Microbiology Flashcards
1
Q
Characteristics of S Pneumonia
A
Rusty coloured sputum.
Usually lobar on CXR
Diplococci gram positive
2
Q
Characteristics of H. Influenza
A
Associated with smoking COPD Kids Elderly Gram negative cocco-bacilli
3
Q
Characteristics of Moraxella . Catarrhalis
A
Associated with smoking
Gram negative coccus
4
Q
Characteristics of S. aureus
A
Associated with recent viral infection
Cavitation on CXR
ETOH, homeless, immunosupressed
Gram positive cocci (grape bunch clusters)
5
Q
Characteristics of Klebsiella pneumonia
A
Alcoholism, elderly, haemoptysis
Gram negative rods
enterobacter
6
Q
Characteristics of bordatella pertussis
A
Whooping cough in unvaccinated kids
Often in travelling community in EMQs
7
Q
Characteristics of mycoplasma pneumonia
A
Common Systemic symptoms Join pain Cold agglutinin test Erythema multiforme Risk of SJS and autoimmune haemolytic anaemia
8
Q
Characteristics of chlamydia pneumonia
A
Hard to diagnose
Obligate intracellular pathogen
Doesn’t stain well
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
10
Q
Most common causes of CAP
A
Haemophilis influenzae
Strep pneumoniae
11
Q
Atypical causes of CAP
A
Legionella
Mycoplasma pneumonia
Coxiella bumetii (Q fever)
Chlamydia psittaci (psittacosis)
12
Q
Characteristics of Chlamydia psittaci
A
Exposure to birds, splenomegaly, rash, haemolytic anaemia
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
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.
15
Q
Encapsulated bacteria
A
Haemophilus influenza
Strep pneumonia
Neisseria menigitides
16
Q
Urine antigen tests for which types of pneumonia?
A
Strep pneumonia
Legionella
17
Q
Pneumonia organisms without a cell wall
Atypical
A
Mycoplasma
Legionella
Chlamydia
Coxiella
18
Q
Legionella extrapulmonary features
A
Low sodium Hepatitis Abdo pain Confusion diarrhoea Lymphopenia
19
Q
Features of coxiella burnetti
A
Common in domestic/farm animals
Transmitted by aerosol or milk
Dx by serology
Sensitive to macrolides
20
Q
Treatment of aspiration pneumonia
A
Cefuroxime and metronidazole
21
Q
Treatment for pseudomonas pneumonia
A
Piptaz
or ciprofloxacin and gentamicin
22
Q
Treatment for mild-moderate pneumonia
A
Amoxicillin or macrolide
23
Q
Causes of pneumonia in HIV
A
PCP
TB
Cryptococcus neoformans
24
Q
Causes of pneumonia in neutropenia
A
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)
```
