Microbiology Flashcards
(222 cards)
1
Q
What are the TORCH infections?
A
Toxoplasmosis Other: syphilis, HIV, HBV, VZV Rubella CMV HSV
2
Q
What are the signs + symptoms of toxoplasmosis in neonates?
A
- Chorioretinitis
- Cerebral calcification -> Low IQ, seizures
- Microcephaly
- Deafness
3
Q
What are the signs + symptoms of congenital rubella syndrome?
A
- Cataracts + other eye things (microophthalmia, retinopathy)
- Deafness
- Cardiac disease (PDA most common)
- Growth retardation, low IQ
- Blueberry muffin rash (due to extramedullary haematopoiesis)
4
Q
How can HSV affect the neonate?
A
- Eyes/skin
- Encephalitis
- Disseminated infection eg. hepatitis, pneumonitis
5
Q
Primary HSV at which gestation has the highest risk for the baby?
A
- 1st trimester infection is bad as can recur later on
- 3rd trimester, esp around delivery has high risk of transmission
6
Q
Define neonatal infection (and early onset, late onset)
A
Infection in the first 6 weeks of life (adjusted for prematurity)
- Early onset: within 48 hours
- Late onset: >48 hours
7
Q
Why is prematurity associated with a high rate of infection?
A
- Less barriers to pathogen entry
- No/low maternal Ig
- Iatrogenic causes (indwelling lines)
8
Q
Which organisms are common causes of early onset neonatal infection? What are some types of infection?
A
- GBS, Listeria, E coli
- Sepsis, pneumonia, meningitis
9
Q
Which organisms are common causes of late onset neonatal infection?
A
Staphylococcus aureus + coagulase -ve staph, Enterococcus, Klebsiella
10
Q
Describe the features of GBS organisms
A
- Gram +ve cocci
- Catalase -ve
- B haemolytic
- Lancefield Group B
11
Q
A 2 day old baby is brought to A&E with a fever, lethargy and poor feeding. The blood culture is positive for Listeria. What other investigations are needed?
A
LP. This is necessary when there are positive blood cultures of GBS, Listeria, and E coli
12
Q
What is the first line antibiotic treatment for early onset neonatal sepsis?
A
Benzylpenicillin + gentamicin, amoxicillin if Listeria present
13
Q
Name some common childhood infections
A
- Usually viral eg. RSV, EBV, CMV, HSV, VZV
- URTI very common
- UTIs common
- Also bacterial pneumonia eg. Strep pneumonia and Haemophilus influenzae
14
Q
Which organisms commonly cause bacterial meningitis in children?
A
In all children:
- Neisseria meningitidis (esp Men B)
- Streptococcus pneumoniae
- Haemophilus influenzae
In neonates: also GBS, E coli, Listeria
15
Q
Describe the characteristics of Streptococcus pneumoniae
A
- Gram +ve diplococci in chains
- A haemolytic
- Optochin sensitive
16
Q
Which medium is best for culturing Haemophilus influenzae?
A
Chocolate agar
17
Q
What type of vaccine against pneumococcus is given to children?
A
Conjugated vaccine. This is effective in children under 2 years of age. Name is Prevenar
18
Q
What are the common pathogens causing respiratory infection in children? What are the treatments?
A
- Viruses!!! eg. RSV. Usually conservative
- Streptococcus pneumoniae: amoxicillin
- Mycoplasma pneumoniae (in older children): azithromycin
19
Q
Describe the presentation of mycoplasma pneumoniae
A
- Outbreaks occur every 3-4 years
- Asymptomatic or non-specific: fever, dry cough, headache, myalgia
- Can also have haemolysis or neurological features
20
Q
What are the haematological features of mycoplasma pneumoniae infection?
A
- IgM antibodies to the I antigen on RBCs
- Cold agglutination
21
Q
Describe some features of HIV infection in children (vertically acquired)
A
- Chronic parotid swelling
- Recurrent/chronic molluscum
- Lymphadenopathy
- Dental + oral problems: caries, gingivitis, thrush
- Encephalopathy
- Shingles
- Failure to thrive
22
Q
What are the risk factors for HIV transmission during pregnancy?
A
- New infection (viraemia)
- HCV coinfection
- Vaginal delivery
- Breastfeeding
- Placental infection/inflammation eg. malaria
23
Q
How can we prevent vertical HIV transmission?
A
- Reduce rates of HIV in mothers pre-pregnancy (contraception, treatment)
- Prevent malaria infection
- C section if high viral load (>50 copies/ml)
- No breastfeeding unless high rate of childhood mortality due to diarrhoeal disease
- Triple ARVs during pregnancy and breastfeeding
- ART to neonates for 4-6 weeks
24
Q
What is IRIS (in the context of HIV)?
A
- Immune reconstitution inflammatory syndrome
- When you treat the HIV, T cell count improves and responds to coexisting infections and creates a huge inflammatory response
- This can cause significant clinical illness
25
Define pneumonia. How does it present?
Inflammation of the lung alveoli
- Fever, productive cough w/ purulent sputum, SOB, chest pain, severe respiratory distress (hypoxia, cyanosis, tachypnoea)
- Raised WCC and acute phase proteins (CRP)
- Consolidation on CXR
26
What are some pathogens that commonly cause community acquired pneumonia? HAP?
CAP:
- Streptococcus pneumoniae
- Haemophilus influenzae
- Klebsiella pneumonia
- Atypicals: mycoplasma pneumo, Legionella, Chlamydia, Coxiella
- Children: also viruses eg. RSV, influenzae
HAP:
- Pseudomonas aeruginosa
- Klebsiella pneumonia
- Staphylococcus aureus
27
What scoring system is used for assessing the severity of pneumonia? Describe.
```
CURB 65:
Confusion (Y/N)
Urea >7
Resp rate >30
BP <90 systolic
>65
```
2+: consider admission
2-5: severe pneumonia
28
Define bronchitis. How does it present?
Inflammation of the medium size airways (bronchi)
| -Fever, cough, SOB is important factor, sputum
29
Which organisms cause bronchitis?
- Viruses common
| - Bacteria: Strep pneumo, HiB
30
Which organisms can cause cavitating lung lesions?
- Staph aureus!
- Klebsiella
- TB
- +/- HiB
31
Describe the characteristics of haemophilus influenzae
- Gram -ve coccobacillus
- Facultative anaerobe
- Grows best on chocolate agar
- Can produce beta-lactamase
- Commonly infects lungs with pre-existing disease eg. smoking, COPD
32
Describe the characteristics of legionella pneumoniae infection (transmission, presentation, diagnosis, treatment)
- Transmitted through infected water droplets (consider aircon, pools/hot-tubs, etc)
- Flu-like prodrome, cough and fever
- Multi-organ involvement: confusion, abdo pain + diarrhoea, hyponatraemia, hepatitis
- Diagnosis: urinary antigens
- Treatment: macrolides (erythro, clarithro)
33
Describe the treatment for atypical pneumonia. Why is this different?
Antibiotics: macrolides + tetracyclines
| -Atypicals do not have cell walls, therefore penicillins are ineffective to treat
34
What medium is Legionella best cultured on?
Buffered charcoal yeast extract
35
Coxiella usually comes from ___. Chlamydia psitacci comes from ___.
Domesticated farm animals eg. aerosol/milk
| Birds
36
Describe the characteristics of Mycoplasma pneumonia infection (presentation, diagnosis, treatment)
- Usually comes around every 3-4 years in outbreaks, esp. schools/unis
- Dry cough, arthralgia, erythema multiforme
- Cold agglutination test
- Treatment with tetracyclines
37
A 60 year old woman is treated for pneumonia. Name some causes of failure to improve on treatment
- Empyema
- Wrong cover eg. atypical organism
- Antibiotic resistance
- Immunodeficiency
38
Describe the presentation of tuberculosis. What is the appearance on CXR? Diagnosis?
- Travel history, high risk area, positive TB contacts
- Prolonged fever, cough, haemoptysis, weight loss, night sweats
- CXR: upper lobe cavitation, lymphadenopathy (Ghon focus= lymph node + primary lesion), miliary TB
- Diagnosis: sputum sample for Ziehl-Neelson stain (AFB appear as red rods), auramine stain, culture for sensitivity
39
Define hospital acquired pneumonia. What are the common organisms? How should it be diagnosed?
Pneumonia developed >48 hours after admission to hospital. Can include VAPs
- Enterobacteriaciae: E coli, Klebsiella
- S aureus
- Pseudomonas
- Acinetobacter baumanii
Get sputum sample from bronchoalveolar lavage
40
Describe the presentation of PCP. What is the diagnosis + treatment?
Pneumocystitis jirovecii pneumonia:
-SOB key feature (insidious onset- worsening)
-Dry cough
-Weight loss
-Bat wing shadowing on CXR
Diagnosed with BAL -> immunofluorescence, silver stain (Grocott-Gomori) shows cysts.
Treat with Septrin (co-trimoxazole)
41
Respiratory tract infections
HIV is a RF for:
Neutropenia is a RF for:
Splenectomy is a RF for:
- HIV: TB, PCP, cryptococcus neoformans
- Neutropenia: fungal (Aspergillus)
- Splenectomy: encapsulated bacteria (S. pneumo, HiB, NMen)
42
Describe the antibiotic treatment of CAPs and HAPs
CAPs:
- Mild/mod: target Gram +ves eg. amoxicillin or macrolide if allergic for 5-7 days
- Mod-severe: cover gram+ves and atypicals with amoxicillin + macrolide (co amox + clarithro) for 2-3 weeks
HAPs: cover everything including good gram-ve
- 1st: ciprofloxacin +/- vancomycin
- 2nd line: Tazocin (pip + tazobactam) + vanc.
43
Which GI infections are notifiable?
- Campylobacter
- Salmonella
- Shigella
- Cholera
- Norovirus
- Listeria
- E coli O157
44
What are the different groups of presentations of GI infection? Broadly speaking what is the pathophysiology of each? What organisms cause each type?
- Febrile diarrhoeal (Inflammatory diarrhoea): caused by exudative inflammation of the bowel. Campylobacter, Shigella, non-typhoid Salmonella, EIEC
- Non-febrile diarrhoeal (Secretory diarrhoea): caused by toxins + dehydration. Cholera, ETEC, EPEC, EHEC
- Febrile, non-diarrhoeal (Enteric fever): caused by interstitial inflammation. Typhoid Salmonella, Yersinia, Brucella
45
Describe the pathophysiology of Cholera infection
- Cholera toxin causes chloride channels to open, causing water to move into the bowel lumen
- Causes ricewater stools and rapid dehydration
46
Name some pathogens that cause rapid-onset diarrhoeal illness
- Staph aureus
- Bacillus cereus
- Salmonella
47
Describe the characteristics of Staphylococcus aureus
- Gram +ve cocci in clusters/tetrads
- Coagulase +ve, catalase +ve
- Forms yellow colonies on blood agar
- Protein A is the main virulence factor
48
Describe the diarrhoeal illness caused by Staph aureus
- Produces enterotoxin that causes rapid-onset secretory diarrhoea and vomiting
- Self-limiting, lasts about 1 day
- Supportive treatment only
49
Describe the characteristics of Bacillus cereus and the infection it causes.
- Gram +ve rod, forms spores
- Typically occurs after eating reheated rice
- Produces toxins (heat stable emetic toxin, heat labile diarrhoeal toxin) that causes food poisoning eg. rapid-onset secretory diarrhoea and vomiting
- Self limiting
50
Name the types of Clostridium and describe the GI infections they cause (transmission, presentation, treatment).
- Gram +ve rods
- Botulinim: produces botulinum toxin -> descending paralysis. Found in cans, honey, formula powder. Treat with antitoxin.
- Perfringens: causes food poisoning from reheated meat. Rapid-onset secretory diarrhoea + cramps.
- Difficile: causes pseudomembranous colitis. After antibiotics treatment (HAI) with 3 C's: cipro, cephalosporin, clindamycin. Treat with metronidazole +/- vanc, stop causative antibiotics.
51
What are the 3 antibiotics that commonly cause C difficile?
Ciprofloxacin
Clindamycin
Cephalosporins
52
Describe the characteristics of Listeria and GI infection with Listeria. What is the treatment?
- Gram +ve V/L shaped rod
- B haemolytic
- Aesculin +ve, tumbling motility
- Found in refrigerated food, unpasteurised cheese
- Causes inflammatory diarrhoea: watery diarrhoea, cramps, fever, vomiting, headache
- Treatment: ampicillin/amoxicillin, ceftriaxone
53
Describe the characteristics of Enterobacteria. What are the different types that cause GI infection?
- Facultative anaerobes
- Glucose/lactose fermenters
- Oxidase negative
Mainly E coli species
-ETEC: toxigenic, causes travellers diarrhoea. Heat labile toxin (stimulates adenyl cyclase) and heat stable (stim guanyl cyclase). Acts on jejunum + ileum
-EIEC: invasive. Dysentery.
-EPEC: paediatric
-EHEC: haemorrhagic. Has verotoxin. O157:H7 can can HUS
Avoid antibiotic treatment. Supportive management
54
Describe the characteristics of Salmonella and the infections they cause.
- Gram -ve rods
- Non-lactose fermenters
- H2S producers (form black colonies)
- Culture on TSI agar, XLD agar, Selenite F broth
- Have different antigens to differentiate types including O (cell wall), H (flagellar), Vi (capsule)
Typhi/paratyphi: cause enteric fever. Multiply in Peyer's patches -> fever, constipation, splenomegaly, rose spots, anaemia. Positive blood cultures. Treat with cef/cipro
Enteritides: causes inflammatory diarrhoea (no blood). From poultry, eggs, meat. Self limiting, supportive treatment.
55
Describe the characteristics of Shigella and the infection it causes.
- Gram -ve rods
- Non-lactose fermenters (as opposed to E coli)
- Non-motile, non-H2S producing
- Also has antigens: O (cell wall), polysaccharide (A-D, best for differentiating)
- Shigella flexneri affects MSMs
- Most effective bacterial enteric pathogen (low number infective dose)
- Causes dysentery w/ blood and mucus, produces Shiga toxin.
- Do not give antibiotics
56
Describe the characteristics of Vibrios and the infections they cause
-Gram -ve, comma shaped
-Late lactose fermenter
-Oxidase +ve
Cholera: O1 group causes epidemics, non-O1 small outbreaks usually from contaminated shellfish. Cause ricewater stools from toxin production.
Parahaemolyticus: from raw seafood. Self limiting diarrhoea for 3 days.
Vulnificus: causes cellulitis from shellfish cuts. VERY bad in HIV +ve -> fatal sepsis.
57
Describe the characteristics of Campylobacter and the infection it causes
- Gram -ve, comma shaped
- Microaerophilic
- Oxidase +ve
- From contaminated food/water. Causes inflammatory diarrhoea, self limiting but can last long time. Treat with azithromycin if immunocompromised.
- Associated with Guillain-Barre and reactive arthritis
58
Describe the characteristics of Yersinia and the infection it causes
- Gram -ve
- Non-lactose fermenter
- Likes cold environments
- Causes enterocolitis (febrile non-diarrhoea), mesenteric adenitis
59
Describe infection with Entamoeba histolytica
- Protozoa: trophozoite/cyst, 4 nuclei
- Flask-shaped ulcers in colon
- Causes diarrhoea, wind, tenesmus, weight loss, RUQ pain (abscess)
- Do stool microscopy (wet mount)
- Treatment: metronidazole +/- paromomycin
60
Describe Giardia infection
- Protozoa, pear-shaped trophozoite.
- 2 nuclei, 4 flagella, suction disk
- Attaches to the duodenum and causes malabsorption -> bad smelling diarrhoea, cramping, lots of wind
- Dx: stool microscopy, string test (swallow string and pull back up)
- Treatment: metronidazole
61
Kinyoun acid fast stain identifies:
Cryptosporidium parvum
| Causes severe diarrhoea in immunocompromised
62
Name the viruses that commonly cause diarrhoea. What are the characteristics of each?
- Norovirus: highly contagious. Diarrhoea and vomiting.
- Rotavirus: affects children. Secretory diarrhoea, with 2x infection leading to immunity
- Poliovirus, enterovirus, Hep A, adenovirus
63
What vaccines against pathogens causing GI infections exist?
- Rotavirus (routine vaccination)
- Cholera
- Salmonella typhi
- Campylobacter
64
Name some bacteria that commonly cause UTI and describe their features
- E coli: Most common. Adhere with p fimbriae
- Proteus: associated with struvite stones
- Staphylococcus saprophyticus: young women
- Klebsiella, Pseudomonas: associated with structural abnormalities and recurrent UTI
65
Name some risk factors for UTI. What is the presentation?
RFs: sex, female, catheter, elderly, incontinent, structural abnormalities
Presentation: dysuria, frequency, urgency, nocturia, smelly/cloudy urine, fever, flank pain, rigors, sepsis, confusion, incontinence
66
How is UTI formally diagnosed?
>10 ^5 cfu/ml is diagnostic of infection/bacteriuria
+ symptoms -> UTI
In practice: symptoms + positive urine dip -> treat
67
What is sterile pyuria? What are some causes?
- Presence of white cells in urine but no growth (MC&S)
| - Caused by STI, stones, tumours, TB
68
Describe the culture part of a urine MC&S
- Use chromogenic agar -> specific colours depending on the organism
- Pink: E coli
- Blue: other coliforms
69
What is a common antibiotic regime used in pyelonephritis
- Broad spectrum PO/IV antibiotics
| - Co-amoxiclav +/- gentamicin
70
What are the different sites of antibiotic action?
Cell well
Ribosome/protein synthesis
DNA/RNA synthesis
Other
71
What are some different antibiotics that inhibit cell wall synthesis? Name some examples of each
Beta lactams: penicillins, cephalosporins, carbapenems
| Glycopeptides: vancomycin, teicoplanin
72
How do beta lactams work? Are they bactericidal or bacteriostatic?
Inhibit transpeptidase PBP (penicillin binding protein), prevent crosslinking of peptidoglycan -> weak cell wall
Bactericidal- only works on rapidly dividing bacteria
73
Which bacteria are sensitive to beta lactams and glycopeptides and why?
Mostly Gram +ve, some have broader action against gram -ve. They have an outer peptidoglycan cell wall compared to gram -ves which have peptidoglycan within the 2 membranes.
Not effective on Chlamydia, Mycoplasma- no peptido.
74
If a patient is allergic to penicillin, which other antibiotics may they be allergic to?
5% chance of allergy to cephalosporins, carbapenems- because they have the same beta-lactam ring.
75
What are some different penicillins, and which bacteria are they effective for?
Penicillin: gram+ve except beta-lactamase
Amoxicillin: broad spectrum- gram +ve, Enterococcus, gram -ve. Not beta-lactamase
Flucloxacillin: gram +ve including beta-lactamase
Piperacillin: broad spectrum. Also Pseudomonas.
76
Which additional agents can be given with beta-lactams to increase their efficacy? What do they do?
Clavulanic acid and Tazobactam eg. Co-amoxiclav, Tazocin
-Inhibit beta-lactamase, increase susceptibility
Increase coverage to broad-spectrum including anaerobes and beta-lactamases
77
What are some types of cephalosporins and which bacteria are they effective for and not effective for?
Cefalexin: UTIs
Cefuroxime: similar to co-amoxiclav eg. gram +
Ceftriaxone (3rd gen): Broad spectrum- gram+ and gram -
Ceftazidime: good for Pseudomonas
Not for anaerobes or ESBL (eg E coli)
78
What are some types of carbopenems and which bacteria are they effective for?
Meropenem
Ertapenem
Broad spectrum: gram +, gram -, ESBLs
79
What are some glycopeptides, which bacteria are they effective against and why?
Vancomycin, teicoplanin
Active against gram + because can't cross gram - outer membrane
Especially for MRSA
80
Name some classes of antibiotics that inhibit protein synthesis and give examples
```
Aminoglycosides: gentamicin, amikacin
Macrolides: erythromycin, azithromycin
Tetracyclines: doxycycline
Chloramphenicol
Oxazolidinones: linezolid
```
81
Describe the MoA of aminoglycosides. Which bacteria are they effective against?
Bind to the 30S ribosome subunit and inhibit protein synthesis.
Broad spectrum: esp gram - and Pseudomonas. Synergistic with beta-lactams
82
Describe the MoA of tetracyclines. Which bacteria are they effective against?
Bind to the 30S subunit and inhibit protein synthesis.
| Intracellular pathogens eg. chlamydia, mycoplasma. Not very good for gram -
83
Describe the MoA of macrolides. Which bacteria are they effective against?
Bind to 50S subunit and inhibit protein synthesis.
| Mild Staph/strep infection, Legionella, mycoplasma
84
Describe the MoA of chloramphenicol. Which bacteria is it effective against?
Bind to 50S subunit and inhibit protein synthesis.
| Broad spectrum but only really used as eye drops for conjunctivitis because aplastic anaemia + grey baby syndrome
85
Describe the MoA of oxazolidinones. Which bacteria are they effective against?
Bind to the 23S of 50S ribosome subunit.
| Gram + cover including MRSA and VRE, not gram -
86
Name some classes of antibiotics that inhibit DNA synthesis and give examples
Fluoroquinolones: ciprofloxacin, levofloxacin
Nitroimidazoles: metronidazole
87
Describe the MoA of fluoroquinolones. Which bacteria are they effective against?
Inhibits DNA gyrase.
Broad spectrum especially gram - and Pseudomonas. Levo is good for gram +
eg. UTIs, atypical pneumonia
88
Describe the MoA of nitroimidazoles. Which bacteria are they effective against?
Cause DNA strand breakage in anaerobic conditions
| Good for anaerobes and protozoa eg. BV, Giardia
89
What is the MoA of rifampicin. Which bacteria is it effective against?
Inhibits RNA polymerase.
| Effective for Mycobacterium and chlamydia
90
What is important to be aware of when using rifampicin?
Monitor LFTs
May interact with other medications due to enzyme inhibition
Can cause orange secretions
91
Name some cell membrane toxins. Which bacteria are they effective against?
Daptomycin: gram + eg MRSA and VRE
Colistin: gram - including Pseudomonas, Klebsiella, Acinetobacter. Toxic- only used for multidrug resistant.
92
What is the MoA of sulphonamides? Which bacteria are they effective against?
Folate metabolism inhibitors.
| Usually combined with trimethoprim eg. co-trimoxazole (Septrin) for PCP
93
What are the different mechanisms of resistance? Give some examples
Inactivation eg. beta-lactamase
Altered target eg. MRSA (changed PBP structure)
Reduced accumulation/efflux
Bypass normal pathways eg. folate inhibitors
94
Which bacteria are beta-lactamases?
Staph aureus, E coli
95
T/F. MRSA is a beta-lactamase
False. It has altered target site
96
What do ESBLs have resistance to?
Cephalosporins and penicillins
| eg. E coli, Klebsiella
97
Which bacteria are carbapenamases?
Enterobactericiae eg. Klebsiella and E coli
98
Which factors need to be taken into account when choosing antibiotics to prescribe?
Host characteristics (age, pregnancy, renal impairment)
Antimicrobial susceptibility (sensitivity testing)
Organism
Site (eg bone, CNS)
99
When would you want to give IV antibiotics?
If there is bone or CNS infection
| If there is sepsis - poor GI perfusion = poor absorption
100
What is the MIC?
Minimum inhibitory concentration: the smallest amount of antibiotic needed to inhibit growth in the lab eg sensitivity
101
What are the key pharmacokinetic factors when using aminoglycosides?
Reaching a high peak concentration -> eg. 1 big dose
| Need to measure the trough concentration to make sure there is elimination (adjust frequency)
102
What are the key pharmacokinetic factors when using carbapenems and cephalosporins?
Having the longest time above the MIC -> frequent dosing
103
What is the Eagle effect?
Bactericidal drugs only work when bacteria are rapidly dividing. When bacterial load is high, there are relatively static, so drugs have no effect
104
Which antibiotics are used in hospital acquired UTI?
Cephalexin or co-amoxiclav
105
What are some ways to minimise surgical site infections?
Pre-op: shower with soap, eradication of S aureus if nasal carriage, antibiotics
Intra-op: ventilation, sterile instruments, skin prep, oxygenation
106
Which organisms commonly cause septic arthritis?
S aureus, Streptococcus, E coli
107
Which organisms commonly cause osteomyelitis?
S aureus, Streptococcus, E coli, Salmonella, TB
108
Which organisms commonly cause prosthetic joint infection?
Usually coagulase negative Staph (eg. not aureus)
| Strep, E coli
109
What is herd immunity? How is the threshold calculated?
Herd immunity is the idea that if enough people in the population are immune to infection, the infection will not transmit among the population.
1-1/R eg. the higher the R, the more people must be vaccinated to have herd immunity
110
What is needed for disease eradication?
- No animal reservoir
- No latency
- Effective vaccine/treatment
- Stable pathogen
111
Name some big pandemic flus. Why do these occur?
1918 Spanish Flu
Asian Flu and Hong Kong Flu in 50s and 60s
Swine Flu 2009
Crossover from animal reservoir -> no human immunity exists
112
What is the natural reservoir for influenza? How does it spread to humans?
Wild fowl.
| Can cross into domestic fowl + pigs -> humans with mutations
113
What is the difference between seasonal flu and pandemic flu?
Seasonal flu is due to antigenic drift (same antigens just small mutations)
Pandemic flu is due to antigenic shift (new antigens, no immunity)
114
Why does influenza affect the lungs?
It requires specific proteases (tryptase) to cleave haemaglutinin from sialic acid in order to enter cells. These enzymes are found in the respiratory tract -> infection occurs there
115
How are influenza viruses named?
According to H and N genes
H: haemaglutinin. Required for entry into cells by binding sialic acid
N: neuraminidase. Required for release after budding.
116
How are viruses able to mutate?
If two viruses infect 1 cell at the same time, the genome may undergo reassortment -> mixing of genes
eg. new deadly virus + old virus with genes to increase transmission -> new deadly virus with increased trans.
117
What are some antiviral drugs used for influenza?
Oseltamivir (Tamiflu): neuraminidase inhibitor
| Baloxivir: polymerase inhibitor
118
How does SARS-CoV2 enter cells?
Binds to ACE2 on epithelial cells of the lungs
119
What type of viruses are the viral hepatitises? What is their transmission?
```
HAV: RNA. Faeco-oral- food + water, MSM
HBV: DNA. Blood, sex, vertical
HCV: RNA. Blood > sex, vertical
HDV: RNA. Blood- only with HBV
HEV: RNA. Faeco-oral
```
120
What is the presentation of Hepatitis A?
Short lived. May be non-specific
| Acute hepatitis: jaundice, RUQ pain, fever
121
What is the risk of developing chronic Hepatitis B infection?
Adults: 5-10%
| Young children: 95%
122
Describe the clinical course of Hepatitis B infection
Infection -> acute hepatitis. This is more likely to be symptomatic in adults
Most people will clear the virus and become seronegative
Some people (10% adults) will not clear the virus, and have chronic HBV infection. HBsAg + for >6 months
123
Describe the HBV serological tests
Several different antigens: HBsAg, HBeAg, HBcAg
Corresponding antibodies: eg anti-HBs
Acute infection:
- HBsAg +, HBeAg +/-
- anti-HBc + (IgM)
Previously infected: HBsAg -, anti-HBs +, anti-HBc (IgG) +
Chronically infected: HBsAg +, anti-HBs -, HBeAg +/-, anti-HBc (IgM) -ve
Vaccinated: HBsAg -, anti-HBs +
124
Interpret this hepatitis serology:
HBsAg-
anti-HBs +
This could mean either previous vaccination or previous infection. Not possible to differentiate
125
What are the consequences of chronic HepB/HepC?
Cirrhosis
| Hepatocellular carcinoma
126
What is the treatment for HepB? Who gets treatment?
```
Pegylated IFNa (less commonly used, poorly tolerated)
Nucleoside analogues eg tenofivir, entecavir
For individuals with high viral load, raised ALT, more severe disease
```
127
What proportion of individuals with HepC become chronically infected?
60-80%
128
What are the tests for HepC? Which is best for acute infection?
HCV RNA. Better for acute infection
| anti-HCV IgG. Rises after the acute infection
129
Interpret this hepatitis serology:
HCV RNA -
anti-HCV IgG +
Previous infection- cleared
130
What is the treatment for HepC? Who gets treatment?
NS3/4 protease inhibitor (-previrs) eg. boceprevir
NS5A inhibitor (-asvirs) eg daclatasvir
Also IFNa and Ribavirin
Give to everyone! High cure rate
131
What are the types of HepD infection?
Coinfection: eg HepD and HepB same time. Acute hepatitis with D, chronic with B
Superinfection: already HepB +, add HepD. Severe infection, worsening liver function + soon cirrhosis
132
What are some symptoms of HepE?
Acute hepatitis
Neuro eg. GBS, encephalitis
Renal eg. GN
133
What type of drug is aciclovir? What is the MoA?
Nucleoside analogue. Gets incorporated into DNA and prevents further elongation -> stops viral replication.
*It requires viral thymidine kinase to activate it, which is only found in infected cells -> selectivity toxicity
134
What is the treatment of VZV infection? Who should be treated?
Aciclovir or valaciclovir (pro-drug, only given PO)
-> foscarnet or cidofivir
Treatment for adults with VZV, shingles in >50s, immunocompromise, children with severe disease
135
What is the treatment of HSV?
Aciclovir- topical or systemic
136
Which cells does CMV establish latency in? HSV? EBV?
CMV: monocytes and dendritic cells
HSV: neurons
EBV: B lymphocytes
137
Who is susceptible to CMV infection? What are the consequences?
Immunosuppressed.
| Reactivation/primary infection can cause encephalitis, pneumonitis, BM suppression, retinitis etc
138
What is the treatment for CMV infection?
Ganciclovir (IV) or valganciclovir (prodrug, PO)
| -> foscarnet (in neutropenia), cidofivir
139
What is the presentation of BK virus?
Usually causes asymp primary infection but then causes chronic carriage in urinary tract
BMT + immunosuppression -> haemorrhagic cystitis, nephritis
140
Who is affected by severe adenovirus infection?
Paediatric transplant patients
141
What are the most common causative pathogens in acute meningitis? Which is most common?
Viral: most common. Coxsackie B + echovirus
Bacteria:
-Neisseria meningitidis (A, B, C): B+C most common.
-Streptococcus pneumoniae
-Haemophilus influenzae
142
What is the most common causative pathogen in chronic meningitis?
TB. In immunosuppressed patients
143
What are some causative pathogens of encephalitis? Which is most common?
```
Viral: many types
-HSV: most common
-Mumps, Measles
-West Nile virus
Bacterial: Listeria
Amoebic: Naegleria fowleri
Toxoplasmosis: immunosuppressed
```
144
What are some common causative pathogens of brain abscess?
S aureus
Streptococcus
Fungi: cryptococcus
Toxoplasmosis
145
Which investigations would you do in suspected meningitis/encephalitis?
Blood tests: FBC, CRP, VBG, culture
LP: MC&S, PCR
Throat swab (Strep), urinary antigens (Strep)
CT/MRI
146
What would you expect to see on LP in bacterial meningitis?
Turbid/purulent CSF
High WCC- polymorphs (100s)
Low glucose (0-2.2)
Normal protein (0.5-3.0)
147
What would you expect to see on LP in viral meningitis?
Clear CSF
High WCC- lymphocytes (15-500)
Normal glucose (Normal)
Normal protein (0.5-1.0)
148
What would you expect to see on LP in TB meningitis?
Clear CSF
High WCC- lymphocytes
Low glucose (0-2.2)
High protein (1.0-6.0)
149
What are prion diseases?
A group of diseases caused by protein-only infectious agent causing spongiform encephalopathy and rapid neurodegeneration and death
150
What is the pathophysiology of prion disease?
Prion enters the brain, triggers the transformation of existing prion protein (alpha-helix to beta-sheet). This is not possible to breakdown -> buildup
Spongiform vacuolisation
151
What are the different types of Prion disease?
Sporadic: Creutzfeldt-Jakob disease
Acquired: Kuru, Variant CJD
Genetic: GSS, FFI
152
Describe the presentation of sporadic CJD (clinical + Ix findings)
Occurs around 65 years. Very rare.
-Rapid dementia
-Myoclonus, cortical blindness, akinetic mutism, LMN signs
-Death within 6 months
Ix: EEG changes, MRI (increased BG signal), CSF (14-3-3 protein, S100), brain biopsy gold standard
153
Describe the presentation of variant CJD (clinical + Ix findings)
Occurs in younger people <30
-Psychiatric symptoms: dysphoria, anxiety, paranoia
-Neurological: ataxia, myoclonus, chorea, dementia
Ix: MRI (pulvinar sign), EEG non-specific, CSF negative, tonsillar biopsy while living- gold standard
154
What are some causes of iatrogenic CJD?
Cadaveric growth hormone, corneal transplant, blood transfusions, etc
155
How is familial prion disease diagnosed?
AD- usually a FHx of neuro
| Neurogenetics is key (mutation in PRNP)
156
What are the common causative pathogens of infective endocarditis? What are they associated with?
- Streptococcus viridans: most common cause subacute
- Staph epidermidis: prosthetic valves, IVDU
- Streptococcus bovis: colorectal cancer
- S aureus/Strep pyogenes: more acute onset, IVDU
- HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
157
How does infective endocarditis present?
- Fever, rigors
- Malaise
- New onset/changed murmur
- Anaemia
- Vascular phenomenon: Janeway lesions, splinter haemorrhages, stroke, septic abscess
- Immune phenomenon: Roth's spots, Osler's nodes, haematuria
158
What is the management of infective endocarditis?
MDT approach with surgeons, cardio, ID, micro
3 sets of cultures from different areas over 12 hours + other bloods and echo
IV ABx for ~6 weeks
-Empirical (prosthetic): vanc + gent + rifampicin
-Empirical (native): pen + gent or fluclox
-Strep viridans: benpen + gent
-MSSA: fluclox
-MRSA: vanc + gent
159
What are some groups of patients who are particularly susceptible to infections?
```
HIV
Transplant + immunosuppressed
Primary immunodeficiencies
Elderly and neonates
Pregnant women
Malnutrition
DM
IVDU
```
160
List the susceptibility to infection from most to least in the following:
Advanced HIV, post-BMT, use of DMARDS/steroids, chemotherapy
DMARDS/steroids
Chemo
Advanced HIV
Post-BMT
161
Name some important viruses in immunocompromised patients and some complications
```
CMV: retinitis, pneumonitis, colitis
EBV: post-transplant lymphoproliferative disease
HSV
VZV: encephalitis, pneumonitis
HPV: cervical cancer
HHV8: Kaposi's sarcoma
Adenovirus (paeds transplant)
```
162
How can opportunistic infections present in immunocompromised hosts?
Unusual pathogen eg. JC virus
Severe infection/different organs eg. CMV retinitis
Low fever or CRP
Frequent reactivation of infection eg HSV
163
After BMT, what is the order of virus-associated complications?
<1 month: HSV (reactivation)
>1 month: EBV, CMV, VZV (community-acquired)
Months-years: malignancy eg. Kaposi's
164
How are opportunistic infections screened for in immunocompromised patients?
In transplants: before transplant serology for everything
| Post: monitor for CMV, EBV, adenovirus in children
165
What is the basic classification of fungal infections? Name some examples
Yeasts: Candida, Cryptococcus, Histoplasma
Moulds: Aspergillus, Dermatophytes
166
Describe the features of Candida (microscopy, culture, etc).
- Purple oval cells, may see budding
| - Grows best on Sabourad agar -> cream coloured colonies
167
What types of infections are caused by Candida? In which patients do these occur?
Vulvovaginitis: common
Oral: immunosuppressed, use of inhaled steroids
Invasive: immunosuppressed
168
Describe the management of Candida infection
- Oral: topical nystatin
- Vulvovaginitis: topical clotrimazole
- Invasive: oral fluconazole (C albicans), amphotericin-B/echinocandins for others
169
How is cryptococcus transmitted? What kind of infections can it cause?
Inhaled aerosol (usually from pigeons, eucalyptus)
Lung disease, meningitis, systemic
Particularly affecting HIV patients
170
Describe the features of Cryptococcus neoformans
Encapsulated yeast in gelatinous matrix
| Stains with India Ink
171
What is the management of Cryptococcus?
Resistant to Echinocandins
- Amphotericin B (Ambisome) is mainstay for several weeks
- Prevent relapse wth fluconazole 8 weeks
172
What is the best way to diagnose cryptococcus?
Antigen test: serum/CSF
| Culture not as good
173
What are the different diseases caused by Aspergillus? Briefly describe.
Invasive Aspergillus: systemic infection
Pulmonary Aspergilloma: colonises cavity eg. previous TB
Allergic bronchopulmonary aspergillosis: obstructive airway disease due to allergic response
174
What are the types of Aspergillus? Describe characteristics. How is it diagnosed?
Flavus, fumigatus
Mould, spore-forming
Dx: sputum MC&S + antigen screen (galactomannan), CXR, histology
175
What is the treatment of Aspergillus infection?
Amphotericin B, voriconazole
176
What are some types of dermatophyte infection? What are the causative organisms? How are they treated?
-Tinea pedis: Trichophyton rubrum
-Tinea corporis (ringworm): Trich.
-Onychomycosis: Trich.
-Pityriasis versicolor: Malassezia furfur
Tx: topical/oral azoles
177
Orbital cellulitis can be caused by which fungal infection? Who is typically affected? How does it present?
Mucorales: causes Mucormycoses
Typically in DM and other immunocomp.
Cellulitis with black pus
178
Which fungus classically causes pneumonia in HIV patients? How does it present? How is it diagnosed? What is treatment?
Pneumocystis jirovecii
Causes pneumonia with dry cough and desaturation on exercise, bilateral patchy shadows
Dx: CXR, BAL for MC&S, PCR
Mx: co-trimoxazole (Septrin)
179
What are some targets of antifungal drugs? Give some examples of different classes
- Cell membrane- inhibit ergosterol production: -azoles (fluconazole), polyenes (amphotericin B)
- Cell wall: echinocandins (Caspofungin, anidulafungin)
- DNA synthesis: flucytosine
180
Describe the MoA of azoles. What are the side effects?
-Bind lanosterol 14a-demethylase
-Inhibit ergosterol production
-Prevent cell membrane formation
SEs: drug interactions (p450), steroidogenesis inhibition (eg cortisol)
181
Describe the MoA of echinocandins. What are they used for?
-Inhibit B-D-glycan synthase
-Prevent cell wall synthesis
Uses: Candida species, Aspergillus
182
What are the different types of Mycobacterium?
-M tuberculosis
Non-tuberculous:
-M avian complex (MAC): includes avian, intracellulare
-M abscessus complex
183
Describe the characteristics of mycobacterium
- Nonmotile rods
- Slow-growing
- Complex cell wall: mycolic acids, waxes, etc
- Stain with auramine, Ziehl-Nielsson
184
What are the features of non-TB mycobacterium? What are some types and what infections are they associated with?
Everywhere in the environment
Don't spread person-to-person
Resistant to anti-TB drugs
-M avian complex: abnormal lungs (cavity), HIV (causes disseminated infection)
-M marinarum: from pools -> skin granulomas
-M ulcerans: causes skin lesions (Buruli ulcer)
-M leprae: Leprosy/Hansen's disease
185
Describe the clinical course of TB infection
- Primary infection: Ghon focus (granuloma + lymph node)
- Usually cleared by the immune system, becomes latent
- May reactivate later as post-primary TB. Can be pulmonary or extra-pulmonary
186
How is TB diagnosed?
CXR
Sputum sample x3 for stain (ZN), culture of Lowenstein-Jensen medium for 6 weeks (gold standard)
+/- BAL
Histology
187
What is the classic histological finding in TB?
Caseating granuloma
188
Which tests can be used for investigation of latent TB infection?
IGRA
| Tuberculin skin test
189
Describe the management of TB infection. What are the side effects?
RIPE x2 months
RI x 4 more months
Rifampicin: drug interaction, orange secretions
Isoniazid: peripheral neuropathy. Give pyridoxone
Pyrazinamide: hepatic toxicity
Ethambutol: visual disturbance
190
What are zoonoses? What are some methods of transmission?
Diseases that pass from animals to humans
- Direct human + animal contact eg farming, animal scratches/bites
- Contact with faeces
- Contaminated foods eg milk
191
How are zoonoses classified? Give some examples
UK vs tropical, farm/wild vs companion
- UK, farm: Campylobacter, Salmonella
- UK, companion: Toxoplasmosis, Bartonella, ringworm
- Tropical, farm: Brucella, Coxiella
- Tropical, companion: rabies
192
Where does Bartonella come from? How does infection present? What is the treatment?
Bartonella henselae: cats, fleas
- Cat scratch disease: macule -> pustule, adenopathy, fever, sweats
- Bacillary angiomatosis: papules, disseminated disease with multiorgan involvement
- Mx: doxycycline/erythromycin. Rifampicin in severe
193
What type of organism is toxoplasma gondii? How does toxoplasmosis present? What is the management?
Parasite
Fever and adenopathy. Abscess + seizures in immunocompromised.
Congenital: chorioretinitis, microcephaly, cerebral calcification
Mx: spiramycin OR pyrimethamine + sulfadiazine.
194
Where does Brucella come from? How does infection present and what can it be confused with? What is the treatment?
Farm animals eg. cows, goats
Transmitted in unpasteurised dairy
FLAWS, back pain, orchitis, abscess -> basically TB
Mx: doxy + gent/rifampicin
195
Where does Coxiella come from? What is the name for the disease it causes and how does it present? What is the treatment?
Farm animals: goats, cattle, sheep
Transmitted in unpasteurised milk
Causes Q fever: fever, flu, pneumonia
Mx: doxy
196
What type of organism causes Rabies? How does it present? What is the management?
Caused by Lyssa virus
Seizures, salivation, agitation, confusion, fever
Mx: must be treated with vaccination before onset of neuro symptoms (test for IgM first)
197
What type of organism causes Rat bite fever? How does it present?
Strep moniliformis, Spirillulin minus
| Fever, arthralgia, rash
198
What are some types of viral haemorrhagic fever?
Ebola, Marburg, Lassa
199
How is leptospirrosis contracted? How does it present?
Through broken skin/swimming in infected water
| High fever, headache, jaundice, myalgia, meningism, carditis, renal failure etc
200
What type of organism causes Lyme disease? How does it present? What is the treatment?
Borrelia burgdorferi- spirochaete bacteria
Erythema migrans, cyclical fever, flu-like symptoms, arthritis, etc
Mx: doxycycline
201
Describe the life cycle of tape worms
1) Eggs ingested by pigs/cows
2) Eggs hatch into larvae -> burrow into flesh -> cyst
3) Humans eat meat -> cyst develop into mature worms in GI tract
202
What is the treatment of tapeworms?
Praziquantel
203
Describe the life cycle of schistosomiasis
- Cercariae in contaminated water invade into tissues
- Larvae move through circulation into lungs -> liver
- Mature in liver and migrate to bowel -> lay eggs
- Eggs excreted in faeces
- Eggs parasitise snails
204
How is filariasis contracted?
Through mosquito/blackfly bites -> larvae enter body
205
What is cysticercosis? How does it present?
Invasion of tissues by Taenia solium larvae (only pig worms, not beef/fish)
Symptoms are often from CNS invasion - seizures, headaches, blindness, etc
206
Name some diseases transmitted by mosquitos
```
Malaria
Dengue
West Nile Virus
Yellow Fever
Zika virus
```
207
What is the vector for malaria? What organism causes malaria?
Anopheles mosquito
| Caused by protozoa: Plasmodium falciparum, P vivax, P ovale, P malariae
208
Describe the life cycle of Plasmodium
- Human bitten by Anopheles mosquito -> sporozoites enters bloodstream
- Moves to the liver where it resides in hepatocytes -> rupture releases merozoites
- Infects erythrocytes, exists as trophozoite -> haemolysis releases gametocytes
- Bitten by Anopheles, gametocytes ingested
* *Hypnozoites can remain in the liver for years in P vivax and ovale
209
Describe the presentation of malaria
- Malaria paroxysms: fevers, chills, rigors, sweats
- Jaundice, anaemia, low platelets
- Severe: parasitaemia, CNS involvement, renal failure, ARDS, circulatory collapse, metabolic acidosis
210
What are the investigations for malaria? What are they used for/what do they show?
FBC, LFTs, U+Es- anaemia, raised LFTs etc
Thick and thin blood film x3 with Giemsa stain
-Thick: screen for parasites
-Thin: species, quantify parasitaemia
Rapid antigen test
211
What is the treatment for malaria?
Falciparum:
-Mild: malarone, riamet (artemisinin combo therapy)
-Severe: IV artesunate > quinine
Non-falciparum: chloroquine, primaquine (good for hypnozoite stage)
212
What is considered severe falciparum malaria?
>2% parasitaemia
213
How is Dengue transmitted? Where is it commonly found?
Aedes mosquito bites
| SE Asia
214
What are the features of Dengue fever? What are the complications?
```
Headache
Myalgia
Rash
Fever
Hepatitis
Reinfection with different serotype -> Dengue haemorrhagic fever
```
215
What are the features of typhoid fever?
```
Fever
Constipation > diarrhoea
Rose spots
Dry cough
Headache
```
216
What are the symptoms of rubella infection?
Usually asymptomatic or mild
- Lymphadenopathy
- Macular rash
- Fever
217
What are the causes of congenital CMV infection?
- Primary infection
| - Reactivation of latent infection
218
How does congenital CMV infection present?
```
Sensorineural hearing loss
Chorioretinitis
Microcephaly
Hepatitis, jaundice
Rash
```
219
How is congenital infection diagnosed?
Detection of pathogen within 21 days of birth/prenatal diagnosis eg amnio and PCR
220
When is the fetus and neonate most susceptible to congenital VZV infection?
13-20 weeks
| Neonate: maternal infection between 7 days prior to and 7 days post delivery
221
When is the fetus most susceptible to parvovirus B19 infection?
Before 20 weeks
222
How is C difficule infection confirmed?
Stool toxin assay
