Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are the TORCH infections?

A 
Toxoplasmosis
Other: syphilis, HIV, HBV, VZV
Rubella
CMV
HSV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the signs + symptoms of toxoplasmosis in neonates?

A
  • Chorioretinitis
  • Cerebral calcification -> Low IQ, seizures
  • Microcephaly
  • Deafness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can HSV affect the neonate?

A
  • Eyes/skin
  • Encephalitis
  • Disseminated infection eg. hepatitis, pneumonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which organisms are common causes of late onset neonatal infection?

A

Staphylococcus aureus + coagulase -ve staph, Enterococcus, Klebsiella

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

Describe the features of GBS organisms

A
  • Gram +ve cocci
  • Catalase -ve
  • B haemolytic
  • Lancefield Group B
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the first line antibiotic treatment for early onset neonatal sepsis?

A

Benzylpenicillin + gentamicin, amoxicillin if Listeria present

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

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

Describe the characteristics of Streptococcus pneumoniae

A
  • Gram +ve diplococci in chains
  • A haemolytic
  • Optochin sensitive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which medium is best for culturing Haemophilus influenzae?

A

Chocolate agar

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

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

What are the haematological features of mycoplasma pneumoniae infection?

A
  • IgM antibodies to the I antigen on RBCs

- Cold agglutination

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

Define pneumonia. How does it present?

A

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

What are some pathogens that commonly cause community acquired pneumonia? HAP?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What scoring system is used for assessing the severity of pneumonia? Describe.

A 
CURB 65:
Confusion (Y/N)
Urea >7
Resp rate >30
BP <90 systolic
>65

2+: consider admission
2-5: severe pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Define bronchitis. How does it present?

A

Inflammation of the medium size airways (bronchi)

-Fever, cough, SOB is important factor, sputum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which organisms cause bronchitis?

A
  • Viruses common

- Bacteria: Strep pneumo, HiB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which organisms can cause cavitating lung lesions?

A
  • Staph aureus!
  • Klebsiella
  • TB
  • +/- HiB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the characteristics of haemophilus influenzae

A
  • Gram -ve coccobacillus
  • Facultative anaerobe
  • Grows best on chocolate agar
  • Can produce beta-lactamase
  • Commonly infects lungs with pre-existing disease eg. smoking, COPD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the characteristics of legionella pneumoniae infection (transmission, presentation, diagnosis, treatment)

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the treatment for atypical pneumonia. Why is this different?

A

Antibiotics: macrolides + tetracyclines

-Atypicals do not have cell walls, therefore penicillins are ineffective to treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What medium is Legionella best cultured on?

A

Buffered charcoal yeast extract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Coxiella usually comes from ___. Chlamydia psitacci comes from ___.

A

Domesticated farm animals eg. aerosol/milk

Birds

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

Describe the characteristics of Mycoplasma pneumonia infection (presentation, diagnosis, treatment)

A
  • Usually comes around every 3-4 years in outbreaks, esp. schools/unis
  • Dry cough, arthralgia, erythema multiforme
  • Cold agglutination test
  • Treatment with tetracyclines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

A 60 year old woman is treated for pneumonia. Name some causes of failure to improve on treatment

A
  • Empyema
  • Wrong cover eg. atypical organism
  • Antibiotic resistance
  • Immunodeficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the presentation of tuberculosis. What is the appearance on CXR? Diagnosis?

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

Define hospital acquired pneumonia. What are the common organisms? How should it be diagnosed?

A

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

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

Describe the presentation of PCP. What is the diagnosis + treatment?

A

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)

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

Respiratory tract infections
HIV is a RF for:
Neutropenia is a RF for:
Splenectomy is a RF for:

A
  • HIV: TB, PCP, cryptococcus neoformans
  • Neutropenia: fungal (Aspergillus)
  • Splenectomy: encapsulated bacteria (S. pneumo, HiB, NMen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the antibiotic treatment of CAPs and HAPs

A

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

Which GI infections are notifiable?

A
  • Campylobacter
  • Salmonella
  • Shigella
  • Cholera
  • Norovirus
  • Listeria
  • E coli O157
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the different groups of presentations of GI infection? Broadly speaking what is the pathophysiology of each? What organisms cause each type?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the pathophysiology of Cholera infection

A
  • Cholera toxin causes chloride channels to open, causing water to move into the bowel lumen
  • Causes ricewater stools and rapid dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Name some pathogens that cause rapid-onset diarrhoeal illness

A
  • Staph aureus
  • Bacillus cereus
  • Salmonella
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe the characteristics of Staphylococcus aureus

A
  • Gram +ve cocci in clusters/tetrads
  • Coagulase +ve, catalase +ve
  • Forms yellow colonies on blood agar
  • Protein A is the main virulence factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe the diarrhoeal illness caused by Staph aureus

A
  • Produces enterotoxin that causes rapid-onset secretory diarrhoea and vomiting
  • Self-limiting, lasts about 1 day
  • Supportive treatment only
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the characteristics of Bacillus cereus and the infection it causes.

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Name the types of Clostridium and describe the GI infections they cause (transmission, presentation, treatment).

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the 3 antibiotics that commonly cause C difficile?

A

Ciprofloxacin
Clindamycin
Cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the characteristics of Listeria and GI infection with Listeria. What is the treatment?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the characteristics of Enterobacteria. What are the different types that cause GI infection?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe the characteristics of Salmonella and the infections they cause.

A
  • 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe the characteristics of Shigella and the infection it causes.

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Describe the characteristics of Vibrios and the infections they cause

A

-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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe the characteristics of Campylobacter and the infection it causes

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Describe the characteristics of Yersinia and the infection it causes

A
  • Gram -ve
  • Non-lactose fermenter
  • Likes cold environments
  • Causes enterocolitis (febrile non-diarrhoea), mesenteric adenitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe infection with Entamoeba histolytica

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Describe Giardia infection

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Kinyoun acid fast stain identifies:

A

Cryptosporidium parvum

Causes severe diarrhoea in immunocompromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Name the viruses that commonly cause diarrhoea. What are the characteristics of each?

A
  • Norovirus: highly contagious. Diarrhoea and vomiting.
  • Rotavirus: affects children. Secretory diarrhoea, with 2x infection leading to immunity
  • Poliovirus, enterovirus, Hep A, adenovirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What vaccines against pathogens causing GI infections exist?

A
  • Rotavirus (routine vaccination)
  • Cholera
  • Salmonella typhi
  • Campylobacter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Name some bacteria that commonly cause UTI and describe their features

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Name some risk factors for UTI. What is the presentation?

A

RFs: sex, female, catheter, elderly, incontinent, structural abnormalities
Presentation: dysuria, frequency, urgency, nocturia, smelly/cloudy urine, fever, flank pain, rigors, sepsis, confusion, incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How is UTI formally diagnosed?

A

> 10 ^5 cfu/ml is diagnostic of infection/bacteriuria
+ symptoms -> UTI
In practice: symptoms + positive urine dip -> treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is sterile pyuria? What are some causes?

A
  • Presence of white cells in urine but no growth (MC&S)

- Caused by STI, stones, tumours, TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe the culture part of a urine MC&S

A
  • Use chromogenic agar -> specific colours depending on the organism
  • Pink: E coli
  • Blue: other coliforms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is a common antibiotic regime used in pyelonephritis

A
  • Broad spectrum PO/IV antibiotics

- Co-amoxiclav +/- gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the different sites of antibiotic action?

A

Cell well
Ribosome/protein synthesis
DNA/RNA synthesis
Other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are some different antibiotics that inhibit cell wall synthesis? Name some examples of each

A

Beta lactams: penicillins, cephalosporins, carbapenems

Glycopeptides: vancomycin, teicoplanin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How do beta lactams work? Are they bactericidal or bacteriostatic?

A

Inhibit transpeptidase PBP (penicillin binding protein), prevent crosslinking of peptidoglycan -> weak cell wall
Bactericidal- only works on rapidly dividing bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Which bacteria are sensitive to beta lactams and glycopeptides and why?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

If a patient is allergic to penicillin, which other antibiotics may they be allergic to?

A

5% chance of allergy to cephalosporins, carbapenems- because they have the same beta-lactam ring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are some different penicillins, and which bacteria are they effective for?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Which additional agents can be given with beta-lactams to increase their efficacy? What do they do?

A

Clavulanic acid and Tazobactam eg. Co-amoxiclav, Tazocin
-Inhibit beta-lactamase, increase susceptibility
Increase coverage to broad-spectrum including anaerobes and beta-lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are some types of cephalosporins and which bacteria are they effective for and not effective for?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are some types of carbopenems and which bacteria are they effective for?

A

Meropenem
Ertapenem
Broad spectrum: gram +, gram -, ESBLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are some glycopeptides, which bacteria are they effective against and why?

A

Vancomycin, teicoplanin
Active against gram + because can’t cross gram - outer membrane
Especially for MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Name some classes of antibiotics that inhibit protein synthesis and give examples

A 
Aminoglycosides: gentamicin, amikacin
Macrolides: erythromycin, azithromycin
Tetracyclines: doxycycline 
Chloramphenicol
Oxazolidinones: linezolid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe the MoA of aminoglycosides. Which bacteria are they effective against?

A

Bind to the 30S ribosome subunit and inhibit protein synthesis.
Broad spectrum: esp gram - and Pseudomonas. Synergistic with beta-lactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Describe the MoA of tetracyclines. Which bacteria are they effective against?

A

Bind to the 30S subunit and inhibit protein synthesis.

Intracellular pathogens eg. chlamydia, mycoplasma. Not very good for gram -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe the MoA of macrolides. Which bacteria are they effective against?

A

Bind to 50S subunit and inhibit protein synthesis.

Mild Staph/strep infection, Legionella, mycoplasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Describe the MoA of chloramphenicol. Which bacteria is it effective against?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Describe the MoA of oxazolidinones. Which bacteria are they effective against?

A

Bind to the 23S of 50S ribosome subunit.

Gram + cover including MRSA and VRE, not gram -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Name some classes of antibiotics that inhibit DNA synthesis and give examples

A

Fluoroquinolones: ciprofloxacin, levofloxacin
Nitroimidazoles: metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Describe the MoA of fluoroquinolones. Which bacteria are they effective against?

A

Inhibits DNA gyrase.
Broad spectrum especially gram - and Pseudomonas. Levo is good for gram +
eg. UTIs, atypical pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Describe the MoA of nitroimidazoles. Which bacteria are they effective against?

A

Cause DNA strand breakage in anaerobic conditions

Good for anaerobes and protozoa eg. BV, Giardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the MoA of rifampicin. Which bacteria is it effective against?

A

Inhibits RNA polymerase.

Effective for Mycobacterium and chlamydia

90
Q

What is important to be aware of when using rifampicin?

A

Monitor LFTs
May interact with other medications due to enzyme inhibition
Can cause orange secretions

91
Q

Name some cell membrane toxins. Which bacteria are they effective against?

A

Daptomycin: gram + eg MRSA and VRE
Colistin: gram - including Pseudomonas, Klebsiella, Acinetobacter. Toxic- only used for multidrug resistant.

92
Q

What is the MoA of sulphonamides? Which bacteria are they effective against?

A

Folate metabolism inhibitors.

Usually combined with trimethoprim eg. co-trimoxazole (Septrin) for PCP

93
Q

What are the different mechanisms of resistance? Give some examples

A

Inactivation eg. beta-lactamase
Altered target eg. MRSA (changed PBP structure)
Reduced accumulation/efflux
Bypass normal pathways eg. folate inhibitors

94
Q

Which bacteria are beta-lactamases?

A

Staph aureus, E coli

95
Q

T/F. MRSA is a beta-lactamase

A

False. It has altered target site

96
Q

What do ESBLs have resistance to?

A

Cephalosporins and penicillins

eg. E coli, Klebsiella

97
Q

Which bacteria are carbapenamases?

A

Enterobactericiae eg. Klebsiella and E coli

98
Q

Which factors need to be taken into account when choosing antibiotics to prescribe?

A

Host characteristics (age, pregnancy, renal impairment)
Antimicrobial susceptibility (sensitivity testing)
Organism
Site (eg bone, CNS)

99
Q

When would you want to give IV antibiotics?

A

If there is bone or CNS infection

If there is sepsis - poor GI perfusion = poor absorption

100
Q

What is the MIC?

A

Minimum inhibitory concentration: the smallest amount of antibiotic needed to inhibit growth in the lab eg sensitivity

101
Q

What are the key pharmacokinetic factors when using aminoglycosides?

A

Reaching a high peak concentration -> eg. 1 big dose

Need to measure the trough concentration to make sure there is elimination (adjust frequency)

102
Q

What are the key pharmacokinetic factors when using carbapenems and cephalosporins?

A

Having the longest time above the MIC -> frequent dosing

103
Q

What is the Eagle effect?

A

Bactericidal drugs only work when bacteria are rapidly dividing. When bacterial load is high, there are relatively static, so drugs have no effect

104
Q

Which antibiotics are used in hospital acquired UTI?

A

Cephalexin or co-amoxiclav

105
Q

What are some ways to minimise surgical site infections?

A

Pre-op: shower with soap, eradication of S aureus if nasal carriage, antibiotics
Intra-op: ventilation, sterile instruments, skin prep, oxygenation

106
Q

Which organisms commonly cause septic arthritis?

A

S aureus, Streptococcus, E coli

107
Q

Which organisms commonly cause osteomyelitis?

A

S aureus, Streptococcus, E coli, Salmonella, TB

108
Q

Which organisms commonly cause prosthetic joint infection?

A

Usually coagulase negative Staph (eg. not aureus)

Strep, E coli

109
Q

What is herd immunity? How is the threshold calculated?

A

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
Q

What is needed for disease eradication?

A
  • No animal reservoir
  • No latency
  • Effective vaccine/treatment
  • Stable pathogen
111
Q

Name some big pandemic flus. Why do these occur?

A

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
Q

What is the natural reservoir for influenza? How does it spread to humans?

A

Wild fowl.

Can cross into domestic fowl + pigs -> humans with mutations

113
Q

What is the difference between seasonal flu and pandemic flu?

A

Seasonal flu is due to antigenic drift (same antigens just small mutations)
Pandemic flu is due to antigenic shift (new antigens, no immunity)

114
Q

Why does influenza affect the lungs?

A

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
Q

How are influenza viruses named?

A

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
Q

How are viruses able to mutate?

A

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
Q

What are some antiviral drugs used for influenza?

A

Oseltamivir (Tamiflu): neuraminidase inhibitor

Baloxivir: polymerase inhibitor

118
Q

How does SARS-CoV2 enter cells?

A

Binds to ACE2 on epithelial cells of the lungs

119
Q

What type of viruses are the viral hepatitises? What is their transmission?

A 
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
Q

What is the presentation of Hepatitis A?

A

Short lived. May be non-specific

Acute hepatitis: jaundice, RUQ pain, fever

121
Q

What is the risk of developing chronic Hepatitis B infection?

A

Adults: 5-10%

Young children: 95%

122
Q

Describe the clinical course of Hepatitis B infection

A

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
Q

Describe the HBV serological tests

A

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
Q

Interpret this hepatitis serology:
HBsAg-
anti-HBs +

A

This could mean either previous vaccination or previous infection. Not possible to differentiate

125
Q

What are the consequences of chronic HepB/HepC?

A

Cirrhosis

Hepatocellular carcinoma

126
Q

What is the treatment for HepB? Who gets treatment?

A 
Pegylated IFNa (less commonly used, poorly tolerated)
Nucleoside analogues eg tenofivir, entecavir
For individuals with high viral load, raised ALT, more severe disease
127
Q

What proportion of individuals with HepC become chronically infected?

A

60-80%

128
Q

What are the tests for HepC? Which is best for acute infection?

A

HCV RNA. Better for acute infection

anti-HCV IgG. Rises after the acute infection

129
Q

Interpret this hepatitis serology:
HCV RNA -
anti-HCV IgG +

A

Previous infection- cleared

130
Q

What is the treatment for HepC? Who gets treatment?

A

NS3/4 protease inhibitor (-previrs) eg. boceprevir
NS5A inhibitor (-asvirs) eg daclatasvir
Also IFNa and Ribavirin
Give to everyone! High cure rate

131
Q

What are the types of HepD infection?

A

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
Q

What are some symptoms of HepE?

A

Acute hepatitis
Neuro eg. GBS, encephalitis
Renal eg. GN

133
Q

What type of drug is aciclovir? What is the MoA?

A

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
Q

What is the treatment of VZV infection? Who should be treated?

A

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
Q

What is the treatment of HSV?

A

Aciclovir- topical or systemic

136
Q

Which cells does CMV establish latency in? HSV? EBV?

A

CMV: monocytes and dendritic cells
HSV: neurons
EBV: B lymphocytes

137
Q

Who is susceptible to CMV infection? What are the consequences?

A

Immunosuppressed.

Reactivation/primary infection can cause encephalitis, pneumonitis, BM suppression, retinitis etc

138
Q

What is the treatment for CMV infection?

A

Ganciclovir (IV) or valganciclovir (prodrug, PO)

-> foscarnet (in neutropenia), cidofivir

139
Q

What is the presentation of BK virus?

A

Usually causes asymp primary infection but then causes chronic carriage in urinary tract
BMT + immunosuppression -> haemorrhagic cystitis, nephritis

140
Q

Who is affected by severe adenovirus infection?

A

Paediatric transplant patients

141
Q

What are the most common causative pathogens in acute meningitis? Which is most common?

A

Viral: most common. Coxsackie B + echovirus
Bacteria:
-Neisseria meningitidis (A, B, C): B+C most common.
-Streptococcus pneumoniae
-Haemophilus influenzae

142
Q

What is the most common causative pathogen in chronic meningitis?

A

TB. In immunosuppressed patients

143
Q

What are some causative pathogens of encephalitis? Which is most common?

A 
Viral: many types
-HSV: most common
-Mumps, Measles
-West Nile virus 
Bacterial: Listeria
Amoebic: Naegleria fowleri 
Toxoplasmosis: immunosuppressed
144
Q

What are some common causative pathogens of brain abscess?

A

S aureus
Streptococcus
Fungi: cryptococcus
Toxoplasmosis

145
Q

Which investigations would you do in suspected meningitis/encephalitis?

A

Blood tests: FBC, CRP, VBG, culture
LP: MC&S, PCR
Throat swab (Strep), urinary antigens (Strep)
CT/MRI

146
Q

What would you expect to see on LP in bacterial meningitis?

A

Turbid/purulent CSF
High WCC- polymorphs (100s)
Low glucose (0-2.2)
Normal protein (0.5-3.0)

147
Q

What would you expect to see on LP in viral meningitis?

A

Clear CSF
High WCC- lymphocytes (15-500)
Normal glucose (Normal)
Normal protein (0.5-1.0)

148
Q

What would you expect to see on LP in TB meningitis?

A

Clear CSF
High WCC- lymphocytes
Low glucose (0-2.2)
High protein (1.0-6.0)

149
Q

What are prion diseases?

A

A group of diseases caused by protein-only infectious agent causing spongiform encephalopathy and rapid neurodegeneration and death

150
Q

What is the pathophysiology of prion disease?

A

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
Q

What are the different types of Prion disease?

A

Sporadic: Creutzfeldt-Jakob disease
Acquired: Kuru, Variant CJD
Genetic: GSS, FFI

152
Q

Describe the presentation of sporadic CJD (clinical + Ix findings)

A

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
Q

Describe the presentation of variant CJD (clinical + Ix findings)

A

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
Q

What are some causes of iatrogenic CJD?

A

Cadaveric growth hormone, corneal transplant, blood transfusions, etc

155
Q

How is familial prion disease diagnosed?

A

AD- usually a FHx of neuro

Neurogenetics is key (mutation in PRNP)

156
Q

What are the common causative pathogens of infective endocarditis? What are they associated with?

A
  • 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
Q

How does infective endocarditis present?

A
  • 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
Q

What is the management of infective endocarditis?

A

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
Q

What are some groups of patients who are particularly susceptible to infections?

A 
HIV
Transplant + immunosuppressed
Primary immunodeficiencies
Elderly and neonates
Pregnant women
Malnutrition
DM 
IVDU
160
Q

List the susceptibility to infection from most to least in the following:
Advanced HIV, post-BMT, use of DMARDS/steroids, chemotherapy

A

DMARDS/steroids
Chemo
Advanced HIV
Post-BMT

161
Q

Name some important viruses in immunocompromised patients and some complications

A 
CMV: retinitis, pneumonitis, colitis
EBV: post-transplant lymphoproliferative disease
HSV 
VZV: encephalitis, pneumonitis
HPV: cervical cancer
HHV8: Kaposi's sarcoma
Adenovirus (paeds transplant)
162
Q

How can opportunistic infections present in immunocompromised hosts?

A

Unusual pathogen eg. JC virus
Severe infection/different organs eg. CMV retinitis
Low fever or CRP
Frequent reactivation of infection eg HSV

163
Q

After BMT, what is the order of virus-associated complications?

A

<1 month: HSV (reactivation)
>1 month: EBV, CMV, VZV (community-acquired)
Months-years: malignancy eg. Kaposi’s

164
Q

How are opportunistic infections screened for in immunocompromised patients?

A

In transplants: before transplant serology for everything

Post: monitor for CMV, EBV, adenovirus in children

165
Q

What is the basic classification of fungal infections? Name some examples

A

Yeasts: Candida, Cryptococcus, Histoplasma
Moulds: Aspergillus, Dermatophytes

166
Q

Describe the features of Candida (microscopy, culture, etc).

A
  • Purple oval cells, may see budding

- Grows best on Sabourad agar -> cream coloured colonies

167
Q

What types of infections are caused by Candida? In which patients do these occur?

A

Vulvovaginitis: common
Oral: immunosuppressed, use of inhaled steroids
Invasive: immunosuppressed

168
Q

Describe the management of Candida infection

A
  • Oral: topical nystatin
  • Vulvovaginitis: topical clotrimazole
  • Invasive: oral fluconazole (C albicans), amphotericin-B/echinocandins for others
169
Q

How is cryptococcus transmitted? What kind of infections can it cause?

A

Inhaled aerosol (usually from pigeons, eucalyptus)
Lung disease, meningitis, systemic
Particularly affecting HIV patients

170
Q

Describe the features of Cryptococcus neoformans

A

Encapsulated yeast in gelatinous matrix

Stains with India Ink

171
Q

What is the management of Cryptococcus?

A

Resistant to Echinocandins

  • Amphotericin B (Ambisome) is mainstay for several weeks
  • Prevent relapse wth fluconazole 8 weeks
172
Q

What is the best way to diagnose cryptococcus?

A

Antigen test: serum/CSF

Culture not as good

173
Q

What are the different diseases caused by Aspergillus? Briefly describe.

A

Invasive Aspergillus: systemic infection
Pulmonary Aspergilloma: colonises cavity eg. previous TB
Allergic bronchopulmonary aspergillosis: obstructive airway disease due to allergic response

174
Q

What are the types of Aspergillus? Describe characteristics. How is it diagnosed?

A

Flavus, fumigatus
Mould, spore-forming
Dx: sputum MC&S + antigen screen (galactomannan), CXR, histology

175
Q

What is the treatment of Aspergillus infection?

A

Amphotericin B, voriconazole

176
Q

What are some types of dermatophyte infection? What are the causative organisms? How are they treated?

A

-Tinea pedis: Trichophyton rubrum
-Tinea corporis (ringworm): Trich.
-Onychomycosis: Trich.
-Pityriasis versicolor: Malassezia furfur
Tx: topical/oral azoles

177
Q

Orbital cellulitis can be caused by which fungal infection? Who is typically affected? How does it present?

A

Mucorales: causes Mucormycoses
Typically in DM and other immunocomp.
Cellulitis with black pus

178
Q

Which fungus classically causes pneumonia in HIV patients? How does it present? How is it diagnosed? What is treatment?

A

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
Q

What are some targets of antifungal drugs? Give some examples of different classes

A
  • Cell membrane- inhibit ergosterol production: -azoles (fluconazole), polyenes (amphotericin B)
  • Cell wall: echinocandins (Caspofungin, anidulafungin)
  • DNA synthesis: flucytosine
180
Q

Describe the MoA of azoles. What are the side effects?

A

-Bind lanosterol 14a-demethylase
-Inhibit ergosterol production
-Prevent cell membrane formation
SEs: drug interactions (p450), steroidogenesis inhibition (eg cortisol)

181
Q

Describe the MoA of echinocandins. What are they used for?

A

-Inhibit B-D-glycan synthase
-Prevent cell wall synthesis
Uses: Candida species, Aspergillus

182
Q

What are the different types of Mycobacterium?

A

-M tuberculosis
Non-tuberculous:
-M avian complex (MAC): includes avian, intracellulare
-M abscessus complex

183
Q

Describe the characteristics of mycobacterium

A
  • Nonmotile rods
  • Slow-growing
  • Complex cell wall: mycolic acids, waxes, etc
  • Stain with auramine, Ziehl-Nielsson
184
Q

What are the features of non-TB mycobacterium? What are some types and what infections are they associated with?

A

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
Q

Describe the clinical course of TB infection

A
  • 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
Q

How is TB diagnosed?

A

CXR
Sputum sample x3 for stain (ZN), culture of Lowenstein-Jensen medium for 6 weeks (gold standard)
+/- BAL
Histology

187
Q

What is the classic histological finding in TB?

A

Caseating granuloma

188
Q

Which tests can be used for investigation of latent TB infection?

A

IGRA

Tuberculin skin test

189
Q

Describe the management of TB infection. What are the side effects?

A

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
Q

What are zoonoses? What are some methods of transmission?

A

Diseases that pass from animals to humans

  • Direct human + animal contact eg farming, animal scratches/bites
  • Contact with faeces
  • Contaminated foods eg milk
191
Q

How are zoonoses classified? Give some examples

A

UK vs tropical, farm/wild vs companion

  • UK, farm: Campylobacter, Salmonella
  • UK, companion: Toxoplasmosis, Bartonella, ringworm
  • Tropical, farm: Brucella, Coxiella
  • Tropical, companion: rabies
192
Q

Where does Bartonella come from? How does infection present? What is the treatment?

A

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
Q

What type of organism is toxoplasma gondii? How does toxoplasmosis present? What is the management?

A

Parasite
Fever and adenopathy. Abscess + seizures in immunocompromised.
Congenital: chorioretinitis, microcephaly, cerebral calcification
Mx: spiramycin OR pyrimethamine + sulfadiazine.

194
Q

Where does Brucella come from? How does infection present and what can it be confused with? What is the treatment?

A

Farm animals eg. cows, goats
Transmitted in unpasteurised dairy
FLAWS, back pain, orchitis, abscess -> basically TB
Mx: doxy + gent/rifampicin

195
Q

Where does Coxiella come from? What is the name for the disease it causes and how does it present? What is the treatment?

A

Farm animals: goats, cattle, sheep
Transmitted in unpasteurised milk
Causes Q fever: fever, flu, pneumonia
Mx: doxy

196
Q

What type of organism causes Rabies? How does it present? What is the management?

A

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
Q

What type of organism causes Rat bite fever? How does it present?

A

Strep moniliformis, Spirillulin minus

Fever, arthralgia, rash

198
Q

What are some types of viral haemorrhagic fever?

A

Ebola, Marburg, Lassa

199
Q

How is leptospirrosis contracted? How does it present?

A

Through broken skin/swimming in infected water

High fever, headache, jaundice, myalgia, meningism, carditis, renal failure etc

200
Q

What type of organism causes Lyme disease? How does it present? What is the treatment?

A

Borrelia burgdorferi- spirochaete bacteria
Erythema migrans, cyclical fever, flu-like symptoms, arthritis, etc
Mx: doxycycline

201
Q

Describe the life cycle of tape worms

A

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
Q

What is the treatment of tapeworms?

A

Praziquantel

203
Q

Describe the life cycle of schistosomiasis

A
  • 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
Q

How is filariasis contracted?

A

Through mosquito/blackfly bites -> larvae enter body

205
Q

What is cysticercosis? How does it present?

A

Invasion of tissues by Taenia solium larvae (only pig worms, not beef/fish)
Symptoms are often from CNS invasion - seizures, headaches, blindness, etc

206
Q

Name some diseases transmitted by mosquitos

A 
Malaria
Dengue
West Nile Virus
Yellow Fever
Zika virus
207
Q

What is the vector for malaria? What organism causes malaria?

A

Anopheles mosquito

Caused by protozoa: Plasmodium falciparum, P vivax, P ovale, P malariae

208
Q

Describe the life cycle of Plasmodium

A
  • 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
Q

Describe the presentation of malaria

A
  • Malaria paroxysms: fevers, chills, rigors, sweats
  • Jaundice, anaemia, low platelets
  • Severe: parasitaemia, CNS involvement, renal failure, ARDS, circulatory collapse, metabolic acidosis
210
Q

What are the investigations for malaria? What are they used for/what do they show?

A

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
Q

What is the treatment for malaria?

A

Falciparum:
-Mild: malarone, riamet (artemisinin combo therapy)
-Severe: IV artesunate > quinine
Non-falciparum: chloroquine, primaquine (good for hypnozoite stage)

212
Q

What is considered severe falciparum malaria?

A

> 2% parasitaemia

213
Q

How is Dengue transmitted? Where is it commonly found?

A

Aedes mosquito bites

SE Asia

214
Q

What are the features of Dengue fever? What are the complications?

A 
Headache
Myalgia
Rash
Fever
Hepatitis
Reinfection with different serotype -> Dengue haemorrhagic fever
215
Q

What are the features of typhoid fever?

A 
Fever
Constipation > diarrhoea
Rose spots
Dry cough
Headache
216
Q

What are the symptoms of rubella infection?

A

Usually asymptomatic or mild

  • Lymphadenopathy
  • Macular rash
  • Fever
217
Q

What are the causes of congenital CMV infection?

A
  • Primary infection

- Reactivation of latent infection

218
Q

How does congenital CMV infection present?

A 
Sensorineural hearing loss
Chorioretinitis
Microcephaly
Hepatitis, jaundice
Rash
219
Q

How is congenital infection diagnosed?

A

Detection of pathogen within 21 days of birth/prenatal diagnosis eg amnio and PCR

220
Q

When is the fetus and neonate most susceptible to congenital VZV infection?

A

13-20 weeks

Neonate: maternal infection between 7 days prior to and 7 days post delivery

221
Q

When is the fetus most susceptible to parvovirus B19 infection?

A

Before 20 weeks

222
Q

How is C difficule infection confirmed?

A

Stool toxin assay

Pathology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions