:

0-1 months
1-6 months
6 months to 5 years
16 years to 30 years

A

0-1 mths- E.coli, GBS, listeria
1-6mths- Chlamydia trachomatis, S aureus, RSV
6mths-5yrs- Mycolpasma, influenza
16-30yrs-M pneumoniae, S pneumoniae

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10
Q

Most common causes of CAP

A

Haemophilis influenzae

Strep pneumoniae

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11
Q

Atypical causes of CAP

A

Legionella
Mycoplasma pneumonia
Coxiella bumetii (Q fever)
Chlamydia psittaci (psittacosis)

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12
Q

Characteristics of Chlamydia psittaci

A

Exposure to birds, splenomegaly, rash, haemolytic anaemia

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13
Q

Components of CURB-65 score

Impact on treatment

A 
CURB-65 score
Confusion
Urea >7 mmol/l
RR >30
BP 65 years

Score 2 = ?admit
Score 2-5 = manage as severe

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14
Q

Pathogens causing bronchitis

Common features

A

Viruses
S. pneumoniae
H. influenzae
M. catarrhalis

Inflammation of medium sized airways.
Mainly in smokers
Cough, fever, increased sputum production, increased shortness of breath.

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15
Q

Encapsulated bacteria

A

Haemophilus influenza
Strep pneumonia
Neisseria menigitides

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16
Q

Urine antigen tests for which types of pneumonia?

A

Strep pneumonia

Legionella

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17
Q

Pneumonia organisms without a cell wall

Atypical

A

Mycoplasma
Legionella
Chlamydia
Coxiella

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18
Q

Legionella extrapulmonary features

A 
Low sodium
Hepatitis 
Abdo pain
Confusion 
diarrhoea
Lymphopenia
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19
Q

Features of coxiella burnetti

A

Common in domestic/farm animals
Transmitted by aerosol or milk
Dx by serology
Sensitive to macrolides

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20
Q

Treatment of aspiration pneumonia

A

Cefuroxime and metronidazole

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21
Q

Treatment for pseudomonas pneumonia

A

Piptaz

or ciprofloxacin and gentamicin

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22
Q

Treatment for mild-moderate pneumonia

A

Amoxicillin or macrolide

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23
Q

Causes of pneumonia in HIV

A

PCP
TB
Cryptococcus neoformans

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24
Q

Causes of pneumonia in neutropenia

A

Aspergillus spp.

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25
Q

Causes of pneumonia in BMT

A

Aspergillus

CMV

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26
Q

Causes of pneumonia after splenectomy

A

Encapsulated organisms:
H. influenza
S. Pneumonia
N. Meningitides

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27
Q

Causes of pneumonia in cystic fibrosis

A 
Pseudomonas aeruginosa 
Burkholderia cepacia (v. high mortality)
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28
Q

Treatment for legionella pneumonia

A

Macrolide plus rifampicin

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29
Q

Treatment for HAP 1st and 2nd line

A

1st line: Ciprofloxacin and vancomycin

2nd line: Piptaz and vancomycin

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30
Q

Treatment for MRSA

A

Vancomycin

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31
Q

Treatment for MSSA

A

Flucloxacillin

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32
Q

Nature of discharge with BV

A

Grey Frothy

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33
Q

Nature of discharge with Gonorrhoea

A

Thick green frothy

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34
Q

Nature of discharge with chlamydia

A

White and cloudy discharge

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35
Q

Features of disseminated gonorrhoea

A

Arthritis
Rash
Septicaemia

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36
Q

After…h post abx treatment for gonorrhea….

A

72h

Repeat culture

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37
Q

Chlamydia serovars:
A, B and C associated with
D-K associated with

A

Trachoma

Genital chlamydia infection, opthalmia neonatorum

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38
Q

Stages of LGV infection

A

Early: primary stage for 3-12 days. Painless genital ulcer, non indurated. Balsanitis, proctitis, cervicitis.
Secondary: painful inguinal swollen lymph nodes (buboes) may rupture. Fever, malaise,. Rarely hepatitis, meningo-encephalitis, pneumonitis). Proctocolitis, hyperplasia, lyphoid tissue

Late LGV: Inguinal lymphadenopathy, abscesses, genital elephantiasis, genital ulcers, frozen pelvis, rectal strictures,, fistulae,

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39
Q

Treatment of LGV

A

Doxycycline 100mg BD for 21 days

Erythromycin 500mg QD for 21 days or azithromycin 1g weekly for 3 weeks

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40
Q

Features of chancroid

A

Haemophilus ducreyi
Gram negative coccibacilli
Multiple ulcers often painful
Diagnosis on chocolate agar

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41
Q

What are clue cells?

A

Clue cells are epithelial cells of the vagina that get their distinctive stippled appearance by being covered with bacteria.

Seen in BV

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42
Q

HPV incubation time

A

3 weeks

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43
Q

Treatment of HPV warts

A

Home: podophyllotoxin solution or cream
Clinic treatment:
1st: cryotherapy
2nd: Imiquimod

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44
Q

Treatment for BV

A

Metronidazole 400mg or 500mg BD 7 days

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45
Q

Describe HPV lesions

A

Warts: pedunculated, papular, planar, carpet, keratinised

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46
Q

Definition of cystitis

A

Inflammation of the bladder often caused by infection

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47
Q

A complicated UTI refers to a UTI in which patient populations?

A

men
pregnant women
children
patients who are hospitalised or in health care–associated settings

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48
Q

Prevalence of bacteriuria in young non-pregnant women will have bacteriuria

A

1% to 3%

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49
Q

Up to …% to …% of the female population will experience a symptomatic urinary tract infection at some time during their life.

A

40% to 50%

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50
Q

Most common organism causing an acute UTI

A

E coli

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51
Q

% of urinary tract infections caused by a single bacterial species

A

95%

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52
Q

List E. coli serogroups causing a large portion of UTIs

A

O1, O2, O4, O6, O7, O8, O75, O150, and O18ab

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53
Q

Organisms that are common causes of UTIs

A 
E. coli (most common)
Proteus mirabilis 
Klebsiella aerogenes 
Enterococcus faecalis 
Staphylococcus saprophyticus 
Staphylococcus epidermis
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54
Q

Host defences preventing UTI

A

Urine flow and micturition
Urine pH, organic acids, osmolality
Urinary tract mucosa (bactericidal activity, cytokines)

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55
Q

Factors increasing risk of UTI in females compared to males

A

Short urethra

Proximity to warm, moist vulvar and perianal areas

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56
Q

Link between UTIs and sexual intercourse

A

Massage of the urethra can force bacteria into the female bladder.

It has been shown that the organisms that cause urinary tract infection in women colonize the vaginal introitus and the periurethral area before urinary infection results

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57
Q

List intra and extrarenal causes of urinary tract obstruction

A

Extrarenal: valves, stenosis, or bands; calculi; extrinsic ureteral compression from a variety of causes; and benign prostatic hypertrophy

Intrarenal: nephrocalcinosis, uric acid nephropathy, analgesic nephropathy, polycystic kidney disease, hypokalemic nephropathy, and the renal lesions of sickle cell trait or disease

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58
Q

Causes of neurogenic malfunction of the urinary tract

A

Poliomyelitis,
Tabes dorsalis,
Diabetic neuropathy,
Spinal cord injuries

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59
Q

What is tabes dorsalis?

A

Slow demyelination of the dorsal columns.
Caused by syphilis
Causes loss of vibration sensation, proprioception and discriminative touch.
Causes weakness, ataxia, loss of coordination, diminished reflexes, parasthesia, urinary incontinence, dementia.

Positive Romberg’s test
Argyll Robertson pupil

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60
Q

UTIs caused by haematogenous spread are usually caused by gram… organisms

A

Gram positive

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61
Q

Kidney abscesses caused by which bacterial species

A

Staph. Aureus

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62
Q

a) Symptoms of UTI in children under 2 years of age

b) Symptoms of UIT in children above 2 years of age

A

a) Failure to thrive
vomiting
fever

b) Urinary frequency
dysuria
abdominal or flank pain

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63
Q

Cause of lower UTI symptoms

A

The bacteria produce irritation of urethral and vesical mucosa

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64
Q

Symptoms of an upper urinary tract infection in older adults

A

Frequency, dysuria, hesitancy, incontinence commonly experienced by older adults without UTI
Abdominal pain, change in mental status

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65
Q

Strongest indicator of a UTI on urinalysis

A

Positive nitrites

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66
Q

According to HPA guidance:

If greater than or equal to… typical symptoms of UTI treat empirically with antibiotics.

A

3

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67
Q

Asymptomatic bacteriuria in pregnancy is associated with

A

Pyelonephritis and premature delivery

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68
Q

According to HPA guidance send urine sample for culture and sensitivity when UTI is suspected in…

A

Pregnancy (plus in all antenatal visits even if asymptomatic)
Suspected UTI in men, or children
Suspected pyelonephritis
Catheterised patients only if features of systemic infection (as bacteriuria is usual)
Failed antibiotic treatment or persistent symptoms (as ESBLs are increasing)
Abnormalities of the GU tract
Renal impairment

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69
Q

UTIs

On microscopy…. is indicative of an infection and … is indicative of contamination

A

White cells

Squamous epithelial cells

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70
Q

Causes of sterile pyuria

A 
Prior treatment with antibiotics
Calculi
Catheterisation
Bladder neoplasm
TB
Sexually Transmitted Disease
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71
Q

UTIs

Culture: when counting colonies >… is considered significant

A

30 colonies

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72
Q

Patients with urinary tract infections usually have at least.. cfu/mL
Patients without have less than… cfu/ml

A

10^5cfu/ml
CFU: colony forming unit

10^4cfu/ml

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73
Q

Empirical treatment of uncomplicated UTI is usually with

A 
Nitrofurantoin 50mg (100mg if severe) QDS 
Trimethroprim 200mg BD

Cephalexin (broad agent) inital treatment in Imperial due to high rate of trimethoprim resistance.

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74
Q

Treatment of pyelonephritis is with…

A

Broad spectrum IV antibiotics:
Co-amoxiclav +/- gentamicin
Cefuroxime +/- gentamicin

Gentamicin added due to risk of ESBL organism

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75
Q

Advice to patients prescribed nitrofurantoin (dose timing)

A

Take after passing urine (but still QDS).
No systemic absorption
Concentrates in the bladder
Don’t use for catheterised patients.

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76
Q

Nitrofurantoin is… spectrum

A

Broad

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77
Q

Duration of antibiotic treatment for UTIs

A

3 days in women with uncomplicated lower tract infection

7 days in men
7 days in women with >7 days symptoms or history of previous UTI caused by antibiotic resistant organisms

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78
Q

Most fungal UTIs are associated with…

A

Indwelling catheters

Treat by removing the catheter

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79
Q

Pathogens causing bacterial meningitis

A 
Neisseria meningitides 
Streptococcus pneumoniae 
M. tuberculosis 
Listeria 
Group B strep (in babies)
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80
Q

Fungal cause of meningitis

A

Cryptococcus neoformans

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81
Q

Pathogens causing chronic meningitis

A

Spirochetes
Cryptococcus
M TB

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82
Q

Most common CNS infection

A

Aseptic meningitis

Most common causes are: Coxsackievirus group B and echoviruses

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83
Q

Viruses causing aseptic meningitis

A

Most common:
Coxsackievirus group B and echoviruses

Other: 
Mumps 
Measles
Varicella-zoster 
Epstein-Barr/ cytomegaloviruses 
Other: myxoviruses, paramyxoviruses, adenoviruses
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84
Q

Most common cause of viral encephalitis

A

HSV

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85
Q

Gram positive diplococci causing meningitis

A

Streptococcus pneumoniae (also alpha-haemolytic)

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86
Q

Gram negative diplococci causing meningitis

A

Neisseria meningitides

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87
Q

Gram positive rod causing meningitis

A

Listeria

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88
Q

Stains with India ink

A

Cryptococcus

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89
Q

Treatment for bacterial meningitis (in hospital)

A

Ceftriaxone 2g iv bd

If immunocompromised give amoxicillin 2g IV 4h (to cover listeria)

Add in corticosteroids e.g. dexamethasone

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90
Q

Treatment for Meningo-encephalitis

A

Aciclovir 10mg/kg IV TDS
Ceftriaxone 2g IV BD

If immunocompromised give amoxicillin 2g IV 4h (to cover listeria)

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91
Q

Low glucose in CSF suggests

A

Bacterial CNS infection

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92
Q

High WCC with high mononuclear cells suggests

A

Viral infections

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93
Q

CSF with high protein, high WCC and mononuclear cells suggests

A

Mycobacterium TB or cryptococcus

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94
Q

Signs/symptoms of hepatitis A

A

feverish, mild, flu like

Then develop jaundice a few weeks later

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95
Q

Duration of hepatitis A incubation period

A

2-6 weeks

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96
Q

Hepatitis A serology

A

Anti-HAV IgM – levels indicate recent infection or vaccination
Anti-HAV IgG – levels indicate previous infection or vaccination

(IgM persists for upto 14 weeks)

EACH COULD ALSO INDICATE VACCINATION

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97
Q

Hepatitis A structure

A

Non enveloped

ssRNA (positive sense)

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98
Q

Hepatitis B structure

A

dsDNA (circular not fully ds)

Lipid envelope

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99
Q

Hepatitis C structure

A

ssRNA positive sense

Enveloped

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100
Q

Hepatitis D structure

A

Enveloped

Negative sense, single-stranded, closed circular RNA

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101
Q

Hepatitis E structure

A

Non-enveloped

Single-strand RNA molecule

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102
Q

Hep B infection is considered chronic if it hasn’t been cleared after…. (time)

A

6 months

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103
Q

Hepatitis B incubation period

A

2-6 months

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104
Q

Hepatitis B serology/blood results

A

Acute infection: ALT rise in first 2 months (also AST)
Virus produces surface antigens. HBsAg indicates chronic or acute infection. Indicates person is infectious.
HbeAg: indicates rapidly replicating virus. (Not produced by everybody so not used for diagnosis)

Anti-HBcAb: indicates actual infection rather than vaccination. IgM if recent infection, IgG if not recent. Rises early, indicates exposure.
Anti-HbsAb: develops later than surface antibody. Indicates immunity and recovery from HBV. Also seen in vaccinated individuals. Not found in chronic carriers.
Anti-HBeAb: develops as viral replication falls. In a carrier indicates low infectivity.

Hep core antigen only in infected liver cells not blood.

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105
Q

Reliable marker of HBV infectivity

A

Viral load

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106
Q

Consequences of chronic HBV infection

A

Liver cirrhosis

HCC

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107
Q

HBV treatment

A

Acute infection normally cleared by immune system
Chronic infection treated with antivirals and IFN (peg-IFN-2alpha). Aim is to suppress replication and prevent liver damage. Treatment doesn’t clear the virus.

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108
Q

Incubation period of hepatitis C

A

2 weeks to 6 months

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109
Q

Most common hepatitis C genotype

A

1

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110
Q

% of people with acute hepatitis C who clear infection

A

20%

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111
Q

Hepatitis C serology/blood results

A

Initial ALT rise
HCV antigen can be detected in blood
Positive anti-HCVAb can indicate current or resolved infection

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112
Q

Treatment of HCV

A

PegIFN alpha2b and ribavarin

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113
Q

Hepatitis D can only infect patients with

A

Hepatitis B

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114
Q

Hepatitis E is transmitted via…

A

Faecal-oral route

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115
Q

Complications of hepatitis D infection

A

If patient already HBV infected then get super infection. Accelerated liver damage (get cirrhosis very quickly)

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116
Q

Hepatitis E strains that only infect humans

A

1 and 2

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117
Q

Hepatitis E incubation period

A

3-8 weeks

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118
Q

Complications of hepatitis E infection

A

Rare: CNS disease – Bell’s palsy, Guillain Barre, other neuropathy
Chronic infection

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119
Q

Treatment of hepatitis E

A

Supportive

Consider ribavarin and pegIFN

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120
Q

Hepatitis E serology

A

HEV RNA becomes detectable in stool and serum during the incubation period
level of IgM antibody peaks early and becomes undetectable during recovery, whereas the level of the IgG antibody continues to increase and persists in the long term.

HEV RNA disappears from serum with recovery, whereas detectable virus usually persists longer in stool (arrows).

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121
Q

Campylobacter incubation period

A

1-10 days

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122
Q

E.Coli 0157 incubation period

A

1-5 days

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123
Q

Shigella incubation period

A

12-96 hours

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124
Q

Salmonella (non typhoidal) incubation period

A

8-48 hours

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125
Q

Vibrio parahaemolyticus incubation period

A

24-72h

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126
Q

Vibrio cholera incubation period

A

1-5 days

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127
Q

Bacillus cereus incubation period

A

1-6h

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128
Q

Staph aureus incubation period

A

2-7h

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129
Q

How does cholera cause diarrhoea

A

The bacteria release cholera toxin which binds to G proteins. Leads to rise in cAMP and then

Opening of chloride channels resulting in massive efflux of water and electrolytes into intestinal lumen

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130
Q

Food poisoning:

If vomiting develops within a few hours of eating the meal the likely organism is…

A

Staph aureus

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131
Q

How do enterotoxin superantigens act (bacterial and viral)

A

Superantigens bind directly to T-cell receptors andMHC molecules outside the peptide binding site

This causes massive cytokine production by CD4 cells ie systemic toxicity and suppression of adaptive response

This allows them to act very quickly e.g. staph aureus.

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132
Q

Features of staph aureus food poisoning

A

1/3 population chronic carriers, 1/3 transient
Spread by skin lesions (eczema) on food handlers

Produces enterotoxin, an exotoxin that can act as a superantigen in the GI tract, releasing IL1 and IL2 causing prominent vomiting and watery, non bloody diarrhoea

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133
Q

Important cytokines in staph aureus food poisoning

A

IL1

IL2

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134
Q

Microbiological features of staph aureus

A

Catalase, coagulase positive gram positive coccus
Appears in tetrads, clusters on gram stain.
Yellow colonies on blood agar

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135
Q

Microbiological features of bacillus cereus

A

Gram positive rod-spores
Heat stable emetic toxin
-not destroyed by reheating
Heat labile diarrhoeal toxin

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136
Q

Features of Bacillus cereus food poisoning

A

food is not cooked to a high enough temperature
and
watery non bloody diarrhoea; self limited
Rarely causes of bacteremia in vulnerable population
Rarely cause cerebral abscesses

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137
Q

Examples of superantigens (in GI infection)

A

Staph aureus enterotoxin

Clostridium pefringens enterotoxin

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138
Q

Features of clostridium pefringens food poisoning

A

reheated food (meat)
Normal flora of colon but not small bowel, where the enterotoxin acts (superantigen)
Incubation 8-16hrs
Watery diarrhoea, cramps,little vomiting lasting 24hrs

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139
Q

Features of chlostridum botulinum food poisoning

A

Source : canned or vacuum packed food (honey / infants)
Ingestion of preformed toxin (inactivated by cooking)
Blocks Ach release from peripheral nerve synapses
Treatment with antitoxin

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140
Q

Treatment of botulinum food poisoning

A

Antitoxin

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141
Q

Treatment of staph aureus food poisoning

A

Nothing

Self limiting

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142
Q

Clinical features of listeria monocytogenes food poisoning

A 
Watery diarrhoea, 
cramps
headache
fever
little vomiting
Perinatal infection, immunocompromised patients
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143
Q

Treatment of C. difficile diarrhoea

A

Metronidazole

Oral vancomycin

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144
Q

Listeria causes outbreaks of…

A

Febrile gastroenteritis

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145
Q

Bacteria causing food food poisoning. Found in refrigerated food.

A

Listeria monocytogenes

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146
Q

Microbiological features of listeria monocytogenes

A

ß haemolytic, aesculin positive with tumbling motility.

Grows in cold

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147
Q

Sources of listeria monocytogenes (food poisoning)

A

Refrigerated food (“cold enhancement”),ie unpasteurised dairy, vegetables. Grows at 4 ºC

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148
Q

Treatment of listeria food poisoning

A

Ampicillin, amoxicillin, ceftriaxone or co-trimoxazole

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149
Q

Microbiological features of E.coli

A

Gram negative
Facultative anaerobe
Oxidase negative
Lactose fermenter

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150
Q

Common cause of travellers diarrhoea

A

E. coli (ETEC)

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151
Q

Source of E.coli infection (GI)

A

Food/water contaminated with human faeces.

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152
Q

Features of enterotoxigenic e.coli

A

ETEC
Traveller’s diarrhoea
Source: food/water contaminated with human faeces.

Enterotoxins :
Heat labile stimulates adenyl cyclase and cAMP
Heat stable stimulates guanylate cyclase.
Act on the jejeunum, ileum not on colon.

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153
Q

Where do the e.coli enterotoxins act in GI infection?

A

jejunum and ileum. Not the colon

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154
Q

Which e.coli subtype causes dysentry

A

EIEC

Enteroinvasive e.coli

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155
Q

Cause of haemolytic uraemic syndrome

A

E. coli. EHEC subtype e.coli O157:H7

The toxin is a shiga-like/verotoxin

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156
Q

Treatment of e.coli food poisoning

A

Self limiting. Avoid antibiotics but can use ciprofloxacin.

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157
Q

Clinical features of haemolytic uraemic syndrome

A

Anaemia
Thrombocytopenia
Renal failure

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158
Q

EPEC causes

A

Infantile diarrhoea

enteropathogenic e. coli

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159
Q

GI infection

Gram negative, oxidase negative, lactose fermenter

A

E. coli

160
Q

GI Infection

Gram-negative, H2S producing, non-lactose fermenter

A 
Salmonellae 
Three species : 
S. typhi (and paratyphi) 	
S.enteritidis
S.cholerasuis,
161
Q

Microbiological features of salmonellae

A

Non lactose fermenters,
H2S producers,
TSI agar,
XLD agar,selenite F broth

Antigens:
Cell wall O (groups A-I)
Flagellar H
Capsular Vi (virulence, antiphagocytic)

162
Q

Salmonella antigens

A

Cell wall O
Flagellar H
Capsular V (virulence prevents phagocytosis)

163
Q

Features of salmonella enteritides

A

transmitted from poultry, eggs, meat

invasion of epi- and sub-epithelial, tissue of small and large bowel

bacteraemia infrequent

self limited non bloody diarrhoea ,usually no treatment (Cipro if required)

Stool positivity

164
Q

Features of salmonella typhi

A 
transmitted only by humans
multiplies in Payer’s patches,
spreads rapidly
bacteraemia, 3% carriers. 
.
Slow onset, fever and constipation,
splenomegaly,rose spots (transient), 
anaemia, leucopaenia,
bradycardia, haemorrhage and
perforation. 
BC pos.           
Treatment : ceftriaxone
Travellers from SE Asia
165
Q

Clinical features of S.typhi infection

A 
Slow onset 
Fever 
Constipation 
Splenomegaly 
Rose spots 
Anaemia and leucopenia 
Relative bradycardia 
Haemorrhage and perforation

Positive blood cultures

166
Q

Treatment of typhoid

A

Ceftriaxone or ciprofloxacin

167
Q

Where does s.typhi multiply

A

Peyer’s patches

168
Q

Sources of s.enteritides infection

A

Meat, poultry, eggs

169
Q

Clinical features of salmonella enteritides

A

Non-bloody diarrhoea (self-limiting)

Infrequent bacteraemia

170
Q

Treatment of salmonella enteritides

A

Usually self-limiting.

Ciprofloxacin if needed

171
Q

GI infection:

Non lactose fermenters, non H2S producers, non motile

A

Shigella

172
Q

Microbiological features of shigella

A

Non lactose fermenters, non H2S producers, non motile

Antigens:
Cell wall O antigens,
Polysaccharide (groups A-D) : 3 species - S.sonnei,

173
Q

Which shigella species most commonly cause infection in MSM population

A

S.flexneri (MSM)

174
Q

Features of shigellae

A

Non lactose fermenters, non H2S producers, non motile.

Antigens:
cell wall O antigens,
polysaccharide (groups A-D) : 3 species - S.sonnei, S.dysenteriae, S.flexneri (MSM)

The most effective enteric pathogen (low ID 50).
No animal reservoir
No carrier state

Dysentery
invading cells of mucosa of distal ileum and colon
producing enterotoxin (Shiga toxin)

Avoid antibiotics (ciprofloxacin if required)

175
Q

Part of GI tract affected by shigella

A

Mainly distal ileum and colon

176
Q

Clinical features of shigella

A 
Mainly affects distal ileum and colon 
Causes mucosal inflammation 
Fever
Pain 
Bloody diarrhoea
177
Q

Infective causes of bloody diarrhoea

A

Shigella

EHEC

178
Q

3 key species of vibrio

A

Cholera
Parahaemolyticus
Vulnificus

179
Q

Which group of vibrio cholera causes epidemics

A

O1

180
Q

How does vibrio cholera cause diarrhoea

A

Produces enterotoxin with A and B subunit which persistantly stimulates adenylate cyclase. This leads to increased cAMP and opening of chloride channels to lumen

181
Q

Clinical features of cholera

A

Rice water stool without inflammatory cells
Loss of water and electrolytes
Massive diarrhoea without inflammation

182
Q

Clinical features of vibrios parahaemolyticus infection (GI)

A

3 days of diarrhoea which is often self limiting

Major cause of diarrhoea in Japan..or when cruising in the Caribbean

183
Q

Treatment of cholera

A

Treat the losses

184
Q

Microbiological features of vibrios

A

Curved, comma shaped, late lactose fermenters, oxidase positive.

185
Q

Clinical features of vibrios vulnificus

A

Cellulitis in shellfish handlers

Fatal septicaemia with D+V in HIV patients

186
Q

Treatment of vibrios vulnificus

A

Doxycycline

187
Q

Treatment of vibrios parahaemolyticus

A

Doxycycline (but condition is often self limiting)

188
Q

GI infection
Bacteria. curved, comma or S shaped
Microaerophilic
Oxidase positive

A

Campylobacter

189
Q

Microbiological features of campylobacter

A

curved, comma or S shaped
Microaerophilic
Oxidase positive
Motile

190
Q

Sources of campylobacter infection

A

Unpasteurised milk

Poultry (and other meat) contaminated with animal faeces

191
Q

Source of vibrios cholerae infection

A

Contamination of water and food from human faeces ( shellfish, oysters, shrimp).

192
Q

Source of vibrios parahaemolyticus

A

Undercooked or raw seafood

193
Q

Vibrios cholerae colonises which part of the GI tract?

A

Small bowel

194
Q

Clinical features of campylobacter jejuni infection

A

Prodrome of headache and fever
Abdo cramps
Bloody foul smelling diarrhoea
Associated with Guillain-Barre, Reiter’s and reactive arthritis

195
Q

Treatment of campylobacter jejunin infection

A

Erythromycin (or ciprofloxacin if first 5-7 days). Only treat if immunocompromised
Self limiting but symptoms can last for weeks (20 days)

196
Q

Features of Reiter’s syndrome

A

Inflammatory arthritis of large joints, inflammation of the eyes in the form of conjunctivitis or uveitis, and urethritis in men or cervicitis in women

197
Q

Features of Yersinia enterocolitica

A

Non lactose fermenter, prefers 4ºC “cold enrichment”

Transmitted via food contaminated with domestic animals excreta.

enterocolitis
mesenteric adenitis with necrotising granulomas

associated with reactive arthritis , Reiter’s and erythema nodosum

198
Q

Microbiological Features of entamoeba hystolytica

A

motile trophozoite in diarrhoea

non motile cyst in non-diarrhoeal illness

Killed by boiling, removed by water filters

4 nuclei

No animal reservoir.

199
Q

Clinical features of entamoeba hystolytica

A

dysentery, flatulence, tenesmus

  • chronic : wt loss,+/- diarrhoea
  • liver abscess (causing RUQ pain)

Diagnosed using stool microscopy (wet mount, iodine and trichome), serology in invasive disease

Ingestion of cysts&raquo_space; trophos in
ileum&raquo_space; colonize cecum, colon&raquo_space; “flask shaped” ulcer

200
Q

Treatment of entamoeba hystolytica

A

metronidazole + paromomycin in luminal disease

201
Q

Microbiological features of giardia lamblia

A

trophozoite “pear shaped”
2 nuclei
4 flagellas and a suction disk.

202
Q

Clinical features of giardia lamblia

A

Ingestion of cyst from fecally contaminated water,food.

Infective process:
Excystation at duodenum
tropho attaches
no invasion

Causes malabsorption of protein and fat.

foul smelling non- bloody diarrhoea, cramps flatulence, no fever

Diagnosis: stool micro, ELISA (enzyme-linked immunosorbent assay), “string test”

203
Q

Treatment of giardia

A

metronidazole

204
Q

Features of cryptosporidium Parvum

A

Cryptosporidium parvum

Infects the jejunum

Severe diarrhoea in the immunocomromised

Oocysts seen in stool by modified Kinyoun acid fast stain

Treatment : reconstitution of immune system

205
Q

Cause of severe diarrhoea. Test using kinyoun acid fast stain

A

cryptosporidium parvum

206
Q

Treatment of cryptosporium parvum infection

A

Reconstitute immune system
nitazoxanide in children
Paramomycin (but minimal effect)

207
Q

Populations commonly affected by giardia

A

travellers, hikers,
day care, mental hospitals,
MSM.

208
Q

Viruses causing secretory diarrhoea

A 
Rotavirus 
Adenovirus 
Norovirus 
Poliovirus 
Enteroviruses e.g. coxsackie
209
Q

Type of nuclear material in rotarvirus

A

dsRNA

210
Q

Features of rotavirus

A

Replicates in mucosa of small intestine
dsRNA virus
Causes secretory diarrhoea without inflammation
Causes watery diarrhoea ? by stimulation of enteric nervous system

211
Q

How many times do you need to be exposed to natural rotavirus infection to develop lifelong immunity

A

Twice

212
Q

Types of adenovirus that cause non-bloody diarrhoea in young children

What ages?

A

40 and 41

Less than 2 years

213
Q

Ages susceptible to rotavirus

A
214
Q

Type of diarrhoea caused by adenovirus

A

Non-bloody

215
Q

Notifiable causes of GI infection

A

Campylobacter, Clostridium sp, Listeria monocytogenes, Vibrio, Yersinia

216
Q

Examples of slow growing non-tuberculous mycobacteria

A

Mycobacterium avium intracellulare
M. marinum
M. ulcerans

217
Q

Difference between infection with mycobacterium avium intracellulare in immunocompetent and immunocompromised individuals

A

Immunocompetent:
May invade bronchial tree
Pre-existing bronchiectasis or cavities

Immunocompromised:
Disseminated infection

218
Q

Mycobacterium avium intracellulare is also known as

A

Mycobacterium avium complex (MAC)

219
Q

Mycobacterium marinum infection causes

A

Skin lesions. Usually multiple. Clusters of nodules or papules. Can be painful or painless.

220
Q

M. ulcerans causes…

A

Chronic painless ulcers

221
Q

List 3 fast growing non-tuberculous mycobacteria

A

M. abscessus,
M. chelonae,
M. fortuitum

222
Q

M. chelonae and M. fortuitum cause

A

Skin and soft tissue infection

223
Q

Treatment of mycobacterium avium intracellulare infection

A

Clarithromycin/azithromycin
Rifampicin
Ethambutol
+/- Amikacin/streptomycin

224
Q

Features of extrapulmonary TB

A

Lymphadenitis
AKA scrofula
Cervical LNs most commonly
Abscesses & sinuses

Gastrointestinal
Swallowing of tubercles

Peritoneal
Ascitic or adhesive

Genitourinary
Slow progression to renal disease
Subsequent spreading to lower urinary tract

Bone & joint
Haematogenous spread
Spinal TB most common
Pott’s disease

Miliary TB
Millet seeds on CXR
Progressive disseminated haematogenous TB
Increasing due to HIV

Tuberculous meningitis

225
Q

Colour of mycobacterium after ZN stain

A

Pink/red

226
Q

Interferon gamma release assays used to test for

A

TB disease. (cannot distinguish between latent and active disease).

227
Q

Tuberculin skin tests have poor sensitivity among which populations?

A

HIV, age, immunosuppressants

Overwhelming TB

228
Q

Disadvantages of using IFN-gamma release assays to test for TB

A

Cannot distinguish latent & active TB

Poor sensitivity in:
HIV, age, immunosuppressants
Overwhelming TB

229
Q

Second line TB medications

A 
Quinolones (Moxifloxacin)
Injectables: Capreomycin, kanamycin, amikacin
Ethionamide/Prothionamide
Cycloserine
PAS (para-aminosalicylic acid)
Linezolid
Clofazamine
230
Q

Key side effects of first line TB medications

A

Rifampicin
Raised transaminases & induces cytochrome P450
Orange secretions

Isoniazid
Peripheral neuropathy (pyridoxine 10mg od)
Hepatotoxicity

Pyrazinamide
Hepatotoxicity

Ethambutol
Visual disturbance

231
Q

First line TB treatment

A 
Duration
3 or 4 drugs for 2/12:
Rifampicin 
Isoniazid
Pyrazinamide
Ethambutol

Then Rifampicin & Isoniazid 4/12
(10/12 if CNS TB)

232
Q

Injectables used to treat TB

A

Capreomycin, kanamycin, amikacin

233
Q

TB is multidrug resistant if it is resistant to….

A

Rifampicin & isoniazid

234
Q

TB is extremely drug resistant if it is resistant to…

A

Rifampicin & isoniazid plus:

fluoroquinolones & at least 1 injectable

235
Q

Challenges diagnosing TB in HIV positive population

A

Clinical history:
Less likely to be classical
Symptoms and signs often absent in population with low CD4 count

Chest X-ray:
More likely extrapulmonary
X-ray changes variable

Smear microscopy & culture:
Less sensitive

Tuberculin skin test
More likely to be negative

236
Q

Challenged treating TB in HIV positive patients

A

Timing of treatment initiation

Drug interactions

Overlapping toxicity

Duration of treatment – adherence

Health care resources

237
Q

Liver and bone ALP can be

differentiated by

A

GGT measurement
Electrophoretic separation
Bone specific ALP immunoassay now available

238
Q

Causes of raised ALP:

>5x Upper limit of normal:

A

5x Upper limit of normal:
Bone ( Pagets, Osteomalacia)
Liver ( cholestasis, cirrhosis)

5 x Upper Limit Normal:
Bone ( tumours, fractures, osteomyelitis)
Liver (infitrative disease,hepatitis)

239
Q

3 forms of CK enzyme

A

CK-MM- skeletal muscles
CK-MB (1 & 2) – cardiac muscles
CK- BB – brain – activity minimal even in severe brain damage

(CK-MM accounts for almost entire normal plasma activity)

240
Q

Markers for MI

A

Myoglobin
Troponin (Cardiac: I or T)
CK-MB (Muscle brain)

241
Q

Troponin T/I peaks… hours post MI

A

12-24 hours post MI

242
Q

Cardiac troponin returns to normal levels… days after acute MI

A

7 days (3-10)

243
Q

Brain natriuretic peptide secreted by…

A

Ventricles

244
Q

Symptoms of primary herpes labialis infection

A

Frequently asymptomatic,

May experience pharyngitis, fever, mouth ulceration and lymphadenopathy

245
Q

Syptoms of herpes labialis recurrence

A

Classically, prodromal tingling followed by localised painful blisters that resolve over 5 – 7 days

246
Q

Herpes genitalis usually caused by which subtype of HSV

A

HSV2

247
Q

Symptoms of primary herpes genitalis infection

A

Frequently asymptomatic,

May experience painful ulceration, fever, lymphadenopathy and urinary retention

248
Q

Signs of herpes encephalitis

A

Fever, Fits, Funny behaviour

Disturbed conscious level, focal neurology

249
Q

Timing of annual chickenpoz peak

A

Spring-summer

250
Q

Adults with chickenpox at higher risk of…

A

Severe disease and Pneumonitis

251
Q

When is chickenpox most infectious

A

Most infectious 1-2 days before rash onset

252
Q

Stages of varicella zoster primary infection

A

Initial localised infection in respiratory tract leads to primary viraemia and seeding of reticuloendothelial organs
Later secondary viraemia leads to disseminated to all tissues and skin and mucosal lesions (chickenpox)

Retrograde transport along neurones from skin permits entry to spinal cord where virus becomes latent
Reactivation and anterograde transport back to innervated skin leads to zoster (shingles)

253
Q

Antivirals used for HSV, VZV

A

Aciclovir (ACV, acyclovir, prototype drug, )

Valaciclovir (vACV prodrug of aciclovir, high bioavailability)

Famciclovir (prodrug of penciclovir, high bioavailability)

254
Q

Pharmacokinetics of aciclovir

A

Oral doses generally well-tolerated
Bioavailability of ACV 15-30%,
t½ = 3 hrs,
Renally-excreted

Poorly soluble in urine so crystallisation of drug in tubules can occur at high IV doses and in renal failure

255
Q

Aciclovir mechanism of action

A

It is a guanosine analogue.
It is converted to aciclovir monophosphate by viral thymidine kinase (in HSV)
Then converted by host cell kinases by host cell enzymes to aciclovir triphosphate
It then competitively inhibits the viral DNA polymerase (it is incorporated into viral DNA and inactivates the polymerase enzyme as further elongation is impossible)

Note: HSV-1 > HSV-2&raquo_space; VZV; susceptibility of other herpesviruses is negligible

256
Q

Aciclovir contains which DNA base within its structure

A

Guanine

257
Q

How does aciclovir exhibit seleective toxicity?

A

Affinity of cellular kinases for ACV is poor but activity of these enzymes in virally-infected cells is greatly increased

Affinity of cellular DNA polymerase for ACV-PPP 10- to 30- fold lower than herpesvirus DNA polymerase

Hence inhibition of DNA synthesis by aciclovir in herpesvirus-infected cells is much greater

258
Q 
Treatment of HSV and VZV (including doses) 
Including:  
Immunocompromised
HSV Encephalitis 
Prevention of recurrence
A

Orogenital HSV – ACV 200mg 5x day for 5 days; vACV 500mg BD for 5 days
Double-dose in immunocompromised; consider IV if extensive
Treat for longer if new lesions appear

Prevention of recurrence: ACV 200 – 400mg BD; vACV 500mg OD (BD if immunocompromised)
VZV: ACV 800mg 5x day for 5 – 7 days; vACV 1G TDS for days
VZV in immunocompromised: IV ACV 10mg / kg 8-hrly for 5 – 7 days

HSV encephalitis: IV ACV 10mg / kg 8-hrly for 14 – 21 days; initiate treatment within 6 hrs of admission

vACV= valaciclovir

259
Q

Advantages of valaciclovir over aciclovir

A

BD dosing in HSV TDS dosing in VZV

Higher bioavailability

260
Q

Treatment of HSV encephalitis

A

HSV encephalitis: IV ACV 10mg / kg 8-hrly for 14 – 21 days; initiate treatment within 6 hrs of admission

261
Q

Famciclovir is a prodrug of

A

Penciclovirq

262
Q

Ganciclovir is used to treat

A

CMV

263
Q

Antiviral used to treat CMV

A

Ganciclovir

264
Q

Key side effect of ganciclovir

A

BM suppression: neutropenia and thrombocytopenia

265
Q

Herpes labialis is usually caused by which HSV subtype

A

HSV 1

266
Q

Consequences of CMV infection in BMT and solid organ transplant patients

A

Marrow suppression, graft rejection, pneumonitis, encephalitis, adrenalitis

267
Q

CMV remains latent (after initial infection) in which cells?

A

Monocytes

268
Q

CMV (in healthy individuals) causes…

A

Mononucleosis-like illness and hepatitis

269
Q

Aciclovir is not effective treatment for CMV because

A

The virus does not produce thymidine kinase

270
Q

Treat CMV in which populations?

A

Immunosuppressed
Pregnant
Congenital
HIV

271
Q

CMV infected cells characteristic appearance

A

Owls eye (due to inclusion bodies)

272
Q

Ganciclovir mechanism of action

A 
Nucleoside analogue (of 2′-deoxy-guanosine) 
It is phosphorylated to ganciclovir monophosphate (by a viral kinase encoded by the cytomegalovirus (CMV) gene UL97 during infection)

Cellular kinases catalyze the formation of ganciclovir diphosphate and ganciclovir triphosphate

Ganciclovir triphosphate is a competitive inhibitor of deoxyguanosine triphosphate (dGTP) incorporation into DNA and preferentially inhibits viral DNA polymerases more than cellular DNA polymerases.

In addition, ganciclovir triphosphate serves as a poor substrate for chain elongation, thereby disrupting viral DNA synthesis by a second route.

273
Q

CMV in immunocompromised adults CMV causes…

A 
Retinitis 
pneumonitis 
Colitis
encephalitis 
Hepatitis
274
Q

Cidofovir mechanism of action

A 
Nucleoside analogue (monophosphate) 
Phosphorylation to diphosphate form is independent of viral enzymes 
The diphsphate competitively inhibits the incorporation of deoxyCYTIDINE triphosphate into viral DNA by viral DNA polymerase. Incorporation of the drug disrupts further chain elongation
275
Q

Foscarnet mechanism of action

A

Foscarnet is a structural mimic of the anion pyrophosphate
It selectively inhibits the pyrophosphate binding site on viral DNA polymerases at concentrations that do not affect human DNA polymerases.
DOES NOT REQUIRE ACTIVATION

276
Q

Which is available as oral preparation: ganciclovir or valganciclovir

A

Valganiclovir

277
Q

Ganciclovir half life

A

18 hours

278
Q

Routes of administration for:
Foscarnet
Cidofovir

A

IV only

IV or topical

279
Q

Major side effects of foscarnet

A

Major side effects are renal impairment and electrolyte disturbance

280
Q

Key adverse effects of cidofovir

A

IV given weekly, nephrotoxic++ (dose dependent) and contraindicated in renal impairment

Requires prior IV hydration and co-treatment with probenecid

281
Q

Pretreatment required before giving cidofovir

A

Requires prior IV hydration and co-treatment with probenecid

282
Q

CMV is excreted in…

A

Breast milk, urine, sweat

283
Q

Treatment of CMV

A

IV Ganciclovir or oral valganiclovir or IV foscarnet
Induction (BD dosing) and maintenance phases (OD dosing)

Cidofovir 2nd line (toxicity)

284
Q

Roseola infantum

a) Symptoms
b) Cause

A

Children under 3 years, high fever (+/- febrile convulsions), coryzal symptoms, then sudden rash (commonly also diarrhoea and cough)

HHV6

285
Q

Effect of HHV6 in immunocompromised individuals

A

encephalitis, marrow suppression, pneumonitis

286
Q

Unique feature of HHV6 (among herpesviruses)

A

HHV-6 is unique among human herpesviruses in that integration of viral DNA into host chromosome can occur

Frequency ~1% of population

Every cell affected

Can be inherited from either parent

Biological significance is unclear

287
Q

Treatment of HHV6 infection

A

Generally supportive – antipyretics

HHV-6 encephalitis in transplant recipients has been treated with FOS and GCV although experience is limited

Important to distinguish chromosomally-integrated HHV-6 – suspect if persistently detectable in every blood sample and confirm with FISH

288
Q

Kaposi sarcoma:

a) associated virus
b) Virus is detected where?

A

a) HHV8

b) Biopsy not blood (as non-lytic part of viral replication cycle)

289
Q

Treatment of HHV8

A

GCV, FOS, CDV all potentially active in vitro but:
NO definitive clinical role for DAA established

HHV-8-associated malignancy usually treated by combination of chemotherapy and immunotherapy

HIV-associated KS may improve with HAART and suppression of HIV replication

290
Q

Treat aciclovir resistant HSV with

A

Foscarnet or cidofovir

Note: Mutations in viral TK (95%) and DNA polymerase (5%)
Mediate cross-resistance to GCV

291
Q

Aciclovir drug resistance usually occurs in which context

A

Immunosupression (TK resistant strains usually less virulent)

292
Q

Ganciclovir resistance most likely to occur in which context

A

Most likely to occur in context of prolonged therapy in immunocompromised

293
Q

2nd line for CMV is

A

foscarnet or cidofovir

294
Q

Mechanisms of aciclovir resistance

A

Mutations in viral TK (95%) and DNA polymerase (5%)

Mediate cross-resistance to GCV

295
Q

Major surface glycoproteins in influenza virus

A

Major surface glycoproteins haemagglutinin (HA) and neuraminidase (NA)

HA facilitates attachment via host cell sialic acid and causes membrane fusion; NA cleave sialic acid and allows virion to exit host cell

296
Q

Examples of Neuraminidase inhibitors

A

Oseltamivir (oral), zanamivir (dry powder inhaler)
IV and nebulised zanamivir can be obtained
Effective for influenza A and influenza B

297
Q

When should neuraminidase inhibitors be used?

A

National surveillance indicates influenza is circulating
Patient is in a ‘risk-group’
Within 48 hours of symptom onset (36 hours for zanamivir)

Risk-groups:
Aged ≥ 65 years
Immunosuppressed
Chronic respiratory disease
Chronic heart disease
Chronic liver disease
Chronic neurological disease
Diabetes mellitus
Pregnant women
Morbid obesity (BMI ≥ 40)
Children
298
Q

Amantidine mechanism of action (treating influenza)

A

Anti-parkinsonian drug, also antiviral activity

Inhibit influenza A matrix protein (M2)
Prevent virus uncoating

Orally absorbed
Only effective for influenza A

NOT currently recommended or used in UK (lack of efficacy and circulating strains generally resistant)

299
Q

Routes of administration of zanamavir

A

Dry powder inhaler

IV and nebulised can be obtained

300
Q

Treatment with neuraminidase inhibitor should be started within… of start of symptoms

A

Within 48 hours of symptom onset (36 hours for zanamivir)

301
Q

Mechanism of action of ribavarin

A

Guanosine analogue
Inhibits viral RNA synthesis (exact mechanism unclear) – broad activity in vitro

Note: Clinical efficacy unclear – effective for Lassa fever, used in combination with interferon for HCV, weak data for nebulised RBV in RSV

302
Q

In children RSV causes

A

Bronchiolitis

303
Q

Cause of croup

A

Parainfluenza viruses

304
Q

Key adverse effects of ribavarin

A

Adverse effects include anaemia and mitochondrial toxicity

305
Q

Palivizumab is…

A

humanized monoclonal antibody (IgG) directed against an epitope in the A antigenic site of the F protein of RSV

306
Q

Antiviral for RSV

A

Ribavarin
Clinical efficacy unclear – effective for Lassa fever, used in combination with interferon for HCV, weak data for nebulised RBV in RSV

Pavilizumab can be used to PREVENT RSV bur will not treat it

307
Q

Classical infections associated with fetal complications

A 
Toxoplasmosis
Other – includes syphilis, parvovirus B19, varicella-zoster
Rubella
Cytomegalovirus
Herpes simplex virus

Influenza is now also known to cause increased morbidity and mortality in pregnant women

308
Q

Infection in pregnancy:

All women are routinely screened at booking (~12 weeks) for:

A

Syphilis
Hepatitis B
HIV
To determine need for antenatal therapy +/- neonatal vaccination (in case of hep B) to prevent vertical transmission

Rubella – IgG to determine immune status and need for post-natal vaccination

309
Q

Features of congenital Rubella syndrome

A

Classic triad:
sensorineural deafness,
eye defects (cataracts, congenital glaucoma, pigmentary retinopathy),
congenital heart disease (pulmonary artery stenosis, PDA)

Also: purpura (‘blueberry muffin’ rash), splenomegaly, microcephaly, mental retardation

310
Q

Risk of congenital rubella syndrome if maternal infection occurs in first… weeks of pregnancy

A

16

311
Q

Rubella infection in weeks 16-20 of pregnancy carries risk of…

A

To baby: minimal risk of deafness only

312
Q

There is no known risk of rubella infection after week… of pregnancy

A

20

313
Q

Features of Rubella infection (in adult)

A

Non-specific febrile illness associated with rash, may have arthralgia and occipital lymphadenopathy

314
Q

Management of rubella

A

No specific antiviral or prophylaxis demonstrated to be effective
Termination of pregnancy offered in case of suspected CRS
Prevention: universal MMR vaccination (give after delivery but before discharge if antenatal testing indicates susceptibility)

315
Q

Infections in pregnancy

Greatest risk where primary CMV infection occurs…

A

During pregnancy or shortly before conception

Relationship between age of gestation and infection unclear

(reactivation / reinfection significant but less risk)

316
Q

CMV is intermittently shed via

A

Saliva and urine

also secreted in breast milk

317
Q

Treatment of congenital CMV infection

A

Antiviral treatment of infant may improve outcome
Key is recognition of infection
6 months of oral valganciclovir recently been demonstrated to be best for long term outcome

Preventative vaccines in development

318
Q

Effects of congenital CMV infection

A

Generalized infection may occur in the infant, and can cause complications such as low birth weight, microcephaly, seizures, petechial rash similar to the “blueberry muffin” rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice).

Though severe cases can be fatal, with supportive treatment most infants with CMV disease will survive. However, from 80% to 90% will have complications within the first few years of life that may include hearing loss, vision impairment, and varying degrees of mental retardation.

Another 5% to 10% of infants who are infected but without symptoms at birth will subsequently have varying degrees of hearing and mental or coordination problems.

The onset of hearing loss can occur at any point during childhood, although commonly within the first decade. It is progressive and can affect both ears.

319
Q

Long term sequelae of congenital CMV

A

Hearing loss
Vision impairment
Varying degrees of mental retardation

320
Q

Initial complications of congenital CMV infection

A

low birth weight, microcephaly, seizures, petechial rash similar to the “blueberry muffin” rash of congenital rubella syndrome, and moderate hepatosplenomegaly (with jaundice).

321
Q

Neonatal HSV routes of infection

A

Direct contact during birth – risk ↑↑ if primary HSV in third trimester

Ascending infection if PROM

Transmission from orolabial HSV (kissing baby, parents, relatives, staff)

322
Q

Management of suspected primary HSV in pregnancy

A

Pregnant women presenting with suspected primary genital HSV should be referred to GUM clinic and obstetrician

Confirm diagnosis and HSV type by lesion swab PCR

Confirm primary infection with type-specific HSV IgG

Offer aciclovir (ACV) treatment and prophylaxis until delivery (↓ viral shedding and transmission)

Caesarean recommended if presenting within 6/52 of delivery or active lesions in labour

Swabs from neonate + neonatal IV ACV empirically until active infection ruled out

323
Q

Management of suspected HSV recurrence (reactivation) in pregnancy

A

Risk of HSV transmission to the neonate from recurrent HSV lesions is low

Women with recurrent HSV will have IgG which may offer some protection of neonate

Vaginal delivery can be offered in the first instance, even if lesions are present shortly before birth

Suppressive therapy with oral aciclovir can be considered from 36 weeks (no evidence of harm)

324
Q

Risk of primary HSV acquisition in pregnancy is highest when?

A

Third trimester

325
Q

Test for congenital CMV infection

A

Congenital infection: urine or saliva for PCR in first 21 days of life

326
Q

Effects of maternal VZV infection in different stages of pregnancy

A

Maternal varicella – 5x increased morbidity in 2nd and 3rd trimester

20 weeks – neonatal zoster; less severe than CVS
7 days before to 7 days after birth – neonatal varicella – severe disseminated infection

327
Q

Features of congenital varicella syndrome

A

Classical: Limb hypoplasia, scarring (dermatomal distribution)

Other features: 
microcephaly
neurological abnormalities:
hydrocephalus
Horner's syndrome

eye abnormalities:
cataracts
chorioretinitis
microphthalmia

3Gs:
growth retardation
gastrointestinal structural defects
genitourinary structural defects

328
Q

Varicella zoster immunoglobulin is effect if used within… of initial exposure

A

10 days

329
Q

Chickenpox infectious period

A

2 days before rash until lesions have crusted over

Note: shingles: only if contact with exposed lesions

330
Q

Parvovirus B19 in pregnancy:

Highest risk at which stage of pregnancy

A

Infection in 1st 20 weeks of pregnancy can result in fetal death, fetal anaemia and hydrops fetalis

Note:
Later infections much reduced risk
Reactivation and reinfection occur but no evidence of risk to fetus

331
Q

Effects of parvovirus B19 in pregnancy (high risk period)

A

Foetal death, foetal anaemia and hydrops fetalis

332
Q

Management of parvovirus B19 in pregnancy

A

Maternal parvovirus B19 infection poses risk to fetus even if asymptomatic

Active fetal management may improve outcome

Exposed pregnant woman: serology for B19V IgG and IgM (+ consider measles / rubella):
B19V-IgG+ve, IgM-ve: past infection, reassure
B19V-IgG-ve, IgM-ve: susceptible, recheck in one month or if illness develops to identify infection (seroconversion to IgG)
B19V-IgM+ve: discuss with medical virology (IgM can be non-specific) and consider referral to fetal medicine

333
Q

Early life acquisition of HBV associated with

A

High risk (90%) of chronic carriage

334
Q

Major route of neonatal HBV acquisition

A

Vertical transmission

335
Q

Prevention of neonatal HBV

A

Can be effectively prevented by neonatal vaccination +/- antenatal antiviral treatment (5-10% risk when treated)

336
Q

Consequences of HBV infection in pregnancy

A

Acute HBV in pregnancy usually not severe and not associated with teratogenicity

Vertical transmission risk, high risk of chronic carriage if acquired early in life.

337
Q

Risk factors for vertical HBV transmission

A

Maternal viral load (very low risk when below 10⁶ copies / mL)
HBeAg positivity – usually indicates high viral replication
No clear association with breastfeeding or mode of delivery (no indication for Caesarean)

338
Q

Diagnosis of HBV in pregnancy

A

HBsAg part of routine antenatal screening
Further HBV markers performed if positive to ascertain status
HBV viral load SHOULD be measured in HBsAg positive pregnant women

339
Q

Management of HBV in pregnancy

A

Refer to hepatologist
HBsAg-positive mother: infant should receive accelerated course of HBV vaccine (1st dose within 12 hours of delivery)
HBeAg-positive mother: as above + infant should also receive HBV immunoglobulin (HBIG) at birth
HBV viral load > 10⁶ copies: as above + antenatal antiviral therapy (lamivudine or tenofovir are used) for 6 – 8 weeks prior to delivery to reduce viral load

340
Q

Consequences of influenza infection in pregnancy

A

Pregnant women identified as at high risk of morbidity and mortality in 2009-10 H1N1 influenza pandemic

Risk to foetus unclear

341
Q

Management of flu in pregnancy

A

Pregnant women should be offered seasonal influenza vaccine

Pregnant women with influenza-like illness during influenza season should be offered empirical antivirals (oseltamivir, zanamivir)

Diagnostic specimens should be taken to confirm / refute diagnosis and assist infection control procedures

342
Q

Pregnant women should be immunised against…

A

Pregnant women should be immunised against diphtheria, tetanus, pertussis, and influenza

343
Q

Which vaccines are not generally given in pregnancy?

A

Live-attenuated vaccines generally not used (but no evidence of harm from MMR or varicella vaccine when inadvertently given) – discuss with medical virologist

344
Q

Major pathogens in surgical site infections (3)

A

Staph.aureus (MSSA and MRSA)
E.coli
Pseudomonas aeruginosa

345
Q

3 levels of surgical site infection

A

Superficial incisional- affect skin and subcutaneous tissue

Deep incisional- affect fascial and muscle layers

Organ/space infection- any part of anatomy other than incision

346
Q

Why does smoking increase risk of surgical site infections?

A

Nicotine delays primary wound healing

Peripheral vascular disease

347
Q

Effect of hair removal on risk of surgical site infections

A

Micro-abrasions caused by shaving with a razor may lead to multiplication of bacteria

Use electric clippers on the day of surgery with single-use head
Hair should not be removed unless it will interfere with the operation

348
Q

Timing of antibiotic prophylaxis for surgery (and reasons)

A

Antibiotic prophylaxis should be given at induction of anaesthesia

Bactericidal concentration of the drug should be established in serum and tissues at time of incision.

Additional doses may be necessary if there has been significant blood loss or if the operation has been prolonged

349
Q

Effect of body temperature on risk of surgical site infections

A

Mild hypothermia appears to increase the risk of SSIs by causing vasoconstriction, decreased delivery of oxygen to wound space and subsequent impairment of neutrophil function

In theatre suite: Measure patients temperature before inducing anaesthesia. Start forced air warming if temperature is below 36ºC
Warm intravenous fluid. Warm irrigation fluid

350
Q

Pathophysiology of septic arthritis

A

Organisms adhere to the synovial membrane, bacterial proliferation in the synovial fluid with generation of host inflammatory response.

Joint damage leads to exposure of host derived proteins such as fibronectin to which bacteria adhere

351
Q

Common causative organisms of septic arthritis

A

Staph. aureus 46%
- Coagulase negative staphylococci 4%

Streptococci 22%:
Streptococcus pyogenes
Streptococcus pneumoniae
Streptococcus agalactiae

Gram negative organisms 
E.coli 
Haemophilus influezae
Neisseria gonorrhoeae
Salmonella

Rare- Lyme, brucellosis, mycobacteria, fungi

352
Q

S. aureus is usally coagulase…

A

Positive

353
Q

Investigations in septic arthritis

A

Blood culture before antibiotics are given

Synovial fluid aspiration for microscopy and culture
ESR,CRP
-Traditionally a synovial count> 50,000 WBC cells/mm3 used to suggest septic arthritis
(Negative culture result does not exclude septic arthritis)

Imaging:
US- confirm effusion and guide needle aspiration
CT- erosive bone change, periarticular soft tissue extension
MRI- joint effusion, articular cartilage destruction, abscess, contiguous osteomyelitis

354
Q

Causative organisms for vertebral osteomyelitis

A

S.aureus- 48.3%
CNS: coagulase negative staphylococci
GNR: Gram negative rod
Strep

355
Q

Most cases of vertebral osteomyelitis are in which region of the spine?

A

Lumbar

356
Q

Symptoms of vertebral osteomyelitis

A

Back pain- 86%
Fever- 60%
Neurological impairment 34%

357
Q

Diagnosis of vertebral osteomyelitis

Duration of treatment

A

MRI: 90% sensitive
Blood cultures
CT/ open biopsy

6 weeks. Longer treatment if undrained abscesses/implant associated

358
Q

Brucella is gram….

A

negative coccobacillus

359
Q

What is a Brodie abscess?

A

Brodie abscess is an intraosseous abscess related to focus of subacute pyogenic osteomyelitis

360
Q

Features of chronic osteomyelitis

Diagnosis using…

A

Pain
Brodies abscess
Sinus tract

MRI
Bone biopsy for culture and histology

361
Q

Presentation of prosthetic joint infections

A

Pain
Patient complains that the joint was ‘never right’
Early failure
Sinus tract

362
Q

Prosthetic joint infections causative organisms

A 
Gram positive cocci
-coagulase negative staphylococci
-staphylococus aureus
Streptococci sp
Enterococci sp

Aerobic gram negative bacilli:
Enterobacteriaceae
Pseudomonas aeruginosa

Anaerobes
Polymicrobial
Culture negative
Fungi

363
Q

Pseudomonas aeruginosa is a gram….

A

negative rod

364
Q

Diagnosis of prosthetic joint infections

A

Radiology- loosening

If CRP>13.5 for prosthetic knee joint infection
CRP> 5 for prosthetic hip joint infection

Joint aspiration
If >1700/ml of WCC correlates with knee PJI
If > 4200/ml of WCC correlates with hip PJI

365
Q

Key lactose fermenting urinary tract

A

Escherichia coli
Klebsiella spp.

Also:
Enterobacter spp.
+Serratia spp.
+Citrobacter spp.

366
Q

Key non lactose fermenting bacteria that cause UTIs

A

Proteus

Pseudomonas

367
Q

Enterococcus are gram….

A

Gram positive cocci

368
Q

Gram positive cocci that forms chains

A

Enterococcus

369
Q

Asymptomatic bacteriuria is common in which population

A

Elderly

370
Q

Piperacillin-tazobactam spectrum of activity

A

Hosp G-ve, some G+ve, anaerobes, Pseud; broad + antipseudomonal

371
Q

Ciprofloxacin spectrum of activity

A

Mainly G-ve, Pseudomonal; broad

372
Q

Gentamicin spectrum of activity

A

G-ve; narrow

373
Q

Meropenem spectrum of activity

A

Hosp G-ve, G+ve, anaerobe, Pseud; broad

374
Q

Colistin spectrum of activity

A

Hosp G-ve inc Carb resistant; broad

375
Q

C. difficile toxins

A

Toxin A and toxin B

376
Q

Treatment of severe and life threatening C. diff colitis

A

Severe: vancomycin at higher doses
Up to 500 mg qds PO / NG
+/- IV metronidazole if unable to tolerate PO
Consider IV immunoglobulin 400mg/kg

Life-threatening- consider colectomy; timing
500 mg qds vancomycin PO 
\+/- intracolonic vancomycin 
\+ metronidazole IV 
\+ IVIG
377
Q

What constitutes ‘severe’ c. diff disease

A 
No validated severity index….
Physiological unstable- P/ BP/ T/ RR
High WCC- >15 (>20?)
Rising or high creatinine >200
Clinical – peritonism, ileus, obstruction
Radiological – colitis 
Age, albumin, others….
378
Q

Rate of c.diff relapse after treatment

A

20%

379
Q

HIV nuclear material

A

ss positive sense RNA (diploid)

380
Q

How many genes in HIV genome?

A

9

(e.g. env, gag, pol) (tat, rev, nef) (vif, vpr, vpu) encoding: 15 Structural, Regulatory & Auxiliary Proteins.

381
Q

Name of HIV surface protein

A

gp120

382
Q

Name of HIV transmembrane protein

A

gp41

383
Q

HIV preferred targets (cells)

A

CD4+ T helper cells (& CD4+ monocytes)

384
Q

Recptor for HIV-1

Examples of co-receptors

A

CD4 molecules

CCR5 and CXCR4

385
Q

Components of natural immunity mobilised in response within hours of HIV infecion

A

Inflammation.
Non-specific activation of macrophages.
Non-specific activation of NK cells and complement.
Release of cytokines and chemokines.
Stimulation of pDCs (plasmacytoid dendritic cells) via toll-like receptors.

386
Q

Role of B cells in HIV immunity

A

Specific humoral responses where neutralising antibodies are produced.

Anti-gp120 and anti-gp41 (Nt) antibodies are thought to be important in protective immunity.
Non-neutralising anti-p24 gag IgG also produced.
HIV remains infectious even when coated with antibodies!

387
Q

In acute HIV infection there is a massive loss of CD4 T cells where?

A

Gut

388
Q

Why does the HIV virus have so many variants?

A

Replication of the retroviral genome depends on 2 steps - Reverse Transcriptase lacks the proof reading mechanisms associated with cellular DNA polymerases and therefore genomes of retroviruses are copied into DNA with low fidelity.

Transcription of DNA into RNA copies is also of low fidelity.

389
Q

Outline the life cycle of HIV

A
  1. Attachment/Entry
  2. Reverse Transcription & DNA Synthesis
  3. Integration
  4. Viral Transcription
  5. Viral Protein Synthesis
  6. Assembly of Virus & Release of Virus
  7. Maturation
390
Q

% of HIV patients who will have rapid progression (AIDS in 2-3 years) without treatment

A

10%

391
Q

% of HIV patients who will be long term non-progressors (stable CD4 counts and no symptoms after 10 years) without treatment

A
392
Q

2 methods of assessing HIV resistance to ART drugs

A

Phenotypic: Viral replication is measured in cell cultures under selective pressure of increasing concentrations of antiretroviral drugs – compared to wild-type

Genotypic: Mutations determined by direct sequencing of the amplified HIV genome (so far limited to sequencing of RT and P)

393
Q

Why does HAART not eradicate HIV in infected people?

A

HAART does not eliminate the virus from the patient (reservoir in resting CD4 T cells).

394
Q

Cause of initial CD4 rise after starting HAART

A

Initial CD4 rise – memory T-cells redistributed

395
Q

Name 3 NNRTIs

A

Nevirapine (Viramune)
Delavirdine (Rescriptor)
Efavirenz (Sustiva)

396
Q

Name 5 NRTIs

A 
Zidovudine (Retrovir, ZVD, AZT)
Didanosine (Videx, ddI)
Stavudine (Zerit, d4T)
Lamivudine (Epivir, 3TC)
Abacavir (Ziagen, ABC)
Emtricitabine (Emtriva, FTC)
Combivir (AZT+3TC)
Epzicom (3TC+ABC)
Trizivir (AZT+3TC+ABC)
397
Q

Name 4 protease inhibitors

A 
Indinavir (Crixivan)
 Nelfinavir (Viracept)
 Ritonavir (Norvir, RIT)
 Saquinavir SGC (Fortovase
 Fosamprenavir (Lexiva, 908)
 Lopinavir+RIT (Kaletra)
 Atazanavir (Reyataz)

Year 5 Pathology (7 decks)

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