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Year 5 Pathology > Microbiology > Flashcards

Flashcards in Microbiology Deck (397):
1

Characteristics of S Pneumonia

Rusty coloured sputum.
Usually lobar on CXR
Diplococci gram positive

2

Characteristics of H. Influenza

Associated with smoking
COPD
Kids
Elderly
Gram negative cocco-bacilli

3

Characteristics of Moraxella . Catarrhalis

Associated with smoking
Gram negative coccus

4

Characteristics of S. aureus

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

5

Characteristics of Klebsiella pneumonia

Alcoholism, elderly, haemoptysis
Gram negative rods
enterobacter

6

Characteristics of bordatella pertussis

Whooping cough in unvaccinated kids
Often in travelling community in EMQs

7

Characteristics of mycoplasma pneumonia

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

8

Characteristics of chlamydia pneumonia

Hard to diagnose
Obligate intracellular pathogen
Doesn't stain well

9

Common causes of pneumonia by age group:

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

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

10

Most common causes of CAP

Haemophilis influenzae
Strep pneumoniae

11

Atypical causes of CAP

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

12

Characteristics of Chlamydia psittaci

Exposure to birds, splenomegaly, rash, haemolytic anaemia

13

Components of CURB-65 score
Impact on treatment

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

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

14

Pathogens causing bronchitis
Common features

Viruses
S. pneumoniae
H. influenzae
M. catarrhalis

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

15

Encapsulated bacteria

Haemophilus influenza
Strep pneumonia
Neisseria menigitides

16

Urine antigen tests for which types of pneumonia?

Strep pneumonia
Legionella

17

Pneumonia organisms without a cell wall
(Atypical)

Mycoplasma
Legionella
Chlamydia
Coxiella

18

Legionella extrapulmonary features

Low sodium
Hepatitis
Abdo pain
Confusion
diarrhoea
Lymphopenia

19

Features of coxiella burnetti

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

20

Treatment of aspiration pneumonia

Cefuroxime and metronidazole

21

Treatment for pseudomonas pneumonia

Piptaz
or ciprofloxacin and gentamicin

22

Treatment for mild-moderate pneumonia

Amoxicillin or macrolide

23

Causes of pneumonia in HIV

PCP
TB
Cryptococcus neoformans

24

Causes of pneumonia in neutropenia

Aspergillus spp.

25

Causes of pneumonia in BMT

Aspergillus
CMV

26

Causes of pneumonia after splenectomy

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

27

Causes of pneumonia in cystic fibrosis

Pseudomonas aeruginosa
Burkholderia cepacia (v. high mortality)

28

Treatment for legionella pneumonia

Macrolide plus rifampicin

29

Treatment for HAP 1st and 2nd line

1st line: Ciprofloxacin and vancomycin
2nd line: Piptaz and vancomycin

30

Treatment for MRSA

Vancomycin

31

Treatment for MSSA

Flucloxacillin

32

Nature of discharge with BV

Grey Frothy

33

Nature of discharge with Gonorrhoea

Thick green frothy

34

Nature of discharge with chlamydia

White and cloudy discharge

35

Features of disseminated gonorrhoea

Arthritis
Rash
Septicaemia

36

After...h post abx treatment for gonorrhea....

72h
Repeat culture

37

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

Trachoma
Genital chlamydia infection, opthalmia neonatorum

38

Stages of LGV infection

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,

39

Treatment of LGV

Doxycycline 100mg BD for 21 days
Erythromycin 500mg QD for 21 days or azithromycin 1g weekly for 3 weeks

40

Features of chancroid

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

41

What are clue cells?

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

Seen in BV

42

HPV incubation time

3 weeks

43

Treatment of HPV warts

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

44

Treatment for BV

Metronidazole 400mg or 500mg BD 7 days

45

Describe HPV lesions

Warts: pedunculated, papular, planar, carpet, keratinised

46

Definition of cystitis

Inflammation of the bladder often caused by infection

47

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

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

48

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

1% to 3%

49

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

40% to 50%

50

Most common organism causing an acute UTI

E coli

51

% of urinary tract infections caused by a single bacterial species

95%

52

List E. coli serogroups causing a large portion of UTIs

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

53

Organisms that are common causes of UTIs

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

54

Host defences preventing UTI

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

55

Factors increasing risk of UTI in females compared to males

Short urethra
Proximity to warm, moist vulvar and perianal areas

56

Link between UTIs and sexual intercourse

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

57

List intra and extrarenal causes of urinary tract obstruction

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

58

Causes of neurogenic malfunction of the urinary tract

Poliomyelitis,
Tabes dorsalis,
Diabetic neuropathy,
Spinal cord injuries

59

What is tabes dorsalis?

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

60

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

Gram positive

61

Kidney abscesses caused by which bacterial species

Staph. Aureus

62

a) Symptoms of UTI in children under 2 years of age
b) Symptoms of UIT in children above 2 years of age

a) Failure to thrive
vomiting
fever

b) Urinary frequency
dysuria
abdominal or flank pain

63

Cause of lower UTI symptoms

The bacteria produce irritation of urethral and vesical mucosa

64

Symptoms of an upper urinary tract infection in older adults

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

65

Strongest indicator of a UTI on urinalysis

Positive nitrites

66

According to HPA guidance:
If greater than or equal to... typical symptoms of UTI treat empirically with antibiotics.

3

67

Asymptomatic bacteriuria in pregnancy is associated with

Pyelonephritis and premature delivery

68

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

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

69

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

White cells
Squamous epithelial cells

70

Causes of sterile pyuria

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

71

UTIs
Culture: when counting colonies >... is considered significant

30 colonies

72

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

10^5cfu/ml
CFU: colony forming unit

10^4cfu/ml

73

Empirical treatment of uncomplicated UTI is usually with

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

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

74

Treatment of pyelonephritis is with...

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

Gentamicin added due to risk of ESBL organism

75

Advice to patients prescribed nitrofurantoin (dose timing)

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

76

Nitrofurantoin is... spectrum

Broad

77

Duration of antibiotic treatment for UTIs

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

78

Most fungal UTIs are associated with...

Indwelling catheters
(Treat by removing the catheter)

79

Pathogens causing bacterial meningitis

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

80

Fungal cause of meningitis

Cryptococcus neoformans

81

Pathogens causing chronic meningitis

Spirochetes
Cryptococcus
M TB

82

Most common CNS infection

Aseptic meningitis
Most common causes are: Coxsackievirus group B and echoviruses

83

Viruses causing aseptic meningitis

Most common:
Coxsackievirus group B and echoviruses

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

84

Most common cause of viral encephalitis

HSV

85

Gram positive diplococci causing meningitis

Streptococcus pneumoniae (also alpha-haemolytic)

86

Gram negative diplococci causing meningitis

Neisseria meningitides

87

Gram positive rod causing meningitis

Listeria

88

Stains with India ink

Cryptococcus

89

Treatment for bacterial meningitis (in hospital)

Ceftriaxone 2g iv bd

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

Add in corticosteroids e.g. dexamethasone

90

Treatment for Meningo-encephalitis

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

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

91

Low glucose in CSF suggests

Bacterial CNS infection

92

High WCC with high mononuclear cells suggests

Viral infections

93

CSF with high protein, high WCC and mononuclear cells suggests

Mycobacterium TB or cryptococcus

94

Signs/symptoms of hepatitis A

feverish, mild, flu like
Then develop jaundice a few weeks later

95

Duration of hepatitis A incubation period

2-6 weeks

96

Hepatitis A serology

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

97

Hepatitis A structure

Non enveloped
ssRNA (positive sense)

98

Hepatitis B structure

dsDNA (circular not fully ds)
Lipid envelope

99

Hepatitis C structure

ssRNA positive sense
Enveloped

100

Hepatitis D structure

Enveloped
Negative sense, single-stranded, closed circular RNA

101

Hepatitis E structure

Non-enveloped
Single-strand RNA molecule

102

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

6 months

103

Hepatitis B incubation period

2-6 months

104

Hepatitis B serology/blood results

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.

105

Reliable marker of HBV infectivity

Viral load

106

Consequences of chronic HBV infection

Liver cirrhosis
HCC

107

HBV treatment

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.

108

Incubation period of hepatitis C

2 weeks to 6 months

109

Most common hepatitis C genotype

1

110

% of people with acute hepatitis C who clear infection

20%

111

Hepatitis C serology/blood results

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

112

Treatment of HCV

PegIFN alpha2b and ribavarin

113

Hepatitis D can only infect patients with

Hepatitis B

114

Hepatitis E is transmitted via...

Faecal-oral route

115

Complications of hepatitis D infection

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

116

Hepatitis E strains that only infect humans

1 and 2

117

Hepatitis E incubation period

3-8 weeks

118

Complications of hepatitis E infection

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

119

Treatment of hepatitis E

Supportive
Consider ribavarin and pegIFN

120

Hepatitis E serology

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).

121

Campylobacter incubation period

1-10 days

122

E.Coli 0157 incubation period

1-5 days

123

Shigella incubation period

12-96 hours

124

Salmonella (non typhoidal) incubation period

8-48 hours

125

Vibrio parahaemolyticus incubation period

24-72h

126

Vibrio cholera incubation period

1-5 days

127

Bacillus cereus incubation period

1-6h

128

Staph aureus incubation period

2-7h

129

How does cholera cause diarrhoea

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

130

Food poisoning:
If vomiting develops within a few hours of eating the meal the likely organism is...

Staph aureus

131

How do enterotoxin superantigens act (bacterial and viral)

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.

132

Features of staph aureus food poisoning

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

133

Important cytokines in staph aureus food poisoning

IL1
IL2

134

Microbiological features of staph aureus

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

135

Microbiological features of bacillus cereus

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

136

Features of Bacillus cereus food poisoning

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

137

Examples of superantigens (in GI infection)

Staph aureus enterotoxin
Clostridium pefringens enterotoxin

138

Features of clostridium pefringens food poisoning

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

139

Features of chlostridum botulinum food poisoning

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

140

Treatment of botulinum food poisoning

Antitoxin

141

Treatment of staph aureus food poisoning

Nothing
Self limiting

142

Clinical features of listeria monocytogenes food poisoning

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

143

Treatment of C. difficile diarrhoea

Metronidazole
Oral vancomycin

144

Listeria causes outbreaks of...

Febrile gastroenteritis

145

Bacteria causing food food poisoning. Found in refrigerated food.

Listeria monocytogenes

146

Microbiological features of listeria monocytogenes

ß haemolytic, aesculin positive with tumbling motility.
Grows in cold

147

Sources of listeria monocytogenes (food poisoning)

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

148

Treatment of listeria food poisoning

Ampicillin, amoxicillin, ceftriaxone or co-trimoxazole

149

Microbiological features of E.coli

Gram negative
Facultative anaerobe
Oxidase negative
Lactose fermenter

150

Common cause of travellers diarrhoea

E. coli (ETEC)

151

Source of E.coli infection (GI)

Food/water contaminated with human faeces.

152

Features of enterotoxigenic e.coli

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.

153

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

jejunum and ileum. Not the colon

154

Which e.coli subtype causes dysentry

EIEC
(Enteroinvasive e.coli)

155

Cause of haemolytic uraemic syndrome

E. coli. EHEC subtype e.coli O157:H7
The toxin is a shiga-like/verotoxin

156

Treatment of e.coli food poisoning

Self limiting. Avoid antibiotics but can use ciprofloxacin.

157

Clinical features of haemolytic uraemic syndrome

Anaemia
Thrombocytopenia
Renal failure

158

EPEC causes

Infantile diarrhoea
(enteropathogenic e. coli)

159

GI infection
Gram negative, oxidase negative, lactose fermenter

E. coli

160

GI Infection
Gram-negative, H2S producing, non-lactose fermenter

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

161

Microbiological features of salmonellae

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

Salmonella antigens

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

163

Features of salmonella enteritides

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

Features of salmonella typhi

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

Clinical features of S.typhi infection

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

Positive blood cultures

166

Treatment of typhoid

Ceftriaxone or ciprofloxacin

167

Where does s.typhi multiply

Peyer's patches

168

Sources of s.enteritides infection

Meat, poultry, eggs

169

Clinical features of salmonella enteritides

Non-bloody diarrhoea (self-limiting)
Infrequent bacteraemia

170

Treatment of salmonella enteritides

Usually self-limiting.
Ciprofloxacin if needed

171

GI infection:
Non lactose fermenters, non H2S producers, non motile

Shigella

172

Microbiological features of shigella

Non lactose fermenters, non H2S producers, non motile

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

173

Which shigella species most commonly cause infection in MSM population

S.flexneri (MSM)

174

Features of shigellae

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

Part of GI tract affected by shigella

Mainly distal ileum and colon

176

Clinical features of shigella

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

177

Infective causes of bloody diarrhoea

Shigella
EHEC

178

3 key species of vibrio

Cholera
Parahaemolyticus
Vulnificus

179

Which group of vibrio cholera causes epidemics

O1

180

How does vibrio cholera cause diarrhoea

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

Clinical features of cholera

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

182

Clinical features of vibrios parahaemolyticus infection (GI)

3 days of diarrhoea which is often self limiting

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

183

Treatment of cholera

Treat the losses

184

Microbiological features of vibrios

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

185

Clinical features of vibrios vulnificus

Cellulitis in shellfish handlers
Fatal septicaemia with D+V in HIV patients

186

Treatment of vibrios vulnificus

Doxycycline

187

Treatment of vibrios parahaemolyticus

Doxycycline (but condition is often self limiting)

188

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

Campylobacter

189

Microbiological features of campylobacter

curved, comma or S shaped
Microaerophilic
Oxidase positive
Motile

190

Sources of campylobacter infection

Unpasteurised milk
Poultry (and other meat) contaminated with animal faeces

191

Source of vibrios cholerae infection

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

192

Source of vibrios parahaemolyticus

Undercooked or raw seafood

193

Vibrios cholerae colonises which part of the GI tract?

Small bowel

194

Clinical features of campylobacter jejuni infection

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

195

Treatment of campylobacter jejunin infection

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

196

Features of Reiter's syndrome

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

Features of Yersinia enterocolitica

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

Microbiological Features of entamoeba hystolytica

motile trophozoite in diarrhoea

non motile cyst in non-diarrhoeal illness

Killed by boiling, removed by water filters

4 nuclei

No animal reservoir.

199

Clinical features of entamoeba hystolytica

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 >> trophos in
ileum >> colonize cecum, colon >> “flask shaped” ulcer

200

Treatment of entamoeba hystolytica

metronidazole + paromomycin in luminal disease

201

Microbiological features of giardia lamblia

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

202

Clinical features of giardia lamblia

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

Treatment of giardia

metronidazole

204

Features of cryptosporidium Parvum

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

Cause of severe diarrhoea. Test using kinyoun acid fast stain

cryptosporidium parvum

206

Treatment of cryptosporium parvum infection

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

207

Populations commonly affected by giardia

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

208

Viruses causing secretory diarrhoea

Rotavirus
Adenovirus
Norovirus
Poliovirus
Enteroviruses e.g. coxsackie

209

Type of nuclear material in rotarvirus

dsRNA

210

Features of rotavirus

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

211

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

Twice

212

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

What ages?

40 and 41
Less than 2 years

213

Ages susceptible to rotavirus

214

Type of diarrhoea caused by adenovirus

Non-bloody

215

Notifiable causes of GI infection

Campylobacter, Clostridium sp, Listeria monocytogenes, Vibrio, Yersinia

216

Examples of slow growing non-tuberculous mycobacteria

Mycobacterium avium intracellulare
M. marinum
M. ulcerans

217

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

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

Immunocompromised:
Disseminated infection

218

Mycobacterium avium intracellulare is also known as

Mycobacterium avium complex (MAC)

219

Mycobacterium marinum infection causes

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

220

M. ulcerans causes...

Chronic painless ulcers

221

List 3 fast growing non-tuberculous mycobacteria

M. abscessus,
M. chelonae,
M. fortuitum

222

M. chelonae and M. fortuitum cause

Skin and soft tissue infection

223

Treatment of mycobacterium avium intracellulare infection

Clarithromycin/azithromycin
Rifampicin
Ethambutol
+/- Amikacin/streptomycin

224

Features of extrapulmonary TB

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

Colour of mycobacterium after ZN stain

Pink/red

226

Interferon gamma release assays used to test for

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

227

Tuberculin skin tests have poor sensitivity among which populations?

HIV, age, immunosuppressants
Overwhelming TB

228

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

Cannot distinguish latent & active TB

Poor sensitivity in:
HIV, age, immunosuppressants
Overwhelming TB

229

Second line TB medications

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

230

Key side effects of first line TB medications

Rifampicin
Raised transaminases & induces cytochrome P450
Orange secretions

Isoniazid
Peripheral neuropathy (pyridoxine 10mg od)
Hepatotoxicity

Pyrazinamide
Hepatotoxicity

Ethambutol
Visual disturbance

231

First line TB treatment

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

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

232

Injectables used to treat TB

Capreomycin, kanamycin, amikacin

233

TB is multidrug resistant if it is resistant to....

Rifampicin & isoniazid

234

TB is extremely drug resistant if it is resistant to...

Rifampicin & isoniazid plus:
fluoroquinolones & at least 1 injectable

235

Challenges diagnosing TB in HIV positive population

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

Challenged treating TB in HIV positive patients

Timing of treatment initiation

Drug interactions

Overlapping toxicity

Duration of treatment – adherence

Health care resources

237

Liver and bone ALP can be
differentiated by

GGT measurement
Electrophoretic separation
Bone specific ALP immunoassay now available

238

Causes of raised ALP:
>5x Upper limit of normal:

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

3 forms of CK enzyme

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

Markers for MI

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

241

Troponin T/I peaks... hours post MI

12-24 hours post MI

242

Cardiac troponin returns to normal levels... days after acute MI

7 days (3-10)

243

Brain natriuretic peptide secreted by...

Ventricles

244

Symptoms of primary herpes labialis infection

Frequently asymptomatic,
May experience pharyngitis, fever, mouth ulceration and lymphadenopathy

245

Syptoms of herpes labialis recurrence

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

246

Herpes genitalis usually caused by which subtype of HSV

HSV2

247

Symptoms of primary herpes genitalis infection

Frequently asymptomatic,
May experience painful ulceration, fever, lymphadenopathy and urinary retention

248

Signs of herpes encephalitis

Fever, Fits, Funny behaviour
Disturbed conscious level, focal neurology

249

Timing of annual chickenpoz peak

Spring-summer

250

Adults with chickenpox at higher risk of...

Severe disease and Pneumonitis

251

When is chickenpox most infectious

Most infectious 1-2 days before rash onset

252

Stages of varicella zoster primary infection

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

Antivirals used for HSV, VZV

Aciclovir (ACV, acyclovir, prototype drug, )

Valaciclovir (vACV prodrug of aciclovir, high bioavailability)

Famciclovir (prodrug of penciclovir, high bioavailability)

254

Pharmacokinetics of aciclovir

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

Aciclovir mechanism of action

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 >> VZV; susceptibility of other herpesviruses is negligible

256

Aciclovir contains which DNA base within its structure

Guanine

257

How does aciclovir exhibit seleective toxicity?

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

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

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

Advantages of valaciclovir over aciclovir

BD dosing in HSV TDS dosing in VZV
Higher bioavailability

260

Treatment of HSV encephalitis

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

261

Famciclovir is a prodrug of

Penciclovirq

262

Ganciclovir is used to treat

CMV

263

Antiviral used to treat CMV

Ganciclovir

264

Key side effect of ganciclovir

BM suppression: neutropenia and thrombocytopenia

265

Herpes labialis is usually caused by which HSV subtype

HSV 1

266

Consequences of CMV infection in BMT and solid organ transplant patients

Marrow suppression, graft rejection, pneumonitis, encephalitis, adrenalitis

267

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

Monocytes

268

CMV (in healthy individuals) causes...

Mononucleosis-like illness and hepatitis

269

Aciclovir is not effective treatment for CMV because

The virus does not produce thymidine kinase

270

Treat CMV in which populations?

Immunosuppressed
Pregnant
Congenital
HIV

271

CMV infected cells characteristic appearance

Owls eye (due to inclusion bodies)

272

Ganciclovir mechanism of action

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

CMV in immunocompromised adults CMV causes...

Retinitis
pneumonitis
Colitis
encephalitis
Hepatitis

274

Cidofovir mechanism of action

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

Foscarnet mechanism of action

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

Which is available as oral preparation: ganciclovir or valganciclovir

Valganiclovir

277

Ganciclovir half life

18 hours

278

Routes of administration for:
Foscarnet
Cidofovir

IV only
IV or topical

279

Major side effects of foscarnet

Major side effects are renal impairment and electrolyte disturbance

280

Key adverse effects of cidofovir

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

Requires prior IV hydration and co-treatment with probenecid

281

Pretreatment required before giving cidofovir

Requires prior IV hydration and co-treatment with probenecid

282

CMV is excreted in...

Breast milk, urine, sweat

283

Treatment of CMV

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

Cidofovir 2nd line (toxicity)

284

Roseola infantum
a) Symptoms
b) Cause

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

HHV6

285

Effect of HHV6 in immunocompromised individuals

encephalitis, marrow suppression, pneumonitis

286

Unique feature of HHV6 (among herpesviruses)

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

Treatment of HHV6 infection

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

Kaposi sarcoma:
a) associated virus
b) Virus is detected where?

a) HHV8
b) Biopsy not blood (as non-lytic part of viral replication cycle)

289

Treatment of HHV8

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

Treat aciclovir resistant HSV with

Foscarnet or cidofovir

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

291

Aciclovir drug resistance usually occurs in which context

Immunosupression (TK resistant strains usually less virulent)

292

Ganciclovir resistance most likely to occur in which context

Most likely to occur in context of prolonged therapy in immunocompromised

293

2nd line for CMV is

foscarnet or cidofovir

294

Mechanisms of aciclovir resistance

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

295

Major surface glycoproteins in influenza virus

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

Examples of Neuraminidase inhibitors

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

297

When should neuraminidase inhibitors be used?

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

Amantidine mechanism of action (treating influenza)

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

Routes of administration of zanamavir

Dry powder inhaler

IV and nebulised can be obtained

300

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

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

301

Mechanism of action of ribavarin

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

In children RSV causes

Bronchiolitis

303

Cause of croup

Parainfluenza viruses

304

Key adverse effects of ribavarin

Adverse effects include anaemia and mitochondrial toxicity

305

Palivizumab is...

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

306

Antiviral for RSV

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

Classical infections associated with fetal complications

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

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

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

Features of congenital Rubella syndrome

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

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

16

311

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

To baby: minimal risk of deafness only

312

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

20

313

Features of Rubella infection (in adult)

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

314

Management of rubella

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

Infections in pregnancy
Greatest risk where primary CMV infection occurs...

During pregnancy or shortly before conception

Relationship between age of gestation and infection unclear

(reactivation / reinfection significant but less risk)

316

CMV is intermittently shed via

Saliva and urine
(also secreted in breast milk)

317

Treatment of congenital CMV infection

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

Effects of congenital CMV infection

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

Long term sequelae of congenital CMV

Hearing loss
Vision impairment
Varying degrees of mental retardation

320

Initial complications of congenital CMV infection

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

321

Neonatal HSV routes of infection

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

Management of suspected primary HSV in pregnancy

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

Management of suspected HSV recurrence (reactivation) in pregnancy

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

Risk of primary HSV acquisition in pregnancy is highest when?

Third trimester

325

Test for congenital CMV infection

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

326

Effects of maternal VZV infection in different stages of pregnancy

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

Features of congenital varicella syndrome

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

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

10 days

329

Chickenpox infectious period

2 days before rash until lesions have crusted over

Note: shingles: only if contact with exposed lesions

330

Parvovirus B19 in pregnancy:

Highest risk at which stage of pregnancy

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

Effects of parvovirus B19 in pregnancy (high risk period)

Foetal death, foetal anaemia and hydrops fetalis

332

Management of parvovirus B19 in pregnancy

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

Early life acquisition of HBV associated with

High risk (90%) of chronic carriage

334

Major route of neonatal HBV acquisition

Vertical transmission

335

Prevention of neonatal HBV

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

336

Consequences of HBV infection in pregnancy

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

Risk factors for vertical HBV transmission

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

Diagnosis of HBV in pregnancy

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

Management of HBV in pregnancy

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

Consequences of influenza infection in pregnancy

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

Risk to foetus unclear

341

Management of flu in pregnancy

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

Pregnant women should be immunised against...

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

343

Which vaccines are not generally given in pregnancy?

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

344

Major pathogens in surgical site infections (3)

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

345

3 levels of surgical site infection

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

Why does smoking increase risk of surgical site infections?

Nicotine delays primary wound healing
Peripheral vascular disease

347

Effect of hair removal on risk of surgical site infections

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

Timing of antibiotic prophylaxis for surgery (and reasons)

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

Effect of body temperature on risk of surgical site infections

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

Pathophysiology of septic arthritis

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

Common causative organisms of septic arthritis

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

S. aureus is usally coagulase...

Positive

353

Investigations in septic arthritis

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

Causative organisms for vertebral osteomyelitis

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

355

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

Lumbar

356

Symptoms of vertebral osteomyelitis

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

357

Diagnosis of vertebral osteomyelitis
Duration of treatment

MRI: 90% sensitive
Blood cultures
CT/ open biopsy

6 weeks. Longer treatment if undrained abscesses/implant associated

358

Brucella is gram....

negative coccobacillus

359

What is a Brodie abscess?

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

360

Features of chronic osteomyelitis
Diagnosis using...

Pain
Brodies abscess
Sinus tract

MRI
Bone biopsy for culture and histology

361

Presentation of prosthetic joint infections

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

362

Prosthetic joint infections causative organisms

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

Pseudomonas aeruginosa is a gram....

negative rod

364

Diagnosis of prosthetic joint infections

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

Key lactose fermenting urinary tract

Escherichia coli
Klebsiella spp.

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

366

Key non lactose fermenting bacteria that cause UTIs

Proteus
Pseudomonas

367

Enterococcus are gram....

Gram positive cocci

368

Gram positive cocci that forms chains

Enterococcus

369

Asymptomatic bacteriuria is common in which population

Elderly

370

Piperacillin-tazobactam spectrum of activity

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

371

Ciprofloxacin spectrum of activity

Mainly G-ve, Pseudomonal; broad

372

Gentamicin spectrum of activity

G-ve; narrow

373

Meropenem spectrum of activity

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

374

Colistin spectrum of activity

Hosp G-ve inc Carb resistant; broad

375

C. difficile toxins

Toxin A and toxin B

376

Treatment of severe and life threatening C. diff colitis

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

What constitutes 'severe' c. diff disease

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

Rate of c.diff relapse after treatment

20%

379

HIV nuclear material

ss positive sense RNA (diploid)

380

How many genes in HIV genome?

9

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

381

Name of HIV surface protein

gp120

382

Name of HIV transmembrane protein

gp41

383

HIV preferred targets (cells)

CD4+ T helper cells (& CD4+ monocytes)

384

Recptor for HIV-1
Examples of co-receptors

CD4 molecules
CCR5 and CXCR4

385

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

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

Role of B cells in HIV immunity

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

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

Gut

388

Why does the HIV virus have so many variants?

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

Outline the life cycle of HIV

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

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

10%

391

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

392

2 methods of assessing HIV resistance to ART drugs

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

Why does HAART not eradicate HIV in infected people?

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

394

Cause of initial CD4 rise after starting HAART

Initial CD4 rise – memory T-cells redistributed

395

Name 3 NNRTIs

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

396

Name 5 NRTIs

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

Name 4 protease inhibitors

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