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Year 5 Pathology > Microbiology Denise > Flashcards

Microbiology Denise Flashcards

1
Q

What congenital infections are currently screened in mothers during pregnancy?

A

Hepatitis B
HIV
Rubella
Syphilis

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2
Q

What congenital infections are currently not screened in mothers during pregnancy but are possible?

A

CMV
Toxoplasmosis
Hepatitis C
Group B Streptococcus

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3
Q

Congenital toxoplasmosis may be asymptomatic at birth but 60% may still go on to suffer long-term sequelae such as….

A

Deafness
Low IQ
Microcephaly

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4
Q

Congenital toxoplasmosis is symptomatic at birth in 40%. What are examples of symptoms?

A 
Choroidoretinitis
Microcephaly/hydrocephalus
Intracranial calcifications
Seizures
Hepatosplenomegaly/jaundice
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5
Q

What is the mechanism of congenital rubella syndrome?

A

The mitotic arrest of cells
Angiopathy
Growth inhibitor effect

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6
Q

How does congenital rubella syndrome affect the eyes?

A

Cataracts
Microphthalmia
Glaucoma
Retinopathy

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7
Q

How does congenital rubella syndrome affect the CVS?

A

Patent ductus arteriosis

Atrial/ventricular septal defect

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8
Q

How does congenital rubella syndrome affect the ears?

A

Deafness

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9
Q

How does congenital rubella syndrome affect the brain?

A

Microcephaly
Meningoencephalitis
Developmental delay

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10
Q

What are some other symptoms of congenital rubella syndrome (not including eyes, CVS, ears, brain)?

A 
Growth retardation
Bone disease
Hepatosplenomegaly
Thrombocytopenia
Rash
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11
Q

Chlamydia trachomatis is a congenital infection transmitted during delivery. The mother may be asymptomatic but the neonate may show…?

A

Neonatal conjunctivitis
Rarely pneumonia

Treat with erythromycin

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12
Q

What is the neonatal period?

A

First 4-6weeks of life

n.b. if the baby is born early (premature), the neonatal period is longer and adjusted for expected birth date

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13
Q

Which organisms are typically involved with neonatal infections?

A

Group B streptococci
E coli
Listeria monocytogenes

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14
Q

What type bacteria and shape are Group B streptococci?

A

Gram +ve coccus
Catalase -ve
B-haemolytic

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15
Q

In neonates, Group B streptococci causes….?

A

Bacteraemia
Meningitis
Disseminated infection e.g. joint infections

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16
Q

What can E coli lead to in neonates?

A

Bacteraemia
Meningitis
UTI

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17
Q

What are early onset sepsis-risk factors (maternal)?

A 
Premature labour
Fever
Foetal distress
Meconium staining
Previous Hx
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18
Q

What are early onset sepsis-risk factors (baby)?

A 
Birth asphyxia
Resp distress
Low BP
Acidosis
Hypoglycaemia
Neutropenia
Rash
Hepatosplenomegaly
Jaundice
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19
Q

What are investigations used for suspected sepsis/infections during childhood?

A 
FBC
C-reactive protein
Urine
Blood culture
Deep ear swab
Lumbar puncture (CSF)
ET secretions if ventilated
Surface swabs
CXR (full body)
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20
Q

What is the treatment for early onset neonatal sepsis?

A

Supportive mgmt

  • Ventilation
  • Circulation
  • Nutrition
  • Antibiotics e.g. benzylpenicillin and gentamicin
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21
Q

What bacteria are causes of late onset sepsis in neonates (after 48-72 hours)?

A

Coagulase negative staphylococci (CoNS)

(Less commonly:
Group B strep
E coli
Listeria monocytogenes
Staph aureus
Enterococcus sp.
Gram negatives (Klebsiella etc)
Candida)
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22
Q

What are clinical features of late onset sepsis in neonates?

A 
Bradycardia
Apnoea
Poor feeding/bilious aspirates/abdo distension
Irritability
Convulsions
Jaundice
Resp distress
Increased CRP
Sudden changes in WCC/platelets
Focal inflammation e.g. umbilicus, drip sites etc
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23
Q

What is the treatment for late onset neonatal sepsis?

A

Treat early
Review and stop Abx if cultures are negative and clinically stable
1st line Abx - cefotaxime and vancomycin
2nd line - meropenem

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24
Q

What is the choice of antibiotics for community acquired late onset neonatal sepsis infections?

A

Cefotaxime, amoxicillin ± gentamicin

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25
Q

Viral infections are very common during childhood. What are some examples?

A

Chickenpox (VZV)
HSV (coldsores/stomatitis)
HHV6, HHV8, EBV, CMV, RSV, enteroviruses etc

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26
Q

Bacterial infections may cause secondary infection in childhood after viral illness. An example is….

A

iGAS disease post-VZV infection

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27
Q

What is the most important bacterial cause of paediatric morbidity and mortality?

A

Meningitis

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28
Q

Diagnosis of meningitis in paeds is confirmed by…?

A 
Clinical features
Blood cultures
Throat swab
LP for CSF if possible
Rapid Ag screen
EDTA blood for PCR
Clotted serum for serology if needed later
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29
Q

What can Streptococcus pneumonia cause?

A

Meningitis
Bacteraemia
Pneumonia

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30
Q

What bacteria is Gram +ve diploccous, a-haemolytic and has >90 capsular serotypes?

A

Streptococcus pneumoniae

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31
Q

Streptococcus pneumoniae has increasing resistance to which drug?

A

Penicillin

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32
Q

What are the bacteria that can cause meningitis at <3 months?

A 
Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae (if unvaccinated)
GBS
E coli
Listeria sp
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33
Q

What are the bacteria that can cause meningitis at 3months-5years of age?

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae (if unvaccinated)

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34
Q

Respiratory tract infections account for what proportion of childhood illnesses?

A

1/3

most viral and upper RTIs

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35
Q

What is the most important bacterial cause of RTIs in children?

A

Streptococcus pneumoniae

Most UK strains remain sensitive to penicillin or amoxicillin

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36
Q

Mycoplasma pneumonia causes RTIs in which age group?

A

Older children

>4years

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37
Q

What is the choice of treatment for myocplasma pneumonia RTIs in children?

A

Macrolides

e.g. azithromycin

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38
Q

What are some classical presentations of mycoplasma pneumonia RTIs in school age children/young adults?

A 
Fever
Headache
Myalgia
Pharyngitis
Dry cough
Incubation period = 2-3weeks

n.b. many are asymptomatic

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39
Q

What are the extrapulmonary manifestations of mycoplasma pneumonia?

A 
Haemolysis
Neurological
Cardiac
Polyarthralgia
Myalgia
Arthritis
Otitis media
Bullous myringitis
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40
Q

What is the mechanism of haemolysis due to mycoplasma pneumonia?

A

IgM antibodies bind to the I antigen on erythrocytes

Cold agglutinins in 60% patients occur

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41
Q

What are some extra-pulmonary neurological manifestations in patients with mycoplasma pneumonia?

A 
Encephalitis (most common)
Aseptic meningitis
Peripheral neuropathy
Transverse myelitis
Cerebellar ataxia
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42
Q

What are the organisms that can cause UTIs?

A

E coli
Other coliforms e.g. Proteus species, Klebsiella, Enterococcus
Coagulas negative Staphylococcus

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43
Q

How are UTIs diagnosed in children?

A

Symptoms if child can give clear Hx
Pure growth >10^5cfu/ml
Pyuria - pus cells on urine microscopy

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44
Q

UTIs are common in children and occur in what % in girls and boys by age 11?

A

Up to 3% girls by age 11

Up to 1% boys by age 11

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45
Q

If treatment for children’s RTI for streptococcus pneumoniae and mycoplasma pneumonia fails to respond, we must consider the bacterial cause to be….?

A 
Whooping cough (Bordetella pertussis especially if child is not vaccinated)
Tuberculosis (including MDRTB and XDRTB)
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46
Q

What is the mechanism of neurological manifestations due to mycoplasma pneumonia?

A

The MoA is currently unknown but it is thought that antibodies cross-react with galactocerebroside

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47
Q

What are 4 important types of CNS infections?

A
  1. Meningitis
  2. Encephalitis
  3. Brain abscess
  4. Spinal infections
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48
Q

What are the 4 routes of entry for CNS infection?

A
  1. Haematogenous spread
  2. Direct implantation
  3. Local extension
  4. PNS into CNS
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49
Q

What are the typical signs and symptoms of meningitis?

A

Fever
Headache
Stiff neck
Vomiting

Light aversion
Drowsiness
Seizures
Non-blanching (petechial/purpuric) rash (in 80% of children)

10% mortality rate

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50
Q

What are the signs and symptoms of encephalitis?

A

Disturbance of brain function

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51
Q

What are the causative agents of encephalitis?

A 
Rabies virus
Arboviruses
Trypanosoma species
Prions
Amoeba
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52
Q

What are the causative agent(s) of myelitis?

A

Poliovirus

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53
Q

What are the signs and symptoms of myelitis?

A

Disturbance of nerve transmission

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54
Q

What region is affected in (i) meningitis, (ii) encephalitis, (iii) myelitis, and (iv) with neurotoxins?

A

(i) Meninges
(ii) Brain
(iii) Spinal cord
(iv) CNS + PNS

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55
Q

What are the signs and symptoms of neurotoxin syndromes?

A

Paralysis
Rigid (tetanus)
OR flaccid (botulism)

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56
Q

What are the causative agents of neurotoxin syndrome?

A

Clostridium tetani

Clostridium botulinum

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57
Q

What is the difference between meningitis and meningoencephalitis?

A

Meningitis is the inflammatory process of meninges and CSF. Meningoencephalitis is the inflammation of meninges AND brain parenchyma.

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58
Q

What mechanisms does neurological damage occur in meningitis?

A

Direct bacterial toxicity
Indirect inflammation with cytokine release and oedema
Shock, seizures and cerebral hypoperfusion

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59
Q

In the UK, around 5% meningitis survivors have long-term neurological sequelae, mainly….

A

Sensorineural deafness

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60
Q

What are some common causative agents of acute meningitis?

A 
Neisseria meningitidis
Strep pneumoniae
Haemophilus influenzae
Listeria monocytogenes
Group B Streptococcus
E coli
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61
Q

How is Neisseria meningitidis transmitted?

A

Person-to-person
Through nasopharyngeal mucosa
From asymptomatic carriers

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62
Q

Pathogenic strains of Neisseria meningitidis are found in what % of carriers?

A

1% of N.meningitidis are pathogenic

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63
Q

Neisseria meningitidis can cause….

A

Meningitis (50% cases)
Septicaemia (7-10%)
Septicaemia AND meningitis (40%)

These clinical differences are important for treatment choice for shock vs only increased ICP.

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64
Q

What 4 processes produce the clinical spectrum for septicaemia?

A
  1. Capillary leak
  2. Coagulopathy
  3. Metabolic derangement (namely acidosis)
  4. Myocardial failure (i.e. multi-organ failure)
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65
Q

How does the capillary leakage process contribute to septicaemia?

A

Leakage of albumin and other plasma proteins results in hypovolaemia

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66
Q

How does the coagulopathy process contribute to septicaemia?

A

Bleeding and thrombosis occur
Due to endothelial injury and platelet-release reactions
Protein C pathway and plasma anticoagulants are also involved

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67
Q

What is an example of chronic meningitis?

A

Tuberculous chronic meningitis

Commoner in immunosuppressed

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68
Q

Which regions does tuberculous chronic meningitis involve?

A

Meninges and basal cisterns of the brain and spinal cord

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69
Q

What can tuberculous chronic meningitis result in?

A

Tuberculous granulomas
Tuberculous abscesses
Cerebritis

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70
Q

What is the most common infection of the CNS?

A

Aseptic meningitis

PC: headache, stiff neck and photophobia ± rash.

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71
Q

What are the causative organism(s) of aseptic meningitis in 80-90% cases?

A

Coxsackievirus group B
Echoviruses

(often in children <1yr)

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72
Q

How is encephalitis transmitted?

A

Commonly from person to person

Or through vectors (mosquitoes, lice, ticks)

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73
Q

West Nile virus is an international cause of which infection?

A

Encephalitis

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74
Q

What organism can cause bacterial encephalitis?

A

Listeria monocytogenes

n.b. toxoplasmosis can also cause CNS encephalitis

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75
Q

What organism(s) can cause amoebic encephalitis?

A

Naegleria fowleri (lives in warm water)
Acanthamoeba
Balamuthia mandrillaris

These can cause brain abscesses, aseptic or chronic meningitis

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76
Q

A focal CNS infection may be indicated by the presence of….?

A

Brain abscess

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77
Q

What are some disorders involved with the pathophysiology of brain abscesses?

A
  1. Otitis media; mastoiditis; paranasal sinuses
  2. Endocarditis (haematogenous spread)
  3. Tuberculous meningitis
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78
Q

What is the most common form of spinal vertebral infection?

A

Pyogenic vertebral osteomyelitis

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79
Q

If pyogenic vertebral osteomyelitis (spinal infection) is left untreated, what can result?

A

Permanent neurological deficits
Significant spinal deformity
Death

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80
Q

What are some risk factors for spinal infections?

A 
Advanced age
IV drug use
Long-term systemic steroids
Diabetes mellitus
Organ transplant
Malnutrition
Cancer
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81
Q

What investigation is the best for detecting parenchymal abnormalities e.g. abscesses and infarction?

A

MRI

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82
Q

What investigations are useful for CNS infections?

A

CSF sample
Brain tissue
MRI (for parenchymal abnormalities e.g. abscesses and infarction)

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83
Q

A 20 year old woman presents with headache and neck stiffness. Gram stain shows Gram +ve cocci. What is the causative pathogen?

A

Strep pneumoniae

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84
Q

A 18 year old man present with headache and neck stiffness. Gram stain shows Gram -ve cocci. What is the causative pathogen?

A

N. meningitidis

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85
Q

A 65 year old presents with headache and neck stiffness. Gram stain shows Gram +ve bacillus/rods. What is the causative pathogen?

A

Listeria monocytogenes

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86
Q

A 45 year old presents with headache and neck stiffness. A Ziehl-Neelsen stain was done and was positive. What is the causative pathogen?

A

Mycobacterium TB

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87
Q

A 35 year old presents with headache and neck stiffness. Indian ink stain tests were done and were positive. What is the causative pathogen?

A

Cryptococcus neoformans

Increased risk in HIV patients

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88
Q

What is the generic treatment plan for meningo-encephalitis?

A

Aciclovir 10mg/kg IV tds
Ceftriaxone 2g IV bd

If >50yrs or immunocompromised add:
amoxicillin 2g IV 4hourly

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89
Q

Define uncomplicated urinary tract infection

A

Infection in a structurally and neurologically normal urinary tract

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90
Q

Define complicated urinary tract infection

A

Infection in a urinary tract with functional or structural abnormalities (including indwelling catheters and calculi).

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91
Q

Complicated urinary tract infections tend to occur in which groups of patients?

A

Men
Pregnant women
Children
Patients who are hospitalised/in healthcare associated settings

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92
Q

More than 95% of urinary tract infections are caused by a single bacterial species. What is the most frequent infecting organism in acute infection?

A

E.coli

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93
Q

Apart from E.coli causing the majority of UTIs, what other organisms can cause them?

A 
Proteus mirabilis 
Klebsiella aerogenes 
Enterococcus faecalis 
Staphylococcus saprophyticus 
Staphylococcus epidermis
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94
Q

What are 3 antibacterial host defences in the urinary tract?

A
  1. Urine (osmolality, pH, organic acids)
  2. Urine flow and micturition
  3. Urinary tract mucosa (bactericidal activity, cytokines)
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95
Q

What is the urethra usually colonised with?

A

BActeria

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96
Q

The female urethra is short and in promiximity to what?

A

The warm and moist vulvar and perianal areas

This makes contamination likely. Bacteria is pushed into the female bladder (risk increases during sex)

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97
Q

Organisms that cause UTIs in women tend to colonise which regions before the urinary infection results?

A

Vaginal introitus

Periurethral area

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98
Q

Once bacteria is within the bladder, bacteria may multiply and where can it pass up?

A

Ureters

Especially if vesicoureteral reflux is present, up to the renal pelvis and parenchyma

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99
Q

How do renal/urinary tract abnormalities interfere and increase infection risk?

A

Obstruction inhibits natural urine flow and resulting stasis occurs

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100
Q

Name extra-renal causes of obstruction of the renal/urinary tract that can increase UTI risk?

A
  • Valves, stenosis, or bands
  • Calculi
  • Extrinsic ureteral compression from a variety of causes
  • Benign prostatic hypertrophy
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101
Q

Name intra-renal causes of obstruction of the renal/urinary tract that can increase UTI risk?

A
  • Nephrocalcinosis
  • Uric acid nephropathy
  • Analgesic nephropathy
  • Polycystic kidney disease
  • Hypokalemic nephropathy
  • Renal lesions of sickle cell trait/disease
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102
Q

Name neurogenic malfunction causes of obstruction of the renal/urinary tract that can increase UTI risk?

A

Poliomyelitis
Tabes dorsalis,
Diabetic neuropathy
Spinal cord injury

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103
Q

The kidney is frequently the site of abscesses in patients with what infections?

A

Staphylococcus aureus bacteremia
Or endocarditis
(Or both. This is by the haematogenous route)

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104
Q

Infection of the kidney with which type of bacteria RARELY occurs by the haematogenous route?

A

Gram-negative bacilli

it is more common with Staph aureus or endocarditis

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105
Q

What do the lower urinary tract symptoms result from?

A

Bacteria causing irritation of urethral and vesical mucosa, causing frequent and painful urination of small amounts of turbid urine

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106
Q

What are the lower UTI symptoms present in patients?

A 
Frequency
Painful urination
Small amounts of turbid urine
Suprapubic heaviness/pain
Grossly bloody urine/bloody tinge at end of micturition

(fever tends to be absent in infections limited to the lower tract)

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107
Q

What are the upper UTI symptoms present in patients?

A

Fever (±rigors)
Flank pain
Frequently lower UTI symptoms too (frequency, urgency, dysuria) - these may occur before the upper tract symptoms by 1-2 days

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108
Q

What are the symptoms of UTIs in older/elderly patients?

A
  • Majority are asymptomatic
  • When they are present, are not diagnostic as many old people have frequency, dysuria, hesitancy, incontinence anyway
  • Atypical upper UTI symptoms e.g. abdo pain, change in mental status
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109
Q

What are the investigations for (i) uncomplicated UTIs/pyelonephritis and (ii) complicated UTIs?

A

(i) Urine dipstick
MSU for urine MC&S
Bloods (FBC, U&Es, CRP, inflammatory markers + renal function)
(ii) The above investigations but also renal USS and IV urography

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110
Q

How can we sample urine for testing in UTIs?

A
  • Midstream clean catch (MSU)
  • Catherisation
  • Suprapubic aspiration
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111
Q

The presence of white cells (pyuria) in the urine under the microscope indicates what?

A

Infection

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112
Q

The presence of squamous epithelial cells in the urine under the microscope indicates what?

A

Contamination of the sample

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113
Q

What are some causes of sterile pyuria (presence of white cells in urine without any apparent infection)?

A
  • Prior treatment with antibiotics
  • Calculi
  • Catheterisation
  • Bladder neoplasm
  • TB
  • Sexually transmitted diseases
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114
Q

The treatment for UTIs is empirical therapy, community based for lower UTIs and local guidance. How many days of therapy should be given for UTIs?

A
  • 3 days of therapy with standard doses for treatment of uncomplicated lower UTIs in women
  • Longer therapy for those with H/O previous UTIs, Abx resistance, >7days symptoms
  • 7 days of therapy in men
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115
Q

What is the treatment for catheter-associated UTIs?

A
  • Remove catheter
  • Aminoglycosides (e.g. gentamin, amikacin) before catheter removal
  • Oral fluconazole is NO more effective than no therapy
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116
Q

Most UTIs with indwelling catheters are caused by which organism?

A

Candida fungal infection

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117
Q

Oral fluconazole is not given to those with Candida fungal UTIs caused by catheters, except in which patients?

A

Renal transplant patients

Patients who are about to undergo elective urinary tract surgery

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118
Q

The kidney itself is NOT uniformly susceptible to infection. What is the susceptibility in the medulla vs the cortex?

A
  • Few organisms are needed to infect the medulla

- 10,000x are needed to infect the cortex

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119
Q

What is pyelonephritis commonly associated with?

A

Sepsis

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120
Q

Pyelonephritis is commonly associated with sepsis so it needs more aggressive treatment such as….?

A

Co-amoxiclav ±/gentamicin

Imaging: calculi, structural cause

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121
Q

What are the complications of pyelonephritis?

A
  • Perinephric abscess
  • Chronic pyelonephritis (scarring, chronic renal impairment)
  • Septic shock
  • Acute papillary necrosis
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122
Q

What are 3 major pathogens in surgical site infections?

A
  1. Staph aureus (MSSA and MRSA)
  2. E.coli
  3. Psuedomonas aeruginosa
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123
Q

What is the pathogenesis mechanism of surgical site infections?

A
  1. Contamination of wound at operation
  2. Pathogenicity and innoculum of microorganisms
  3. Host immune response
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124
Q

What are the 3 levels of surgical site infection?

A
  1. Superficial incisional - skin and subcutaneous tissue
  2. Deep incisional - fascial and muscle layers
  3. Organ/space infection
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125
Q

The presence of pus with cluster cocci with a surgical site infection is most likely to be which of the organisms:

(a) E.coli
(b) Enterobacter
(c) Neisseria meningitides
(d) MRSA

A

MRSA

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126
Q

Diabetes increases the risk of surgical site infection by 2-3x. How can this be managed?

A

Control blood glucose
Aim for HbA1C <7

This is because DM is associated with post-operative hyperglycaemia

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127
Q

Rheumatoid arthritis increases the risks of surgical site infections. How can this be managed?

A

Stop disease modifying agents for 4 weeks pre- and 8 weeks post-operatively.

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128
Q

Why is there greater risk of surgical site infection in patients with obesity (BMI>35 have 5-7x greater risk)?

A

Adipose tissue is poorly vascularised

Poor oxygenation of tissues and functioning of the immune response increases SSI risk

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129
Q

Why is there greater risk of surgical site infection in patients who smoke?

A

Nicotine delays primary wound healing
Peripheral vascular disease
Therefore encourage tobacco cessation

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130
Q

Why is pre-operative showering encouraged?

A
  • Microorganisms colonising skin may contaminate exposed tissues and cause surgical site infections
  • Patients should wash using soap on operation day or the day before
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131
Q

Why is hair removal is not encouraged before operations?

A

Micro-abrasions caused by shaving with a razor may lead to multiplication of bacteria in surgical site infections
(Use electric clippers on the day of surgery with single-use head)

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132
Q

Staph aureus contaminates the nasal region in what % of people?

A

20-30%

High RF for surgical site infections

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133
Q

Why does mild hypothermia during surgery appear to increase the risk of surgical site infections?

A

Vasoconstriction
Decreased O2 delivery to the wound space
Subsequent impairment of neutrophil function

therefore peri-operatively give high O2

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134
Q

Give 4 bone and joints infections that will increase the risks of surgical site infections?

A
  1. Septic arthritis
  2. Vertebral osteomyelitis
  3. Chronic osteomyelitis
  4. Prosthetic joint infection
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135
Q

What are the risk factors for septic arthritis?

A
  • RhA, OA, crystal-induced arthritis
  • Joint prosthesis
  • IV drug abuse
  • Diabetes, chronic renal disease, chronic liver disease
  • Immunosuppression, steroids
  • Trauma: intra-articular injection, penetrating injury
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136
Q

What is the pathophysiology of septic arthritis?

A

Organisms adhere to the synovial membrane
Bacteria proliferate in synovial fluid and generate a host inflammatory response
Joint damage exposes host-derived proteins e.g. fibronectin, to which bacteria adhere

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137
Q

Staph aureus has receptors that can recognise selected host proteins. What is an example of a receptor that it has?

A

Fibronectin binding protein

binds to fibronectin which is a host-derived protein that is exposed from joint damage

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138
Q

Kingella kingae is a bacteria that can adhere to the synovial membrane in septic arthritis. How does it adhere?

A

Bacterial pili

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139
Q

Some strains of Staph aureus produce what cytotoxin that has been associated with fulminant infections in septic arthritis?

A

Cytotoxin PVL

Panton-Valentine Leucocidin

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140
Q

What are the causative organisms of septic arthritis?

A
  1. Staph aureus (46%)
  2. Coagulase negative staph (4%)
  3. Streptococci (22%) - pyogenes, pneumoniae, agalactiae
  4. Gram negative organisms - E.coli, HI, Neisseria, §
  5. Rare: Lyme, brucellosis, mycobacteria, fungi
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141
Q

What are the clinical features of septic arthritis?

A
  • 1-2 week H/O red, painful, swollen restricted joint
  • Monoarticular in 90%
  • Knee is involved in 50%
  • Patients with rheumatoid arthritis may show more subtle signs of joint infection
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142
Q

Is septic arthritis polyarticular or monoarticular?

A

Monoarticular in 90%

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143
Q

What signs may be present on imaging of septic arthritis?

A

USS - joint effusion
CT - erosive bone change, periarticular soft tissue extension
MRI - effusion, articular cartilage destruction, abscess, contiguous osteomyelitis

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144
Q

What is the treatment for septic arthritis?

A
  • Antibiotics (up to 6 weeks therapy can be given)

- Drainage

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145
Q

Vertebral osteomyelitis can be classified into which 2 categories?

A
  1. Acute haematogenous

2. Exogenous - after disc surgery, or implant associated

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146
Q

What are the causative organisms of vertebral osteomyelitis?

A
  1. Staph aureus (48.3%)
  2. Coagulase negative staph
  3. Gram negative rods
  4. Strep
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147
Q

Where can vertebral osteomyelitis infections be localised to and in what %?

A

Cervical (10.6%)
Cervico-thoraco (0.4%)
Lumbar (43.1%)

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148
Q

What are the symptoms of vertebral osteomyelitis?

A 
Back pain (86%)
Fever (60%)
Neurological impairment (34%)
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149
Q

How is vertebral osteomyelitis diagnosed?

A

MRI - 90% sensitive
Blood cultures
CT/open biopsy

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150
Q

What is the treatment for vertebral osteomyelitis?

A

6 weeks of treatment (flucocloxacillin usually)

Longer treatment if undrained abscesses or implant associated

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151
Q

What are 3 characteristic features of chronic osteomyelitis?

A

Pain
Brodies’ abscess
Sinus tract

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152
Q

How is chronic osteomyelitis diagnosed?

A

MRI

Bone biopsy for culture and histology

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153
Q

What is the treatment for chronic osteomyelitis?

A

Radical debridement down to living bone

Remove sequestra, and remove infected bone and soft tissue

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154
Q

What are signs of prothetic joint infections?

A

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

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155
Q

Define sinus tract

A

A narrow opening or passageway under the skin that can extend in any direction through soft tissue and results in dead space with potential for abscess formation

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156
Q

What are the causative organisms for prosthetic joint infections?

A
  • Gram +ve cocci (CoNS, Staph aureus, strep, entero)
  • Aerobic gram -ve bacilli (entero, pseudomonas)
  • Anerobes
  • Polymicrobial
  • Cultural negative
  • Fungi
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157
Q

How are prosthetic joint infections diagnosed?

A
  • Radiology: loosening
  • CRP >13.5 (prosthetic knee joint)
  • CRP >5 (hip joint)
  • Joint aspiration where WCC >1700/ml (knee)
  • WCC >4200/ml (hip)
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158
Q

What does the ‘Endo Klinik single stage revision’ treatment for prosthetic joint infection involve?

A
  • Aspirate joint to identify pathogen
  • Removal of infected tissue, foreign material, dead bone
  • Re-implant new prosthesis with antibiotic impregnated cement
  • IV antibiotics
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159
Q

What does the ‘two stage revision’ treatment for prosthetic joint infection involve?

A
  • Remove prosthesis
  • Take samples for MC+S and histology
  • 6 weeks IV antibiotics
  • Stop Abx for 2 weeks
  • Re-debride and sample at second stage
  • Re-implant with antibiotic impregnated cement
  • No further antibiotics if samples clear
160
Q

A 70year old women had a 1994 right total hip replacement, and 1998 revision of acetabular component. X-ray shows lysis around the distal part of the femoral component. H/O diabetes. What is the likely pathogen involved here:

(a) Coagulase negative staphylococci
(b) Staph aureus
(c) E.coli
(d) Haemophilus influenzae

A

Coagulase negative staphylococci

Rx: IV vancomycin and oral rifampicin

8 weeks later had second stage revision and cultures showed no growth.

161
Q

How do leucocyte derived proteases and cytokines act as host factors contributing to the pathogenesis of septic arthritis?

A

Cartilage degradation

Bone loss

162
Q

How does raised intra-articular pressure (a host factor) contribute to the pathogenesis of septic arthritis?

A

Impaired capillary blood flow

Cartilage and bone ischaemia and necrosis

163
Q

Name 4 host factors involved in the pathogenesis of septic arthritis

(n.b. bacterial factors include binding proteins, synovial membrane adherence and cytotoxins)

A
  • Leucocyte derived proteases and cytokines
  • Raised intra-articular pressure
  • Genetic deletion of macropage-derived cytokines
  • Absence of IL-10
164
Q

How does the genetic deletion of macrophage-derived cytokines (a host factor) contribute to the pathogenesis of septic arthritis?

A

E.g. lymphotoxin-a, TNF-a, IL-1 receptor

When present, these reduce host response normally in S.aureus sepsis in animal models.

i.e. genetic variation in cytokine expression increases susceptibility to septic arthritis

165
Q

How does the absence of IL-10 (a host factor) contribute to the pathogenesis of septic arthritis?

A

IL-10 absence in KO mice increases the severity of staphylococcal joint disease

i.e. genetic variation in cytokine expression increases susceptibility to septic arthritis

166
Q

Which groups are the most vulnerable to GI infections?

A

Infants

Elderly

167
Q

What are 6 reportable GI infections?

A 
Campylobacter
Salmonella
Shigella
E.coli 0157
Listeria
Norovirus
168
Q

For Campylobacter, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 1-10 days
(b) 2-20 days
(c) Poultry

169
Q

For E.coli 0157, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 1-5 days
(b) 1-4 days
(c) HUS, verotoxin

170
Q

For Shigella, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 12-96hrs
(b) 5-7 days
(c) Small infective dose, outbreaks

171
Q

For Salmonella (non-typhoidal, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 8-48hrs
(b) 4-7 days
(c) Rare cause systemic diagnosis

172
Q

For Vibrio parahaemolyticus, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 24-72hrs
(b) 2-10 days
(c) Shellfish

173
Q

For Vibrio cholera, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 1-5 days
(b) Variable
(c) ‘Ricewater stools’, endemic

174
Q

For Bacillus cereus, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 1-6hrs
(b) <1 day
(c) Heat stable emetic toxin i.e. rice

175
Q

For Staph aureus, what is the:

a) incubation period
(b) duration (days
(c) associated risk factors?

A

(a) 2-7hrs
(b) <1 day
(c) Preformed toxins

176
Q

What does the mechanism of cholera GI infection involve?

A
  • Cholera (secretory-diarrhoea) toxin
  • Superantigens
  • Host responses causing inflammation
177
Q

Describe the mechanism of cholera disease involving cholera toxin (secretory diarrhoea toxin)?

A
  • Cholera toxin binds to proteins
  • Via cAMP, Cl- channels open at the apical membrane of enterocytes
  • Cl- efflux into the lumen occurs
  • H2O and electrolytes are lost
178
Q

Describe the mechanism of cholera disease involving superantigens?

A
  • Superantigens bind directly to T-cell receptors and MHC molecules
  • This occurs OUTSIDE the peptide binding site
  • Massive cytokine production by CD4 cells occur
  • This causes systemic toxicity and suppression of adaptive response
179
Q

Describe the host responses in bacteraemia mechanism of disease?

A

Inflammatory diarrhoea or enteric fever (interstitial inflammation)

180
Q

Staphylococcus aureus can cause food poisoning. What is its method of transmission?

A

1/3 of the population are chronic carriers, and 1/3 transiently carry it.
It is spread by skin lesions on food handlers.

181
Q

What features do Staphylococcus aureus bacteria (that cause food poisoning) show on MC+S?

A
  • Catalase, coagulase positive Gram positive coccus
  • In tetrads/clusters on Gram stain
  • Yellow colonies on blood agar
182
Q

Staphylococcus aureus bacteria (that cause food poisoning) produces what toxin, which induces what clinical features?

A
  • An enterotoxin (exotoxin) that can act as a superantigen in the GI tract is produced
  • Releases IL-1 and IL-2
  • Causes prominent vomiting and watery, non-bloody diarrhoea
183
Q

What is the treatment for the prominent vomiting, and watery, non-bloody diarrhoea caused by the enterotoxins and superantigens in Staph aureus food poisoning?

A

Do not treat

Self-limiting

184
Q

What are gram-positive rods (spore-forming) that cause food poisoning?

A

Bacillus cereus

spores germinate in reheated fried rice

185
Q

What are the 2 toxins involved in Bacillus cereus?

A
  • Heat stable emetic toxin (not destroyed by reheating rice)

- Heat labile diarrhoeal toxin (food is not cooked to a high enough temperature)

186
Q

What are the clinical features of Bacillus cereus?

A

Watery, non-bloody diarrhoea (self-limiting)
Rare cause of bacteraemia in vulnerable populations
Cerebral abscesses (rare)

187
Q

What is a gram-positive anaerobe that can cause botulism and food poisoning?

A

Clostridia

  • Clostridium botulinum = botulism
  • Clostridium pefringens = food poisoning
188
Q

What is the source of clostridium botulinum (botulism)?

A

Canned or vacuum packed foods
Ingestion of preformed toxin (inactivated by cooking)
e.g. in honey for infants

189
Q

What is the mechanism of clostridium botulinum gram +ve anaerobe that causes botulism, and the treatment?

A
  • Blockade of ACh release from peripheral nerve synapses

- Treat with antitoxin

190
Q

What is the source of Clostridium pefringens (food poisoning)?

A

Reheated food (meat)

191
Q

What is the incubation period and clinical features for Clostridium perfringens (food poisoning, Gram +ve anaerobe)?

A

Incubation = 8-16hours
Watery diarrhoea
Cramps
Little vomiting lasting 24hrs

192
Q

What is the mechanism of clostridium botulism (gram +ve anaerobe) causing food poisoning?

A

The enterotoxin acts as a superantigen, and affects the colon (but not the small bowel small bowel)

193
Q

Pseudomembranous colitis can occur with Clostridium difficile which is antibiotic-related colitis. This occurs in how many hospitalised patients, and mainly with which antibiotics?

A

3-30% patients

Cephalosporins, cipro and clindamycin are often involved

194
Q

What is the treatment for closteridium difficile?

A

Metrodinadazole
Vancomycin
(taken orally)
Stop other Abx where possible

195
Q

Listeria monocytogenes presents in a population as…?

A

Outbreaks of febrile gastroenteritis

196
Q

What does the stain for Listeria monocytogenes show?

A

Gram-positive rod
B-haemolytic
Aersculin positive
Tumbling motility

197
Q

What is the source for Listeria monocytogenes GI infection?

A

Refrigerated food (cold enhancement) i.e. unpasteurised dairy
Vegetables
(Grows at 4 degrees c)

198
Q

What are the clinical symptoms of Listeria monocytogenes?

A 
Watery diarrhoea
Cramps
Headache
Fever
Little vomiting
199
Q

What patient groups are particularly susceptible to Listeria monocytogenes?

A 
Perinatal infection (pregnant women)
Immunocompromised patients
200
Q

What is the treatment for Listeria monocytogenes?

A

Ampicillin

201
Q

Describe features of enterobacteriacae?

A

Facultative anerobes
Glucose/actose fermenters (LF)
Oxidase negative

202
Q

E.coli is also described as traveller’s diarrhoea. What is the source of E.coli?

A

Food/water contaminated with human faeces

203
Q

What are the enterotoxins involved with the mechanism of disease in E.coli and where do they act?

A
  • Heat labile stimulates adenyl cyclase and cAMP
  • Heat stable stimulates guanylate cyclase

These act on jejeunum and ileum, not on colon

204
Q

Name the various types of E.coli that match up with the features:

(a) Toxigenic, main cause of traveller’s diarrhoea
(b) Pathogenic, infantile diarrhoea
(c) Invasive, dysentery
(d) Haemorrhagic, can cause HUS

A

(a) ETEC = toxigenic, main cause of traveller’s diarrhoea
(b) EPEC = pathogenic, infantile diarrhoea
(c) EIEC = invasive, dysentery
(d) EHEC = haemorrhagic (O157), can cause HUS (H7)

205
Q

What bacteria is a non-lactose fermenter and H2S producer?

A

Salmonella

tests use TSI agar, XLD agar and selenite F broth

206
Q

What are the 3 species of Salmonellae?

A
  1. S. typhi (and paratyphi)
  2. S. enteritidis
  3. S. cholerasuis
207
Q

What antigens are produced by Salmonellae?

A
  • Cell wall O (groups A-I)
  • Flagellar H
  • Capsular Vi (virulence, anti-phagocytic)
208
Q

How is Salmonella enteritidis (enterocolitis) transmitted?

A

Poultry
Eggs
Meat

209
Q

How is Salmonella typhi (typhoid/enteric fever) transmitted?

A

Only by humans

Multiplies in Payer’s patches

210
Q

What regions does Salmonella enteritidis invade to cause enterocolitis?

A

Epithelial and sub-epithelial tissue of small and large bowel

211
Q

What are the clinical symptoms and signs of enterocolitis (Salmonella enteritidis)?

A

Non-bloody diarrhoea (self-limiting, no treatment needed)
Bacteraemia is rare
Stool positivity diagnoses

212
Q

What are the clinical symptoms and signs of typhoid/enteric fever (Salmonella typhi)?

A 
Slow onset fever
Constipation
Splenomegaly
Rose spots
Anaemia + leukopenia
Bradycardia
Haemorrhage and perforation
213
Q

How is salmonella typhi (typhoid/enteric fever) diagnosed and treated?

A

Diagnosis is with a positive blood culture

Treatment = ceftriaxone

214
Q

What bacteria is a non-lactose fermenter, non-H2S producer and non-motile?

A

Shigellae

215
Q

What antigens are present with Shigellae?

A
  • Cell wall O antigens

- Polysaccharide (groups A-D): S.sonnei, S.dysenteriae, S.flexneri (MSM)

216
Q

What is the most effective enteric pathogen?

A

Shigella

Due to low infectious dose required (50)
n.b. it has no animal reservoir or carrier state

217
Q

Dysentery (caused by Shigellae dysenteriae) involves what processes?

A
  • Invasion of cells of mucosa of distal ileum and colon

- Shiga enterotoxin is produced

218
Q

What is the treatment for Shigellae infections?

A

Avoid antibiotics

But ciprogloxacin given if required

219
Q

What are some features of Vibrios (cholera) bacteria?

A

Curved
Comma-shaped
Late lactose fermenters
Oxidase positive

220
Q

What are the types of Vibrio cholera?

A
  • O1 group = endemics, with various biotypes and serotypes

- Non-O1 group = sporadic or non-pathogens

221
Q

How is vibrio transmitted?

A

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

222
Q

What is the mechanism of action for vibrio cholerae?

A

Colonisation of small bowel
Secretion of enterotoxin with A and B subunit, which persistently stimulate adenylate cyclase and cAMP
Opens Cl- channels and causes massive diarrhoea (rice water stool) without inflammatory cells

223
Q

What is the treatment for vibrio cholerae infection?

A

Treat the losses (i.e. supportive)

± Doxycycline

224
Q

What are the species of Vibrios?

A
  • Vibrios cholera (O1 and non-O1 group)
  • Vibrio parahaemolyticus
  • Vibrio vulnificus
225
Q

How is Vibrio parahaemolyticus transmitted?

A

Ingestion of raw or undercooked seafood (i.e. oysters)
Major cause of diarrhoea in Japan
Self-limiting (3days)

226
Q

How is vibrio vulnificus transmitted?

A

Cellulitis in shellfish handlers

In HIV patients, it induces sepsis, D+V.

227
Q

What is the treatment for vibrios pathogens?

A

Doxycycline

228
Q

What are the features of. Campylobacter bacteria?

A 
Curved, comma or S-shaped
Micro-aerophilic
C.jejuni at 42 degrees C
Oxidase positive
Motile
229
Q

Campylobacter is self-limiting but symptoms can last for weeks (up to 20 days). We only treat campylobacter in which patients and using which treatment?

A

Only treat if immunocompromised

Rx macrolides

230
Q

How is campylobacter transmitted?

A

Contaminated food and water with animal faeces

poultry, meat, unpasteurised milk

231
Q

What are the clinical features of Campylobacter?

A

Watery, foul-smelling diarrhoea
Bloody stool
Fever and severe abdominal pain

232
Q

What are 3 long-term sequelae that may occur post-Campylobacter infection?

A

GBS syndrome
Reactive arthritis
Reiter’s syndrome

233
Q

What is the treatment for campylobacter?

A

Erythromycin or ciprofloxacin if infection is in the first 4-5 days

234
Q

What can Yersinia enterocolitica cause?

A

Enterocolitis

Mesenteric adenitis

235
Q

What conditions is Yersinia enterocolitica associated with?

A

Reactive arthritis

Reiter’s syndrome

236
Q

What are some features of Yersinia enterocolitica bacteria?

A

Non-lactose fermenter

Prefers 4 degrees C i.e. ‘cold enrichment’

237
Q

How is Yersinia enterocolitica transmitted?

A

Via contaminated food with domestic animal faeces

238
Q

What condition is caused by Mycobacteria (M.Tuberculosis, M.Avium Intracellulare)?

A

Tuberculosis

239
Q

Give 3 examples of protozoa

A

Entamoeba histolytica
Giardia lamblia
Cryptosporidium parvum

240
Q

What are the features of the protozoa, entamoeba histolytica, in (i) diarrhoea, and (ii) non-diarrhoeal illness?

A

(i) Motile trophozoite in diarrhoea
(ii) Non-motile cyst in non-dirrhoeal illness

4 nuclei, no animal resevoir

241
Q

How is entamoeba histolytica removed normally?

A

Killed by boiling or removed by water filters

242
Q

What is the mechanism of action of entamoeba histolytica?

A

Ingestion of cysts leads to trophozoites in the ileum
These colonise the caecum and colon
Results in ‘flask-shaped’ ulcers

243
Q

What are the acute and chronic clinical features of entamoeba histolytrica?

A

Acute: dysentery, flatulence, tenesmus
Chronic: weight loss, ±diarrhoea, liver abscess

244
Q

How is entamoeba histolytica confirmed on diagnosis?

A

Stool microbiology shows wet mount, iodine and trichrome

Serology confirms in invasive disease

245
Q

What is the treatment for entamoeba histolytica protozoal infection?

A

Metronidazole and peromomycin in luminal disease

246
Q

What protozoa has the features of a ‘pear-shaped’ trophozoite, 2 nuclei, 4 flagella and a suction disc?

A

Giardia lamblia

247
Q

How is giardia lamblia protozoal infection transmitted?

A

Ingestion of cyst from faecally contaminated water or food

248
Q

What is the mechanism of action of giadia lamblia infection?

A

Excystation at duodenum
Pear-shaped trophozoite attaches
No invasion
Results in malabsorption of protein and fat

249
Q

What groups of people are likely to suffer from Giardia lamblia infection?

A 
Travellers
Hikers
Day-care
Psychiatric hospitals
MSM
250
Q

What are the clinical features of giardia lamblia?

A

Foul-smelling, non-bloody diarrhoea
Cramps
Flatulence
No fever

251
Q

How is the diagnosis made for giardia lamblia, and what is the treatment?

A

Stool MC+S
ELISA
‘String test’

Rx = metronidazole

252
Q

Stool MC+S for using the modified Kinyoun acid fast stain is used for the diagnosis of which infection, and what is shown?

A

Oocysts are seen in the stool by modified Kinyoun acid fast stain with Cryptosporidium parvum (protozoal infection affecting jejenum)

253
Q

Give 3 reasons why norovirus tends to cause outbreaks?

A
  • Low infectious dose needed (18-1000 viral particles)
  • Environmental resilience (survives in 0-60 degrees)
  • No long immunity against it
254
Q

GII.4 is currently the predominant stain of what infection?

A

Norovirus

255
Q

A dsRNA ‘wheel-like’ virus refers to which virus?

A

Rotavirus

256
Q

Rotavirus replicates in which region?

A

The mucosa of the small intestine

257
Q

What are the clinical features of rotavirus?

A
  • Secretory diarrhoea (with no inflammation)

- Watery diarrhoea (mechanism unknown, but may be caused by stimulation of the enteric nervous system)

258
Q

Rotavirus is common and by age 6 most children globally have antibodies to at least one type. What confers lifelong immunity to rotavirus?

A

Exposure to natural rotavirus infection twice confers lifelong immunity

259
Q

What types of adenovirus cause non-bloody diarrhoea below 2 years of age?

A

Types 40 and 41

260
Q

In immunocompromised patients, what types of adenovirus cause non-bloody diarrhoea and infection?

A

ANY type

261
Q

Using which investigations can we detect and diagnose adenovirus GI infections?

A

Stool MC+S
Antigen detection
PCR

262
Q

Poliovirus, enteroviruses (coxsackie, ECHO), hepatitis A are all transmitted via which route?

A

Faecal-oral route

263
Q

Vaccines for cholera exist for serogroups O1 and O139 in which 2 forms?

A

(a) Inactivated, whole cell with B-subunit of toxins

(b) Live attenuated, but not recommended

264
Q

Vaccines are available/being tested for which GI infection pathogens?

A
  • Cholera
  • Campylobacter
  • ETEC
  • Salmonella typhi
  • Rotavirus
265
Q

Bacterial organisms that can cause vertebral oseomyelitis include…

A

Brucella

Salmonella

266
Q

What two techniques can be used for the surgical treatment of chronic osteomyelitis?

A
  • Modified Lautenbach technique

- Papineau technique (this has a higher success rate)

267
Q

What are the mechanisms that antibiotics target

A
  1. inhibitors of cell wall synthesis
  2. inhibitors of protein synthesis
  3. inhibitors of DNA, RNA synthesis enzymes (DNA gyrase)
  4. inhibitors of folate metabolism
  5. cell membrane toxins
268
Q

Which antibiotics are inhibitors of cell wall synthesis?

A
  • B-lactams: penicillins, cephalosporins, carbapenems

- Glycopeptides: vancomycin, teicoplanin

269
Q

B-lactams (cell wall synthesis inhibitors, bactericidal) include

A
  • penicillins e.g. piperacillin
  • cephalosporins
  • carbapenems

Active against rapidly dividing bacteria. Ineffective against bacteria that lack cell walls (e.g. Mycoplasma + Chlamydia).

270
Q

Glycopeptides (cell wall synthesis inhibitors) include

A
  • Vancomycin

- Teicoplanin

271
Q

B-lactamase inhibitors are useful for protecting penicillins from enzymatic breakdown and include coverage to S.aureus, GRam negatives and anerobes. What are 2 examples?

A
  • Clavulanic acid (given with amoxicillin = co-amoxiclav)

- Tazobactam (given with piperacillin = piptaz)

272
Q

What is a 1st generation cephalosporin?

A

Cephalexin

273
Q

What is a 2nd generation cephalosporin?

A

Cefuroxime

Active against many b-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes.

274
Q

What are three 3rd generation cephalosporins?

A
  • Cefotaxime
  • Ceftriaxone
  • Ceftazidime [useful against Psuedomonas].
275
Q

Extended spectrum B-lactamase (ESBL) will produce organisms that are resistant to….

A

ALL cephalosporins

Therefore carbapenems must be used to treat ESBL enzyme infections

276
Q

Carbapenems include…

A

Meropenem
Imipenem
Ertapenem

Useful for treating ESBL infections

277
Q

Carbapenemase enzymes are seen in which severe infections

A

Multi-drug resistant Acinetobacter and Klebsiella species

278
Q

How are b-lactams excreted?

A

Renally excreted

Relatively non-toxic with short half-life

279
Q

Glycopeptides are bactericidal and inhibit cell wall synthesis (like b-lactams!). What are 2 examples

A

Vancomycin [treats MRSA]
Teicoplanin

n.b. these are nephrotoxic. Active against Gram +ves

280
Q

Which antibiotics are inhibitors of protein synthesis (5 types)?

A
  • Aminoglycosides: gentamicin, amikacin, tobramycin
  • Tetracyclines
  • Macrolides: erythromycin, clindamycin
  • Chloramphenicol
  • Oxazolidinones: linezolid
281
Q

Aminoglycosides (inhibitors of protein synthesis) examples and side effects

A
  • Gentamicin
  • Amikacin
  • Tobramycin

Bactericidal. Otoxic and nephrotoxic. Active versus pseudomonas aeruginosa.

282
Q

Tetracyclines (inhibitors of protein synthesis):

(a) are useful against which pathogens?
(b) what are the side effects?

A
  • Active against most bacteria INCLUDING intracellular pathogens e.g. chlamydia, mycoplasma, rickettsia
  • Widespread resistance however

SE: Light-sensitive rash
- Contraindicated in pregnancy and children

283
Q

Macrolides (inhibitors of protein synthesis) examples, and which pathogens are they active against

A
  • Erythromycin
  • Clarithromycin
  • Azithromycin

Active against staph + strep in those allergic to penicillin. Also active against Campylobacter + Legionella

284
Q

Chloramphenicol (inhibitor of protein synthesis) is a bacteriostatic, with broad anti-bacterial activity, rarely used drug now. Why is it rarely used?

A

Risk of aplastic anaemia

Grey baby syndrome in neonates

285
Q

Oxazolidinones (inhibitor of protein synthesis) - what is an example and what is it active against?

A

Linezolid

Highly active against gram +ve organisms, including MRSA and VRE. But it is expensive.

286
Q

Linezolid is an oxazolidinone (inhibitor of protein synthesis). It is highly active against gram +ve organisms, including MRSA and VRE. It is expensive and may cause which side effect?

A

Thrombocytopenia

287
Q

Inhibitors of DNA synthesis antibiotics include…

A
  • Quinolones: ciprofloxacin, levofloaxin, moxifloxacin

- Nitroimidazoles: metronidazole, tinidazole

288
Q

Quinolones (or fluoroquinolones) are inhibitors of DNA synthesis by DNA gyrase. They are bactericidal. What are examples and what are they active against?

A
  • Ciprofloxacin
  • Levofloxacin

Active versus gram -ve including Pseudomonas aeruginosa. Active against gram +ves too and intracellular like chlamydia.

289
Q

Nitroimidazoles are inhibitors of DNA synthesis. Rapidly bactericidal. Examples and what is it active against?

A
  • Metronidazole
  • Tinidazole

Active versus anaerobes and protozoa e.g. Giardia

290
Q

Nitroimidazoles are inhibitors of DNA synthesis that are rapidly bactericidal e.g. metronidazole. These are related compounds to….

A

Nitrofurans

e.g. nitrofurantoin

291
Q

Inhibitors of RNA synthesis antimicrobials include…

A

Rifamycins:

  • rifampicin
  • rifabutin
292
Q

Rifamycins (inhibit RNA synthesis) are effective vs mycobacteria + chlamydia. What should be monitored, and why shouldn’t these be given alone?

A
  • Monitor LFTs - hepatitis
  • Do not give alone as resistance (Chr mutatio) develops rapidly
  • RNA polymerase is the target for these bactericidal drugs.
  • A single amino acid change occurs in the b-subunit of RNA polymerase
293
Q

2 cell membrane toxins used for anti-microbial use are…

A
  • Daptomycin: gram +ve. MRSA and VRE as alternative to linezolid.
  • Colistin: gram -ve, e.g. psuedomonas, acinetobacter, Klebsiella. basically for multi-resistant infections. nephrotoxic.
294
Q

Inhibitors of folate metabolism antimicrobial drugs examples

A
  • Sulfonamides

- Diaminopyrimidines e.g. trimethoprim

295
Q

Inhibitors of folate metabolism antimicrobial drugs include sulfonamides and diaminopyrimidines e.g. trimethoprim. Combined use of the two is useful for….

A

Pneumocystis jiroveci pneumonia

otherwise, use alone is rare due to common sulphonamide resistance.

296
Q

Methicillin Resistant Staphylococcus aureus (MRSA) mechanism of resistance

A
  • mecA gene encodes a novel penicillin binding protein (2a)

- B-lactams cannot bind to these well. Low affinity for B-lactam binding.

297
Q

What are 3 yeast

A
  • Candida
  • Cryptococcus
  • Histoplasma
298
Q

What are 3 moulds?

A
  • Aspergillus
  • Dermatophytes
  • Agents of mucormycosis
299
Q

Characteristic ‘germ tubes’ are produced by which pathogen?

A

Yeast - candida albicans

300
Q

Which candida is common in patients with indwelling catheters or drug abuse?

A

Candida endophthalmitis

301
Q

B D Glucan assay serology is useful for diagnosis of which pathogen?

A

Yeast - candida albicans

302
Q

Treatment of candidasis

A
  • Echinicandin empirically and for non-albicans Candida
  • Fluconazole for Candida albicans
  • Ambisome (e.g. CNS)
  • Fluconazole (e.g. urine) - Voriconazole (e.g. CNS) for organ-based disease
303
Q

Cryptococcosis caused by Cryptococcus neoformans risk is increased in patients with….

A

impaired T-cell immunity:

  • AIDS patients who have CD4 T cells usually <200/ml
  • T cell immunosuppressants post-solid organ transplant
304
Q

Cryptococcus neoformans can cause meningitis and space-occupying lesions in the brain and lung. There is increased resistance to ….

A

Amphotericin B

305
Q

India ink stain helps to confirm diagnosis of

A

Cryptococcus neoformans

n.b. it grows from Eucalyptus leaves

306
Q

Management of cryptoccocosis

A
  • 3 weeks of Amphotericin B +/- flucytosine
  • Repeat LP for pressure management
  • Secondary suppression with fluconazole
307
Q

Methenamine silver (GMS) stain shows fungus balls indicates…

A

Aspergillus

308
Q

Management of aspergillosis

A
  • Voriconazole
  • Ambisome
    (Caspofungin/Itraconazole are less good)

At least 6 weeks of therapy

309
Q

Onchomycosis refers to

A

thickening and discolouration of nails

Can be caused by trichophyton, epidermophyton, microsporum spp

310
Q

Pityriasis versicolor

A

Fungal infection
Reaction to sun
Caused be Malassezia furfur
Dark/orangey rash patch

311
Q

Mucormycosis is….

A

Cellulitis of the orbit and face progress with discharge of black pus from the palate and nose.

Brain involvement - LOC

312
Q

Mucormycosis - cellulitis of the orbit and face with discharge of black pus from palate and nose. This tends to occur in which patients?

A

Immunocompromised
Poorly controlled DM

Caused by rhizopus spp, rhizomucor spp, mucor spp

313
Q

Treatment of mucormycosis

A

Surgical debridement
Amphotericin
Posaconazole

314
Q

Gram positive spore forming anaerobe

A

C-difficile

315
Q

What 3 factors influence SSI risk?

A
  1. host defence
  2. wound environment
  3. pathogens
316
Q

High ESR, with FDG-PET/CT showing highly increased FDG uptake of the aorta, subclavian arteries, and femoral arteries. What is the likely diagnosis?

A

Increased FDG = increased glycolysis and inflammation.
The inflammation of vessels = large vessel vasculitis.
Patient was given corticosteroids and ESR normalised.

317
Q

High ferritin levels are associated with which 2 syndromes

A
  • Adult onset Still’s disease

- Macrophage activation syndrome

318
Q

The IGRA test for TB is not good for distinguishing between latent vs active TB. What does IGRA stand for?

A

IFN gamma release assay

319
Q

HACEK are rare causes of bacterial infective endocarditis which grows a negative blood culture. What does HACEK stand for?

A 
Haemophilus
Aggregatibacter
Cardiovacterium
Eikenelia
Kingella
320
Q

What diagnostic test should be done if there is clinical suspicion of infective endocarditis

A

Total transthoracic echocardiogram

321
Q

Duke’s criteria for infective endocarditis: 2 major or 1 major + 3 minor criteria are needed.
What are major criteria?

A
  1. persistent bacteraemia (>2 positive blood cultures)
  2. TTE shows vegetation
  3. Serology for BArtonella, Coxiella or Brucella
322
Q

Duke’s criteria for infective endocarditis: 2 major or 1 major + 3 minor criteria are needed.
What are minor criteria?

A
  • Predisposition (murmur, IVDU)
  • Inflammatory markers
  • Immune complexes: splinters, RBCs in urine
  • Embolism
  • Atypical TTE
  • 1 positive blood culture
323
Q

Giant cell arteritis criteria

A 
Age >50 - most important
Headache [not needed for Dx]
Jaw claudication
ESR >45
Visual changes
Ischaemic tongue
High risk of stroke/blind
324
Q

What is the gold standard test for giant cell arteritis

A

Temporal biopsy

325
Q

Adult onset stills can present with…

A

salmon pink rash
ferritin is really high
DDx: macrophage activation syndrome

326
Q

Malignant causes of fever

A
  • Lymphoma
  • Leukaemia - BM biopsy
  • Renal cell carcinoma
  • HCC/liver mets
327
Q

Treatment of salmonella GI infection

A

Supportive
Ciprofloxacin
Azithromycin

328
Q

Treatment of campylobacter GI infection

A

Supportive

Self-limiting usually

329
Q

Bartonella henselae (gram -ve rod) is found in kittens. it causes 2 diseases

A
  • cat scratch disease

- bacillary angiomatosis [in immunocompromised]

330
Q

Cat scratch disease (caused by Bartonella henselae (Gram -ve rod) presents with a macule at the site of innoculation. It becomes pustular. What is the treatment?

A
  • Erythromycin
  • Doxycycline

[add rifampicin for the disseminated bacillary angiomatosis disease]

331
Q

Bacillary angiomatosis (caused by Bartonella henselae (Gram -ve rod) presents with a as a disseminated multi-organ disease with BV involvement. Skin papules exist. What is the treatment?

A
  • Erythromycin
  • Doxycycline
  • Rifampicin

n.b. cat scratch disease is not disseminated and also caused by Bartonella. It is treated with erythro + doxy only.

332
Q

Toxoplasmosis treatment

A

Spiramycin

Pyrimethamine plus sulfadiazine

333
Q

Brucellosis increased risk with

A

unpasteurised milk/diary

334
Q

Brucellosis treatment

A

Doxycycline plus:

Gentamicin or rifampicin

335
Q

Unpasteurised diary products can lead to

A

Brucellosis
Coxiella burnetii (Q fever) - milk
Listeria

336
Q

Treatment of Coxiella burnetii (Q fever) which is caught from cows/unpasteurised MILK

A

Doxycycline

hydroxychloroquine

337
Q

Treatment of Lyssa virus (rabies)

A

Immunoglobulin

Vaccination

338
Q

Treatment of rat bite virus

A

Penicillins

Rats can also cause hantavirus pulmonary syndrome with has supportive management only.

339
Q

Viral haemorrhagic fever treatment

A

Supportive

340
Q

What is the resevoir for Lyssa virus (Rabies)

A

Bats

  • bat bite with fever, most worrying is rabies i.e. LYSSA virus.
341
Q

Slow-growing mycobacterium examples?

A
  • Mycobacterium avium complex (MAC) or m.avium intracellulare (MAI)
  • Myobacterium tuberculosis complex: M.bovis BCG, M.tuberculosis
  • M. marinum
  • M. ulcerans
342
Q

Rapid-growing mycobacterium tend to cause skin and soft-tissue infections. What are some examples?

A
  • Mycobacterium abscessus
  • M. chelonea
  • M. fortuitum
343
Q

Ungrouped example of mycobacterium i.e. it is neither rapid nor slow-growing

A

Mycobacterium leprae

344
Q

What kind of vaccine is rubella

A

Live attenuated

345
Q

Mycobacterium avium intracellulare (MAI) a.k.a M. avium complex (MAC) is a slow-growing non-tuberculous mycobacteria. How does it affect those who are:

(a) Immunocompetent?
(b) Immunosuppressed?

A

MAI or MAC affects

(a) immunocomponent by invading bronchial tree. Usually in those with pre-existing lung disease e.g. bronchiectasis, cavities
(b) immunosuppressed by causing disseminated infection.

346
Q

M.ulcerans is a non-tuberculous mycobacterium that is slow-growing. It can cause….

A
  • Skin lesions e.g. Bairnsdale ulcer, Buruli ulcer

- Chronic progressive painless ulcer

347
Q

M.marinum is a slow growing non-tuberculous mycobacteria that can cause

A

swimming pool granulomas

348
Q

Rapid growing non-tuberculous mycobacteria e.g. m.abscessus, m.chelonea, m.fortuitum can cause ….

A

skin and soft tissue infections

found in hospital settings in patients with vascular catheters/devices

349
Q

Treatment of mycobacterium avium complex (MAC) a.k.a intracellular (MAI)

A

Clarithromycin/azithromycin
Rifampicin
Ethambutol
± Amikacin/streptomycin

350
Q

Treatment of rapid growing non-tuberculous mycobacterium is based on

A

Susceptibility testing

usually macrolife based e.g. clarithromycin

351
Q

2 types of mycobacterium leprae

A
  • paucibacillary tuberculoid

- multibacillary lepromatous

352
Q

lifetime risk of developing active TB from latent TB

A

10%

353
Q

What type of vaccine is the m.bovis (bacille calmette-guerin BCG) injection?

A

Live attenuate M.bovis strain

For babies in high prevalence communities. 70-80% efficacy preventing severe childhood TB. Protection wanes over time.

354
Q

Ghon focus/complex is typically seen in CXR of..

A

tuberculosis

it is a granuloma in the lungs with ipsilateral lymphadenopathy.

355
Q

Rare allergic reactions can occur with TB including which feature

A

Erythema nodosum

occasionally disseminated/miliary

356
Q

Risk factors for TB reactivation

A
  • immunosuppression
  • chronic alcohol excess
  • malnutrition
  • ageing
357
Q

What is scrofula

A

Lymphadenitis

usually in cervical lymph nodes. abscesses and sinuses can occur. can be present with extra-pulmonary TB.

358
Q

Gastrointestinal TB sign

A

Swallowing of tubercles

359
Q

Pott’s disease refers to

A

Spinal TB

haematogenous spread to bones and joints of TB.

360
Q

Features of miliary TB

A
  • Millet seeds on CXR
  • Progressive disseminated haematogenous TB
  • Increasing due to HIV
361
Q

Gold standard for TB

A

Sputum culture

can take up to 6 weeks.

362
Q

The tuberculin skin tests (Mantoux) induces what type of hypersensitivity reaction?

A

Type 4 delayed hypersensitivity reaction

n.b. Does not distinguish between active vs latent infection of TB, only previous exposure. IGRAs are the same in this respect.

363
Q

TB management

A 
Rifampicin (6 months)
Isoniazid (6 months)
Pyrazinamide (2 months)
Ethambutol (2 months)
\+ pyridoxine
364
Q

Rifampicin [6 months] side effects

A
  • Raised transaminases
  • Cytochrome P450 inducer
  • Orange secretions
365
Q

vitamin D given for TB

A

pyridoxine 10mg OD

  • helps to prevent peripheral neuropathy, a SE of isoniazid.
366
Q

Isoniazid [6months] side effects

A
  • Peripheral neuropathy (pyridoxine 10mg OD helps avoid this)
  • Hepatotoxicity
367
Q

Pyrazinamide [2 months] side effects

A

hepatotoxicity

368
Q

Ethambutol [2 months] side effects

A

visual disturbance

369
Q

If there is CNS tuberculosis, the therapy (RIPE) is given for what time period instead?

A

10 months

rather than 6 months

370
Q

Multi-drug resistant TB (MDR) refers to the resistance to…

A

rifampicin and isoniazid

371
Q

Extremely drug-resistant TB (XDR) refers to the resistance to….

A

fluoroquinolones and at least 1 injectable

372
Q

Treatment for multi-drug resistant TB

A

4-5 drug regimen combination, longer duration:

  • Quinolones
  • injectable aminoglycosides e.g. amikacin
  • PAS
  • cycloserine
  • ethionamide
373
Q

Types of helminths

A
  • Cestodes (tape worms) e.g. hydatid
  • Trematodes (flukes) e.g. schistosomiasis
  • Nematodes (roundworms) e.g. hookworms, strongyloides
374
Q

Hydatid is a dog tapeworm. Complications in humans arise from ….

A

Hydatid lead to cysts:

  • Mass effect
  • Cyst rupture
375
Q

Treatment of hydatid tapeworm and cysteicercosis (dying worms and cysts)

A

Worms - praziquantel

Cysts - PAIR procedure, albendazole, steroids

376
Q

Treatment of schistosomiasis (trematodes, a.k.a. flukes)

A

Praziquantel

377
Q

Treatment of roundworms such as stronglyoides

A

Ivermectin

378
Q

Myiasis is the parasitisation of human flesh by…

A

fly larvae

local damage as the maggot eats necrotic flesh.

379
Q

Treatment of myiasis

A

Removal of larva by asphyxiation or surgery

380
Q

Shingles occurs as a reactivation of latent VZV in the dorsal root ganglia. What is a complication?

A

Post-herpetic neuralgia

381
Q

Acyclovir action

A

inhibits DNA synthesis

HSV1 > HSV2&raquo_space;> VZV

382
Q

HSV encephalitis is treated with

A

IV Acyclovir

for 21 days

383
Q

Where does CMV virus remain latent

A

Blood monocytes and dendritic cells

It becomes reactivated following immunosuppression

384
Q

CMV antiviral drugs

A

Ganciclovir
Vanganciclovir
Foscarnet
Cidofovir

385
Q

side effect of ganciclovir (CMV antiviral)

A

bone marrow toxicity

386
Q

side effect of foscarnet and cidofovir (CMV antiviral)

A

nephrotoxic

387
Q

Treatment of post-transplant lymphoproliferative disease (B cell over-activation due to EBV)

A
  • Reduce immunosuppression

- Rituximab (anti-CD20)

388
Q

BK virus can lead to lifelong carriage in the kidneys and urinary tract. It can lead to what problems in the immunocompromised?

A
  • Haemorrhagic cystitis - in bone marrow transplant patients

- BK nephritis - in renal transplant patients

389
Q

Treatment of BK virus haemorrhagic cystitis

A
  • Bladder washouts
  • Reduce immunosuppression
  • Cidofovir (+ probenicid)
390
Q

Treatment of BK nephropathy

A
  • Reduce immunosuppresion

- IV Ig

391
Q

Treatment of adenovirus

A
  • Cidofovir
  • IV Ig
  • Brincidofovir
392
Q

HSV resistance to acyclovir usually has mutations in which enyzme?

A

Viral thymidine kinase (95%)

5% is DNA polymerase
These must be treated with foscarnet or cidofovir.

393
Q

CMV resistance to ganciclovir involves which genetic mutation most commonly?

A

Protein kinase gene

Give foscarnet or cidofovir instead

394
Q

Immunoglobulin preparations

(a) prophylactic
(b) post-exposure prophylaxis
(c) therapeutic

A

(a) palivizumab (RSV)
(b) VZV Ig, Hepatitis B Ig, human rabies Ig
(c) IV Ig for CMV, rituximab for EBV-driven PTLD

395
Q

Treatment for non-falciparum malaria (e.g. vivax or ovale)

A

Chloroquinine

And primaquinine after checking not G6PD deficient

396
Q

Treatment for falciparum malaria

A

IV artesunate

or IV quinine and doxycycline

397
Q

Antiviral treatment for chickenpox and shingles (VZV) after acyclovir

A
  • acyclovir 1st line
  • valacyclovir - acyclovir prodrug
  • famcyclovir
  • 2nd line = foscarnet or cidofovir for acyclovir-resistant virus.

Year 5 Pathology (6 decks)

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