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Path Laz (condensed) (COPY) > Micro > Flashcards

Micro Flashcards

1
Q

Name three organisms that cause acute meningitis.

A

Neisseria meningitidis

Streptococcus pneumoniae

Haemophilus influenzae

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2
Q

How many serotypes of N. meningitidis are there?

A

3 – A, B and C

NOTE: the meningitis vaccine is for meningitis C (although there is one available for meningitis B)

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3
Q

List some other, rarer bacterial causes of acute meningitis.

A

Listeria monocytogenes

Group B Streptococcus

Escherichia coli

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4
Q

How long does N. meningitidis take to cause infection?

A

< 10 days

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5
Q

Outline the presentation of TB meningitis.

A

Similar presentation to acute meningitis but takes weeks to present

Tends to occur in immunocompromised patients

Involves the meninges and basal cisterns of the brain and spinal cord

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6
Q

hat is a typical MRI feature of TB meningitis?

A

Leptomeningeal enhancement

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7
Q

What is the most common infections of the CNS?

A

Aseptic meningitis

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8
Q

What are the most common causative organisms in aseptic meningitis?

A

Coxsackie group B viruses

Echoviruses

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9
Q

Which age group is susceptible to aseptic meningitis?

A

< 1 year

NOTE: normally self-resolving after 1-2 weeks

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10
Q

List some viruses that cause encephalitis

A

Mumps

Measles

Enteroviruses

Herpes viruses

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11
Q

What is becoming a leading cause of encephalitis worldwide?

A

West Nile virus

NOTE: this is transmitted by mosquitoes and birds

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12
Q

Which bacterium is associated with causing encephalitis?

A

Listeria monocytogenes

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13
Q

Name two types of amoeba that cause encephalitis.

A

Naegleria fowleri

Acanthamoeba species and Balamuthia mandrillaris

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14
Q

What is toxoplasmosis and how is it spread?

A

Obligate intracellular parasite

Spread via oral, transplacental or organ transplant route

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15
Q

Name a common spinal infection.

A

Pyogenic vertebral osteomyelitis

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16
Q

What are some long-term consequences of Pyogenic vertebral osteomyelitis?

A

Permanent neurologic defects

Significant spinal deformity

Death

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17
Q

Describe the typical CSF analysis results of Bacterial meningitis

A

Turbid

High polymorphs

High protein

Low glucose

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18
Q

Describe the typical CSF analysis results of Aseptic meningitis

A

Clear

High lymphocytes

High protein

Normal glucose

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19
Q

Describe the typical CSF analysis results of Tuberculous meningitis

A

Clear

High lymphocytes

High protein

Low glucose

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20
Q

Describe the Gram-stain and microscopic appearance of S. pneumoniae

A

Gram-positive alpha-haemolytic diplococci

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21
Q

Describe the Gram-stain and microscopic appearance of N. meningitidis

A

Gram-negative non-haemolytic diplococci

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22
Q

Describe the Gram-stain and microscopic appearance of L. monocytogenes

A

Gram-positive rods

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23
Q

Describe the Gram-stain and microscopic appearance of TB

A

Stains positively with Ziehl-Neelsen (red and blue)

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24
Q

Describe the Gram-stain and microscopic appearance of Cryptococcus

A

Stains positively with India ink (appears like an orbit – yeast in the middle with a capsule around the outside)

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25
Q

What is the generic therapy used in meningitis?

A

Ceftriaxone 2 g IV BD

If > 50 years or immunocompromised = amoxicillin 2 g IV 4 hourly

NOTE: this is because ceftriaxone does NOT cover Listeria

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26
Q

What is the generic therapy used in meningo-encephalitis?

A

Aciclovir 10 mg/kg IV TDS

Ceftriaxone 2 g IV BD

If > 50 years or immunocompromised = amoxicillin 2 g IV 4 hourly

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27
Q

Name the specific therapy for meningitis caused by S. pneumoniae

A

Pen G 18-24 mu/day

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28
Q

Name the specific therapy for meningitis caused by N. meningitidis

A

Ceftriaxone 4 g/day

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29
Q

Name the specific therapy for meningitis caused by H. influenzae

A

Cefotaxime 12 g/day

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30
Q

Name the specific therapy for meningitis caused by Group B Streptococcus

A

Pen G 18-24 mu/day

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31
Q

Name the specific therapy for meningitis caused by Listeria

A

Ampicillin 12 g/day

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32
Q

Name the specific therapy for meningitis caused by Gram-negative bacilli

A

Cefotaxime 12 g/day

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33
Q

Name the specific therapy for meningitis caused by Pseudomonas

A

Meropenem 6 g/day

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34
Q

List some reportable GI infections.

A

Campylobacter

Salmonella

Shigella

Escherichia coli O157

Listeria

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35
Q

What are the main characteristics of secretory diarrhoea?

A

Watery diarrhoea (no inflammatory cells in stool)

No fever

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36
Q

What are the main characteristics of inflammatory diarrhoea?

A

Fever

Diarrhoea (inflammatory cells present, may be bloody)

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37
Q

List some examples of severe GI infections that produce a fever with little stool changes.

A

Salmonella typhi

Enteropathogenic Yersinia

Brucella

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38
Q

What type of organism is Staphylococcus aureus?

A

Catalase and coagulase positive, Gram-positive coccus that appears in clusters

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39
Q

What type of toxin is produced by Staphylococcus aureus?

A

Enterotoxin – this is an exotoxin that can act as a superantigen in the GI tract triggering the release of IL1 and IL2

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40
Q

How is Staphylococcus aureus spread and what kind of GI symptoms can it cause?

A

Spread by skin lesions on food handlers

Causes prominent vomiting and watery, non-bloody diarrhoea

NOTE: it is self-limiting so does not require treatment

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41
Q

What type of organism is Bacillus cereus?

A

Gram-positive rods that are spore-forming

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42
Q

What type of GI symptoms does B. cereus cause?

A

Watery, non-bloody diarrhoea

NOTE: it can cause bacteraemia and cerebral abscesses in vulnerable populations

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43
Q

Clostridium botulinum

A

· From canned food

· Causes disease due to preformed toxin which blocks acetylcholine release at peripheral nerve synapses resulting in paralysis

· Treated with antitoxin

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44
Q

Clostridium perfringens

A

· From reheated food

· Generates a superantigen that mainly affects the colon

· Causes watery diarrhoea and cramps that last 24 hours

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45
Q

Which antibiotics are most commonly implicated in C. difficile colitis?

A

Cephalosporins

Clindamycin

Ciprofloxacin

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46
Q

How is C. difficile colitis treated?

A

Metronidazole

Vancomycin

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47
Q

What type of organism is Listeria monocytogenes?

A

Gram-positive, rod-shaped, facultative anaerobe

Beta-haemolytic, aesculin-positive with tumbling motility

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48
Q

What GI symptoms does Listeria tend to cause?

A

Watery diarrhoea, cramps, headache, fever and a little vomiting

NOTE: it comes from refrigerated food (e.g. unpasteurised dairy)

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49
Q

How is Listeria infection treated?

A

Ampicillin

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50
Q

What type of organisms are Enterobacteriaceae?

A

Facultative anaerobes

Lactose fermenters

Oxidase-negative

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51
Q

Name and describe the different types of E. coli infection

A

ETEC – toxigenic, main cause of travellers’ diarrhoea

EPEC – pathogenic, infantile diarrhoea

EIEC – invasive, dysentery

EHEC – haemorrhagic, caused by E. coli O157:H7

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52
Q

What causes haemolytic uraemic syndrome?

A

EHEC shiga-liked verocytotoxin

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53
Q

What type of bacteria are Salmonellae?

A

Non-lactose fermenting, Gram-negatives

Produce hydrogen sulphide (form black colonies)

Grows on TSI agar, XLD agar and selenite F broth

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54
Q

List three species of Salmonella.

A

Salmonella typhi (and paratyphi)

Salmonella enteritidis

Salmonella choleraesuis

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55
Q

Describe the presentation of Salmonella enteritidis.

A

Enterocolitis – loose stools

Transmitted by poultry, eggs and meat

Self-limiting diarrhoea that is non-bloody

No fever

Bacteraemia is rare

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56
Q

Describe the presentation of Salmonella typhi.

A

Transmitted only by humans

Multiplies in Peyer’s patches and spreads via the endoreticular system

Slow onset fever and constipation

May cause splenomegaly, rose spots, anaemia and leucopaenia

Blood cultures may be positive

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57
Q

Which subset of patients are at increased risk of Salmonella bacteraemia?

A

Sickle cell patients

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58
Q

How is Salmonella typhi treated?

A

Ceftriaxone

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59
Q

What are some key microbiological features of Shigella?

A

Non-lactose fermenter

Does NOT produce hydrogen sulphide

Non-motile

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60
Q

List some types of Shigella.

A

Shigella sonnei

Shigella dysenteriae

Shigella flexneri (MSM)

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61
Q

What is the most effective bacterial enteric pathogen and why?

A

Shigella – it has the lowest infective dose (50)

NOTE: Shigella has no animal reservoir and no carriers

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62
Q

How does Shigella infection manifest?

A

Dysentery – severe diarrhoea with blood and mucus in the faeces

NOTE: Shigella produces shiga toxin

NOTE: avoid antibiotics when treating Shigella

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63
Q

What are the microbiological features of Vibrio?

A

Comma-shaped

Late lactose-fermenters

Oxidase-positive

Gram-negative

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64
Q

What type of GI disturbance does Vibrio cholerae cause?

A

Produce watery diarrhoea without inflammatory cells

Treat the losses (water and electrolytes)

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65
Q

Vibrio parahaemolyticus

A

caused by ingestion of raw/undercooked seafood, causes self-limiting diarrhoea, grows on salty agar

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66
Q

Vibrio vulnificus

A

causes cellulitis in shellfish handlers, can cause fatal septicaemia with D&V in HIV patients, treated with doxycycline

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67
Q

What are the main microbiological features of Campylobacter?

A

Comma-shaped

Microaerobphilic

Oxidase-positive

Gram-negative

Motile

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68
Q

Describe the presentation of Campylobacter jejuni infection.

A

Watery, foul-smelling diarrhoea, bloody stools, fever and severe abdominal pain

NOTE: transmitted by food and water that has been contaminated by animal faeces

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69
Q

How is Campylobacter infection treated?

A

Only treated if immunocompromised

Erythromycin or ciprofloxacin

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70
Q

What are some complications of Campylobacter infection?

A

Guillain-Barre syndrome

Reactive arthritis

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71
Q

What are the key microbiological features of Entamoeba histolytica?

A

Motile trophozoite in diarrhoeal illness

Non-motile cyst in non-diarrhoeal illness

Killed by boiling

Contains four nuclei

No animal reservoir

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72
Q

Describe the presentation of GI infection by Entamoeba histolytica.

A

Dysentery, flatulence, tenesmus, liver abscess

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73
Q

How is Entamoeba histolytica infection diagnosed and treated?

A

Diagnosis: stool microscopy, serology of invasive disease

Treatment: metronidazole + paromomycin

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74
Q

What are the key microbiological features of Giardia lamblia?

A

Pear-shaped trophozoites

Two nuclei

Four flagellae and a suction disc

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75
Q

Outline the pathophysiologiy of GI disease caused by Giardia.

A

Transmitted by ingestion of cyst from faecally contaminated water

Excystation in the duodenum leads to trophozoite attachment

Results in malabsorption of protein and fat

Presentation: foul-smelling non-bloody diarrhoea, cramps, flatulence, NO fever

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76
Q

How is Giardia infection diagnosed and treated?

A

Stool microscopy

ELISA

String test

Treatment: metronidazole

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77
Q

What are the main features of Cryptosporidium parvum?

A

Causes severe diarrhoea in the immunocompromised

Oocysts can be seen in the stool using modified Kinyoung acid fast stain

Treated by boosting the immune system

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78
Q

What is rotavirus and what does it cause?

A

dsRNA virus

Replicates in the mucosa of the small intestine and causes secretory diarrhoea with no inflammation

NOTE: exposure to natural infection twice will confer lifelong immunity

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79
Q

Which causes of diarrhoeal illness have available vaccines?

A

Cholera (serogroup O1)

Campylobacter

ETEC

Salmonella typhi

Rotavirus (rotarix (live, monovalent), rotateq (pentavalent), rotashield (used if risk of intussusception))

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80
Q

What are some features of HIV encephalopathy?

A

Basal ganglia calcification

White matter changes

Atrophy

Vasculopathy/stroke

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81
Q

What is an effective barrier to HIV transmission from mother to baby?

A

Healthy placenta

NOTE: there are conditions that can damage the placenta (e.g. malaria, toxoplasmosis)

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82
Q

State a perinatal risk factor for HIV transmission.

A

Prolonged rupture of membranes

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83
Q

List some classes (with examples) of antiretroviral drugs.

A

NRTI (e.g. zidovudine)

NNRTI (e.g. efavirenz)

Integrase inhibitors (e.g. raltegravir)

Protease inhibitors (e.g. lopinavir)

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84
Q

Describe the typical clinical findings in Pneumocystis jirovecii pneumonia.

A

Widespread, bilateral ground-glass shadowing with reduced exercise tolerance and low saturations

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85
Q

How is PCP treated?

A

Co-trimoxazole

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86
Q

Which investigation can be used to confirm a diagnosis of PCP?

A

Bronchoalveolar lavage cytology

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87
Q

Which stain is used to identify PCP?

A

Silver stain (Grocott-Gomori stain)

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88
Q

What is Cryptococcus?

A

Yeast that causes fungal meningoencephalitis

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89
Q

What is Actinomyces and what does it cause?

A

Gram-positive rod that causes lung abscesses in immunocompromised patients (particularly alcoholics)

NOTE: it’s closely associated with Nocardia

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90
Q

Describe the histological features of Actinomyces.

A

Basophilic sulfur granules

Gram-positive rods that branch as they grow

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91
Q

List some indicators of severe disease in people with C. difficile infection.

A

High temperature

High heart rate

High WCC

Rising creatinine

Clinical or radiological signs of severe colitis

Failure to respond to therapy at 72 hours

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92
Q

What is the rapid plasma reagent test?

A

Test for active syphilis

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93
Q

What is a characteristic finding of CJD on a diffusion-weighted MRI?

A

Increased signal in the cortex of the right parietal lobe

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94
Q

What is a possible physiological role of the normal prion protein?

A

It may have some role in copper metabolism

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95
Q

Which gene mutation is associated with prion diseases?

A

PRNP

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96
Q

Give some examples of inherited prion diseases.

A

Fatal familial insomnia

Gerstmann-Straussler-Sheinker syndrome

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97
Q

Describe the clinical features of sporadic CJD.

A

Rapid dementia

Myoclonus

Cortical blindness

Akinetic mutism

LMN signs

NOTE: usually in older people (> 65)

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98
Q

Describe the EEG appearance in sporadic CJD.

A

Periodic, triphasic complexes

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99
Q

Describe the MRI appearance of sporadic CJD.

A

Increased signal in the basal ganglia

Increased intensity on DWI MRI of the cortex and basal ganglia

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100
Q

Which markers will be raised in the CSF of a patient with CJD?

A

14-3-3

S100

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101
Q

What is the only way of confirming a diagnosis of CJD?

A

Brain biopsy (usually at autopsy)

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102
Q

Describe the histological appearance of CJD.

A

Spongiform vacuolisation

NOTE: there are amyloid plaques but these are different from the plaques seen in Alzheimer’s disease

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103
Q

List the differential diagnosis for CJD.

A

Alzheimer’s disease

Vascular dementia

CNS neoplasms

Cerebral vasculitis

Paraneoplastic syndromes

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104
Q

Describe the clinical features of vCJD.

A

Younger age of onset (20s)

Psychiatric onset (dysphoria, anxiety, delusions, hallucinations)

Followed by neurological symptoms (peripheral sensory symptoms, ataxia, myoclonus, chorea, dementia)

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105
Q

What is a characteristic MRI feature of vCJD?

A

Pulvinar sign – high intensity in the putamen

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106
Q

How is the use of CSF markers different in vCJD?

A

14-3-3 and S100 are NOT useful in vCJD

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107
Q

Which investigation is most useful for vCJD?

A

Tonsillar biopsy – prions localise in lymphoid tissue

NOTE: this is not useful in CJD

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108
Q

What is the inheritance pattern of inherited prion diseases?

A

Autosomal dominant

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109
Q

What are some alternative diagnoses for someone presenting with features suggestive of prion disease?

A

Spinocerebellar ataxia

Huntington’s disease

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110
Q

Describe the clinical features of Gerstmann-Straussler-Sheinker syndrome.

A

Slowly progressive ataxia

Diminished reflexes

Dementia

NOTE: PRNP P102L mutation is most common

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111
Q

Describe the clinical features of fatal familial insomnia.

A

Untreatable insomnia

Dysautonomia (blood pressure and heart rate dysregulation)

Ataxia

Thalamic degeneration

NOTE: PRNP D178N mutation is most common

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112
Q

Outline the principles of treatment of CJD.

A

Symptomatic – clonazepam for clonus

Delaying prion conversion – quinacrine, pentosan, tetracycline

Anti-prion antibody – blocks progression in mice but cannot access CNS

Depletion of neuronal cellular prion protein – blocks neuronal cell loss and reverses early spongiosis in mice

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113
Q

In which groups of patients are UTIs considered ‘complicated’?

A

Men

Pregnant women

Children

Hospitalised patients

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114
Q

Which organism most commonly causes UTI?

A

E. coli

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115
Q

List some other organisms that cause UTI.

A

Proteus mirabilis

Klebsiella aerogenes

Enterococcus faecalis

Staphylococcus saprophyticus

Staphylococcus epidermidis (can cause infection in the presence of prosthesis (e.g. procedures, indwelling catheters))

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116
Q

List some symptoms of upper UTI.

A

Fever (and rigors)

Flank pain

Lower urinary tract symptoms

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117
Q

List some investigations for uncomplicated UTI.

A

Urine dipstick

MSU for urine MC&S

Bloods – FBC, CRP, U&E

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118
Q

List some further investigations that may be considered in complicated UTIs.

A

Renal ultrasound scan

IV urography

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119
Q

What are nitrites in the urine specific for?

A

They are produced by E. coli

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120
Q

List some patient groups in whom culture and sensitivities should be performed.

A

Pregnancy

Children

Pyelonephritis

Men

Catheterised

Failed antibiotic treatment

Abnormalities of the genitourinary tract

Renal impairment

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121
Q

What does the presence of squamous epithelial cells in the urine suggest?

A

Contamination

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122
Q

What is the microbiological definition of UTI?

A

Culture of single organisms > 105 colony forming units/mL with urinary symptoms

NOTE: this threshold may be reduced for organisms that are known to cause UTI (e.g. E. coli and S. saprophyticus)

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123
Q

In which patient groups should screening of the urine for white cells before MC&S NOT be performed?

A

Immunocompromised patients, pregnant women and children

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124
Q

List some causes of sterile pyuria.

A

STIs (e.g. chlamydia)

TB

Prior antibiotic treatment (MOST COMMON)

Calculi

Catheterisation

Bladder cancer

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125
Q

What type of agar is used for urine culture? What do the colours suggest?

A

Chromogenic agar

· Pink = E. coli

· Blue = other coliforms

· Light blue = Gram-positives

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126
Q

Outline the treatment options for Uncomplicated UTI in women

A

Cefalexin 500 mg BD PO for 3 days

OR

Nitrofurantoin 50 mg POQ QDS for 7 days (check renal function)

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127
Q

Outline the treatment options for UTI in pregnant or breastfeeding women

A

Cefalexin 500 mg BD PO for 7 days

2nd line: co-amoxiclav 625 mg TDS PO for 7 days

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128
Q

Outline the treatment options for UTI in men

A

Cefalexin 500 mg BD PO for 7 days

OR

Ciprofloxacin 500 mg BD PO for 14 days if suspicion of prostatitis

Chronic prostatitis: ciprofloxacin 500 mg BD PO for 4-6 weeks

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129
Q

Outline the treatment options for Pyelonephritis or systemically unwell with a UTI

A

Co-amoxiclav 1.2 g IV TDS

Consider adding IV amikacin or gentamicin

Penicillin allergy: ciprofloxacin 400 mg IV BD

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130
Q

Outline the treatment options for Catheter-associated UTI

A

Remove catheter (but give stat doses before removal of infected catheter)

Gentamicin 80 mg STAT IV/IM 30-60 mins before procedure

OR

Amikacin 140 mg STAT IV/IM 30-60 mins before procedure

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131
Q

In which patients do Candida UTIs tend to occur?

A

Patients with indwelling catheters

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132
Q

Which part of the kidney is more susceptible to infection?

A

Renal medulla

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133
Q

What is the main treatment option for pyelonephritis?

A

Co-amoxiclav with or without gentamicin

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134
Q

List some complications of pyelonephritis.

A

Perinephric abscess

Chronic pyelonephritis (scarring, renal impairment)

Septic shock

Acute papillary necrosis

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135
Q

How is hepatitis A spread?

A

Faecal-oral

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136
Q

Describe the natural history of hepatitis A infection.

A

2-6 weeks after the infection you will develop hepatitis (transaminitis)

This will be accompanied by a rise in IgM

A more gradual rise in IgG will follow

NOTE: hepatitis A infection is often subclinical

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137
Q

What is the diagnostic test for hepatitis A?

A

Anti-hepatitis A IgM

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138
Q

Which antibodies will be present if someone has received a hepatitis A vaccine?

A

High IgM and high IgG but NO transaminitis

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139
Q

How is hepatitis B transmitted?

A

Sexually transmitted

Blood products

Mother-to-baby

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140
Q

What is the risk of chronic hep b infection in adults and babies?

A

5-10% in adults

95% in babies

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141
Q

What serological features is suggestive of recent HBV infection?

A

Anti-HBV IgM antibodies

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142
Q

What serological feature is suggestive of chronic HBV infection?

A

Prolonged presence of HBsAg

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143
Q

What are some possible consequences of HBV infection?

A

Hepatocellular carcinoma

Cirrhosis

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144
Q

List the HBV disease stages.

A

Immune tolerant

Immune reactive

Inactive HBV carrier state

HBeAg negative chronic HBV

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145
Q

What is a strong indicator of risk of cirrhosis in people with hepatitis B infection?

A

HBV DNA level (copies/mL)

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146
Q

List some treatment options for chronic HBV.

A

Interferon alpha - not in liver transplant pts

Lamivudine

Tenofovir

Entecavir

Emtricitabine

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147
Q

What class of drugs are most antivirals used for hepatitis C?

A

Protease inhibitors

Inhibitors of non-structural components

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148
Q

Outline the serological changes that take place following HCV infection.

A

Anti-HCV antibodies develop after the acute infection has resolved (i.e. ALT has returned to normal)

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149
Q

How is HCV treated?

A

Early treatment with peginterferon alfa

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150
Q

What is the main difference in the treatment of genotype 1 and non-genotype 1 HCV?

A

Genotype 1 – high-dose long-lasting ribavirin is required for high cure rates

Non-genotype 1 – ribavirin does NOT increase cure rates

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151
Q

What is the difference between hepatitis D co-infection and superinfection?

A

Co-infection

· This happens when you are inoculated with HBV and HDV at the same time (e.g. sharing a needle with someone infected by both viruses)

· Anti-HDV IgM will rise after inoculation causing hepatitis

Superinfection

· This happens when someone with chronic hepatitis B infection is inoculated by HDV

· This is more severe than coinfection

· Patients can develop cirrhosis within 2-3 years

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152
Q

Which patient group has a high mortality if infected by hepatitis E?

A

Pregnant women

NOTE: mainly associated with genotype 1

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153
Q

List some rare complications of hepatitis E.

A

CNS disease (e.g. Bell’s palsy)

Chronic infection

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154
Q

Outline the treatment of hepatitis E.

A

Supportive

Ribavirin

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155
Q

Outline the serological changes that take place in hepatitis E infection.

A

Acute infection is accompanied by a rise in IgM anti-HEV antibody

Rarely you can get persistently high levels of HEV RNA

NOTE: it generally responds well to ribavirin

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156
Q

Name three major pathogens that cause surgical site infections.

A

Staphylococcus aureus

Escherichia coli

Pseudomonas aeruginosa

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157
Q

How is a surgical site infection caused by MRSA treated?

A

IV linezolid

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158
Q

Who should be offered nasal decontamination?

A

Patients who are found to be carrying S. aureus

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159
Q

List some organisms that can cause septic arthritis.

A

Staphylococcus aureus

Streptococci (pyogenes, pneumoniae, agalactiae)

Gram-negative organisms (E. coli, H. influenzae, N. gonorrhoeae and Salmonella)

Coagulase-negative staphylococci

RARE: Lyme disease, Brucellosis, Mycobacteria, Fungi

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160
Q

Describe the clinical features of septic arthritis.

A

1-2 week history of red, painful, swollen joint with restricted movement

NOTE: 90% monoarticular, 50% knee involvement

NOTE: patients with rheumatoid arthritis may have more subtle signs

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161
Q

List some investigations for septic arthritis.

A

Blood culture before antibiotics

Synovial fluid aspiration (send for MC&S, WCC > 50,000/mL is considered septic arthritis)

ESR and CRP

Ultrasound

CT (for bone erosion)

MRI (for joint effusion, articular cartilage destruction, abscess)

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162
Q

List some organisms that can cause vertebral osteomyelitis.

A

Staphylococcus aureus

Coagulase-negative staphylococcus

Gram-negative rods

Streptococcus

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163
Q

In which region of the vertebral column is vertebral osteomyelitis most common?

A

Lumbar

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164
Q

What are the symptoms of vertebral osteomyelitis?

A

Back pain

Fever

Neurological impairment

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165
Q

List some investigations for vertebral osteomyelitis.

A

MRI

Blood cultures

CT-guided/open biopsy

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166
Q

How is vertebral osteomyelitis treated?

A

Antibiotics (at least 6 weeks)

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167
Q

Outline the presentation of chronic osteomyelitis.

A

Pain

Brodie’s abscess

Sinus tract

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168
Q

How is chronic osteomyelitis diagnosed?

A

MRI

Bone biopsy for culture and histology

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169
Q

How is chronic osteomyelitis treated?

A

Radical debridement down to living bone

Remove sequestra (dead bone tissue) and infected bone tissue

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170
Q

Which organism most commonly causes prosthetic joint infection?

A

Coagulase-negative staphylococcus

Others: streptococci, enterococci, enterobacteriaciae, Pseudomonas aeruginosa, anaerobes

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171
Q

How is prosthetic joint infection diagnosed?

A

Radiology – shows loosening of the prosthesis

CRP > 13.5 for prosthetic knees

CRP > 5 for prosthetic hips

Joint aspiration (>1700/mL if knee; >4200/mL if hip)

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172
Q

List 5 HAIs in order of prevalence.

A

Pneumonia

Surgical site infection

UTI

Blood stream infection

Gastrointestinal infection

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173
Q

What type of bacterium is C. difficile?

A

Gram-positive spore-forming anaerobe

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174
Q

Define pyrexia of unknown origin.

A

A fever > 38.3 degrees lasting > 3 weeks with an uncertain diagnosis after 7 days in hospital

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175
Q

List some causes of PUO in HIV patients.

A

TB/NTM

PCP

Cryptococcal meningitis

Non-Hodgkin lymphoma

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176
Q

List some differentials for PUO.

A

Infection

· Infectious endocarditis

· HIV

· TB

Inflammation

· Polymyalgia rheumatica

· Still’s disease

· Sarcoidosis

· ANCA-associated vasculitis

· Rheumatoid arthritis

Malignancy

· Malignant lymphoma

· Castleman’s disease

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177
Q

List some routine diagnostic tests that should be requested in patients with PUO.

A

FBC

U&E

Total protein

LFTs

CRP

Blood cultures

Urine culture

HIV test – VERY IMPORTANT

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178
Q

List some infectious causes of PUO.

A

Bacteria

· TB/NTM

· Enteric fever (e.g. Salmonella typhi)

· Zoonoses

Viruses

· EBV/CMV

· HIV

· Hepatitis

Fungi

· Cryptococcosis

· Histoplasmosis

Parasites

· Malaria

· Amoebic liver abscess

· Schistosomiasis

· Toxoplasmosis

· Trypanosomiasis

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179
Q

Which organ will always light up in PET-CT?

A

Kidneys (FDG is excreted renally)

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180
Q

List two causes of very high ferritin.

A

Adult-onset Still’s disease

Macrophage activation syndrome

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181
Q

Why is a transthoracic echocardiogram an important investigation to perform in PUO?

A

To rule out infective endocarditis (important differential for PUO)

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182
Q

Outline the major and minor criteria for infective endocarditis.

A

Major

· Persistent bacteraemia (> 2 positive blood cultures)

· Vegetations on echocardiogram

· Positive serology for Bartonella, Coxiella or Brucella

Minor

· Predisposition (murmur, IVDU)

· Raised inflammatory markers

· Immune complexes (RBC in urine)

· Embolic phenomena (Janeway lesions)

· Atypical echo

· 1 positive blood culture

2 major + 1 minor OR 3 minor = infective endocarditis

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183
Q

List some key features of GCA.

A

Headache

Jaw claudication

Scalp tenderness

Changes in vision (50%)

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184
Q

How is GCA treated?

A

High dose prednisolone

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185
Q

Outline the key features of Adult-onset Still’s disease.

A

Salmon pink rash

Arthralgia

Sore throat

Lymphadenopathy

Fever

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186
Q

List some malignant causes of PUO.

A

Lymphoma (especially Non-Hodgkin)

Leukaemia

Renal cell carcinoma

Hepatocellular carcinoma and liver metastases

NOTE: lymphoma causes a high LDH

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187
Q

List some miscellaneous causes of PUO.

A

Subacute thyroiditis

Addison’s disease

PE

Dressler’s syndrome

Drugs – idiosyncratic or adverse drug reaction

NOTE: 25% of drug reactions will cause eosinophilia and a rash

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188
Q

Give examples of zoonoses in the UK that are transmitted by Farm/wild animals

A

Campylobacter

Salmonella

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189
Q

Give examples of zoonoses in the UK that are transmitted by Companion animals

A

Toxoplasmosis

Bartonella

Ringworm

Psittacosis

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190
Q

Give examples of zoonoses in tropical countries that are transmitted by Farm/wild animals

A

Brucella

Coxiella

Rabies

VHF

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191
Q

Give examples of zoonoses in tropical countries that are transmitted by Companion animals

A

Rabies

Tick-borne diseases

Spirilum minus

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192
Q

Which two diseases are caused by Bartonella henselae?

A

Cat scratch disease

Baciliary angiomatosis

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193
Q

Cat Scratch Disease presentation

A

Macule at site of inoculation

Becomes pustular

Regional adenopathy

Systemic symptoms (FLAWS)

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194
Q

Cat scratch disease management

A

Erythromycin

Doxycycline

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195
Q

Bacillary angiomatosis presentation

A

Skin papules

Disseminated

Leads to bursting of blood vessels in various organs and tissues

Can be FATAL

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196
Q

Bacillary angiomatosis management

A

Erythromycin

Doxycycline

Rifampicin

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197
Q

Toxoplasmosis presentation

A

Fever

Adenopathy

Stillbirth

Infants with progressive visual, hearing, motor and cognitive issues

Seizures

Neuropathy

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198
Q

Toxoplasmosis management

A

Spiramycin

Pyrimethamine + sulfadizine

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199
Q

Brucellosis presentation

A

Fever (and rest of FLAWS)

Back pain

Orchitis

Focal abscess (psoas or liver)

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200
Q

Brucellosis management

A

Doxycycline + gentamicin or rifampicin

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201
Q

Which organism causes Q fever?

A

Coxiella burnetii

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202
Q

Coxiella burnetii presentation

A

Fever

Flu-like illness

Pneumonia

Hepatitis

Endocarditis

Focal abscess (paravertebral, discitis)

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203
Q

Coxiella burnetii management

A

Doxycycline

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204
Q

Which infectious agent causes Rabies?

A

Lyssa virus

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205
Q

Rabies presentation

A

Seizures

Excessive salivation

Hydrophobia

Agitation

Confusion

Fever

Headache

NOTE: 100% mortality

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206
Q

Rabies management

A

Immunoglobulin

Vaccine

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207
Q

Which two infectious agents can cause rat bite fever?

A

Streptobacillus moniliformis

Spirilum minus

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208
Q

Rat bite fever presentation

A

Fevers

Polyarthralgia

Maculopapular progressing to purpuric rash

Can progress to endocarditis

209
Q

Rat btie fever management

A

Penicillins

210
Q

Hentavirus pulmonary syndrome presentation

A

Fever

Flu-like illness

Myalgia

Respiratory failure (USA)

Bleeding and renal failure (SE asia)

211
Q

Viral haemorrhagic fever presentation

A

Fever

Myalgia

Flu-like illness

BLEEDING

212
Q

What type of bacterium is Streptococcus pneumoniae?

A

Gram-positive cocci in chains

Alpha-haemolytic and optochin-sensitive

213
Q

List the main organisms that cause CAP.

A

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

Staphylococcus aureus

Klebsiella pneumoniae

214
Q

List the most prevalent pathogens causing CAP in 0-1 months

A

Escherichia coli

Group B Streptococcus

Listeria monocytogenes

215
Q

List the most prevalent pathogens causing CAP in 1-6 months

A

Chlamydia trachomatis

Staphylococcus aureus

RSV

216
Q

List the most prevalent pathogens causing CAP in 6 months – 5 years

A

Mycoplasma pneumoniae

Influenza

217
Q

List the most prevalent pathogens causing CAP in 16-30 years

A

Mycoplasma pneumoniae

Streptococcus pneumoniae

218
Q

Typical CAP causes

A

Streptococcus pneumoniae

Haemophilus influenzae

219
Q

Atypical CAP causes

A

Legionella

Mycoplasma

Coxiella burnetii

Chlamydia psittaci

220
Q

What is the CURB-65 score? How is it interpreted?

A

Confusion

Urea > 7 mmol/L

Respiratory rate > 30/min

BP < 90 systolic, < 60 diastolic

Score of 2 = consider hospital admission

Score of more than 2 = severe pneumonia that may need ITU admission

221
Q

Outline the presentation of bronchitis.

A

Cough

Fever

Increased sputum production

Increased SOB

222
Q

Which organisms cause bronchitis?

A

Viruses

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

223
Q

List some bacterial causes of cavitating lung lesions.

A

Staphylococcus aureus

Klebsiella pneumoniae

TB

224
Q

What type of bacterium is H. influenzae?

A

Gram-negative cocco-bacilli

225
Q

What is a common feature of bacteria that cause atypical pneumonia?

A

They have NO cell wall

226
Q

List four atypical organisms.

A

Mycoplasma

Legionella

Chlamydia

Coxiella

227
Q

Which type of antibiotics do not work on atypical bacteria?

A

Penicillins

NOTE: this is because they act on cell walls

228
Q

Which type of antibiotics do work on atypical bacteria?

A

Antibiotics that interfere with protein synthesis (macrolides, tetracyclines)

229
Q

List some clinical features of Legionella pneumophila infection.

A

Confusion

Abdominal pain

Diarrhoea

Lymphopaenia

Hyponatraemia

230
Q

Urinary antigens are associated with which causes of pneumonia?

A

Streptococcus pneumoniae

Legionella pneumophila

231
Q

What is an empyema?

A

Collection of pus within the pleural cavity

232
Q

What is the classical CXR feature of TB?

A

Upper lobe cavitation

233
Q

Which types of staining are used when investigating TB?

A

Auramine staining

Ziehl-Neelsen stain

NOTE: they are red rods

234
Q

List some organisms that cause HAP.

A

Enterobacteriaciae (MOST COMMON – e.g. E. coli, K. pneumoniae)

Staphylococcus aureus

Pseudomonas

Haemophilus influenzae

Acinetobacter baumanii

Fungi (e.g. Candida)

235
Q

Describe the typical presentation of Pneumocystic jirovecii pneumonia.

A

Dry cough

Weight loss

SOB

Malaise

Walk test – desaturation on exertion

236
Q

What is the treatment for PCP?

A

Co-trimoxazole (septrin)

237
Q

What are the main features of allergic bronchopulmonary aspergillosis?

A

Chronic wheeze

Eosinophilia

Bronchiectasis

238
Q

What is an aspergilloma?

A

Fungal ball often forming within a pre-existing cavity

May cause haemoptysis

239
Q

How is invasive aspergillosis treated?

A

Amphotericin B

240
Q

What is the treatment for mild-to-moderate CAP?

A

Amoxicillin

OR erythromycin/clarithromycin (if penicillin allergic)

241
Q

What is the treatment for moderate-to-severe CAP?

A

Co-amoxiclav AND clarithromycin

242
Q

What are the 1st and 2nd line treatment options for HAP?

A

1st = ciprofloxacin +/- vancomycin

2nd = tazocin AND vancomycin

243
Q

Which antibiotics are used to treat HAP caused by MRSA

A

Vancomycin

244
Q

Which antibiotics are used to treat HAP caused by Pseudomonas

A

Tazocin OR ciprofloxacin +/- gentamicin

245
Q

List three types of mycobacterial complex.

A

Mycobacterium tuberculosis complex

· Mycobacterium tuberculosis

· Mycobacterium bovis

Mycobacterium avium complex

· Mycobacterium avium

· Mycobacterium intracellulare

Mycobacterium abscessus complex

· Mycobacterium abscessus

· Mycobacterium massiliense

· Mycobacterium bolletii

246
Q

Describe the morphology of mycobacteria.

A

Non-motile rod-shaped bacteria

Relatively slow-growing

Cell wall composed of mycolic acids, complex waxes and glycoproteins

Acid-alcohol fast

247
Q

What is used as a screening test for mycobacterial infections?

A

Auramine stain

248
Q

How are non-tuberculous mycobacterial infections transmitted?

A

NOT person-to-person

From the environment

May be colonising rather than infecting

249
Q

List three examples of slow-growing non-tuberculous mycobacteria and the diseases that they cause.

A

Mycobacterium avium intracellulare

· May invade bronchial tree or pre-existing bronchiectasis/cavities

· Disseminated infection in immunocompromised patients

Mycobacterium marinum

· Swimming pool granuloma

Mycobacterium ulcerans

· Skin lesions (e.g. Bairnsdale ulcer, Buruli ulcer)

· Chronic progressive painless ulcer

250
Q

List three examples of rapid-growing non-tuberculous mycobacteria.

A

Mycobacterium abscessus

Mycobacterium chelonae

Mycobacterium fortuitum

251
Q

How is Mycobacterium avium intracellulare treated?

A

Clarithromycin/azithromycin

Rifampicin

Ethambutol

+/- streptomycin/amikacin

252
Q

What is the most common cause of death by infectious agent in the world?

A

1 = HIV

2 = TB

253
Q

Describe the natural history of primary TB.

A

Usually asymptomatic

Ghon focus (granuloma in the lungs)

Controlled by cell-mediated immunity

Occasionally causes disseminated/military TB

254
Q

What is post-primary TB?

A

Reactivation or exogenous re-infection

Happens > 5 years after primary infection

255
Q

List some risk factors for reactivation of TB.

A

Immunosuppression

Chronic alcohol excess

Malnutrition

Ageing

256
Q

List some types of extra-pulmonary TB.

A

Lymphadenitis (scrofula) – cervical lymph nodes most commonly

Gastrointestinal – due to swallowing of tubercle

Peritoneal – ascitic or adhesive

Genitourinary

Bone and joint – due to haematogenous spread (e.g. Pott’s disease)

Miliary TB

Tuberculous meningitis

257
Q

Why is it important to take 3 sputum samples when investigating suspected TB?

A

Increases the sensitivity of the smear microscopy

258
Q

What is the histological hallmark of TB?

A

Caseating granuloma

259
Q

What are the disadvantages of the tuberculin skin test?

A

Cross-reacts with BCG

Cannot distinguish between active and latent TB

260
Q

List some side-effects of Rifampicin

A

Raised transaminases

CYP450 induction

Orange secretions

261
Q

List some side-effects of Isoniazid

A

Peripheral neuropathy (give with pyridoxine)

Hepatotoxicity

262
Q

List some side-effects of Pyrazinamide

A

Hepatotoxicity

263
Q

List some side-effects of Ethambutol

A

Visual disturbance

264
Q

Describe the treatment regimen for TB.

A

RIPE for 2 months

Followed by rifampicin and isoniazid for 4 more months

265
Q

What is multi-drug resistant TB?

A

Resistant to rifampicin and isoniazid

266
Q

What are the diagnostic challenges of HIV and TB coinfection?

A

Clinical presentation is less likely to be classical

Symptoms may be absent if CD4+ count is low

More likely to have extra-pulmonary manifestations

Tuberculin skin test more likely to give false-negative

Low sensitivity for IGRAs

267
Q

List three examples of neuraminidase inhibitors.

A

Oseltamivir (Tamiflu) – oral

Zanamivir (Relenza) – inhaled or IV

Peramivir – IV

268
Q

List two examples of polymerase inhibitors.

A

Favipiravir

Baloxavir

269
Q

What type of vaccine is the seasonal influenza vaccine used in high risk groups?

A

Purified fraction containing HA and NA of an inactivated virus

NOTE: often needs to be given with an adjuvant

270
Q

What type of flu vaccine is given to school-aged children?

A

Live-attenuated vaccine

NOTE: this is a cold-adapted virus that is sprayed into the child’s nose

This provides broader and more cross-reactive immunity

271
Q

What is a possible complication of shingles?

A

Post-herpetic neuralgia

272
Q

What are two 2nd line treatment options for aciclovir-resistant VZV infection?

A

Foscarnet

Cidofovir

NOTE: they inhibit viral DNA synthesis

273
Q

HSV encephalitis is a medical emergency. How should it be treated?

A

IMMEDIATE treatment with IV aciclovir 10 mg/kg TDS without waiting for test results

If confirmed, treat for 21 days

274
Q

What is HSV meningitis and how should it be treated?

A

Usually self-limiting

Immunocompromised patients and those who are unwell enough to require hospital admission require treatment

IV aciclovir for 2-3 days followed by oral aciclovir for 10 days

275
Q

In which cells does CMV lie dormant?

A

Monocytes and dendritic cells

276
Q

List some consequences of CMV infection in immunocompromised patients.

A

Bone marrow suppression, retinitis, pneumonitis, hepatitis, colitis and encephalitis

277
Q

What is a characteristic histological feature of CMV infection?

A

Owl’s eye inclusions

278
Q

What is the 1st line treatment option for CMV infection?

A

Ganciclovir (IV)

279
Q

What is a major side-effect of ganciclovir?

A

Bone marrow toxicity

NOTE: therefore, its use is limited in bone marrow transplant patients

280
Q

What is a major side-effect of foscarnet?

A

Nephrotoxicity

281
Q

What is a major side-effect of cidofovir?

A

Nephrotoxicity (requires hydration and probenecid)

282
Q

What are three strategies for the treatment of CMV in transplant patients?

A

TREAT established disease

PROPHYLAXIS with ganciclovir or valganciclovir (mainly in solid organ transplant patients)

PRE-EMPTIVE THERAPY for bone marrow transplant patients (monitoring for the appearance of CMV in PCR of the blood and starting antiviral therapy when the viral load reaches a threshold)

283
Q

In which cells does EBV cause continuous low-grade viral replication?

A

B cells

284
Q

What is post-transplant lymphoproliferative disease?

A

Polyclonal expansion of B cells associated with immunosuppression used in organ transplants (due to breakdown of immunosurveillance keeping the B cells and EBV in check)

This predisposes to lymphoma

285
Q

How is post-transplant lymphoproliferative disease treated?

A

Reduce immunosuppression

Rituximab (anti-CD20)

286
Q

Name two examples of neuraminidase inhibitors.

A

Oseltamivir (Tamiflu) – oral

Zanamivir (Relenza) – dry powder

287
Q

Outline the treatment of BK haemorrhagic cystitis.

A

Bladder washouts

Reduce immunosuppression

Cidofovir IV (may consider intravesical)

288
Q

Outline the treatment of BK nephropathy.

A

Reduce immunosuppression

IVIG

NOTE: cidofovir cannot be used because it is nephrotoxic

289
Q

In which subgroup of patients is adenovirus a major issue?

A

Paediatric transplant patients

290
Q

Outline the treatment of adenovirus infection in transplant patients.

A

Cidofovir IV

IVIG

Brincidofovir (prodrug of cidofovir currently undergoing clinical trials)

291
Q

What are the main treatment options for drug resistant HSV and CMV infection?

A

Foscarnet and cidofovir

292
Q

What is the herd immunity threshold?

A

Threshold = 1 – 1/R0

293
Q

What are the three main types of memory cell?

A

Memory B cells

Memory killer T cells

Memory T helper cells

294
Q

List examples of inactivated vaccines

A

Influenza

Polio

Cholera

295
Q

List examples of live attenuated vaccines

A

MMR

Yellow fever

296
Q

List examples of toxoid vaccines

A

Diphtheria

Tetanus

297
Q

List examples of subunit vaccines

A

Hepatitis B

HPV

298
Q

List examples of conjugate vaccines

A

Haemophilus influenzae type B

299
Q

List examples of heterotypic vaccines

A

BCG

300
Q

List some contraindications for vaccines.

A

Previous anaphylactic reactions

Anaphylactic reaction to egg is contraindicated with the influenza vaccine

Immunocompromised and pregnant women should not receive live attenuated vaccines

If acutely unwell on the day of vaccination

DTP is contraindicated if evidence of neurological abnormality

301
Q

List some examples of serious reactions associated with the following DTP vaccination

A

Encephalopathy

Shock

Anaphylaxis

302
Q

List some examples of serious reactions associated with the following polio vaccination

A

Guillain-Barre syndrome

Polio

303
Q

List some examples of serious reactions associated with the following measles vaccination

A

Anaphylaxis

Thrombocytopaenia

304
Q

List some examples of serious reactions associated with the following rubella vaccination

A

Acute arthritis

305
Q

List some examples of serious reactions associated with the following T/ DT/ Td vaccination

A

Guillain-Barre syndrome

Brachial neuritis

Anaphylaxis

306
Q

List some examples of serious reactions associated with the following Hep B vaccination

A

Anaphylaxis

307
Q

Which infections are screened for in pregnancy?

A

HIV

Hepatitis B

Syphilis

308
Q

What are the possible outcomes for neonates with congenital toxoplasmosis?

A

Asymptomatic (60%) at birth but go on to develop long-term sequelae such as deafness, low IQ and microcephaly

Symptomatic (40%) at birth

· Choroidoretinitis

· Microcephaly/hydrocephalus

· Intracranial calcifications

· Seizures

· Hepatosplenomegaly/jaundice

309
Q

What is the triad of features in congenital rubella syndrome?

A

Cataracts

Congenital heart disease (PDA is most common)

Deafness

Other features: microphthalmia, glaucoma, retinopathy, ASD/VSD, microcephaly, meningoencephalopathy, developmental delay

310
Q

How is herpes simplex virus transmitted to the neonate?

A

Lesions in the genital tract can transmit HSV to the neonate

It causes a blistering rash and can cause disseminated infection with liver dysfunction and meningoencephalitis

311
Q

How if Chlamydia trachomatis transmitted to the neonate and what disease does it cause in the neonate?

A

During delivery

Causes neonatal conjunctivitis or pneumonia

NOTE: it is treated with erythromycin

312
Q

What type of bacterium is Group B Streptococcus?

A

Gram-positive coccus

Catalase negative

Beta haemolytic

313
Q

What type of organism is E. coli and which diseases can it cause in the neonate?

A

Gram-negative rods

Can cause bacteraemia, meningitis and UTI

NOTE: the K1 antigen is particularly problematic

314
Q

What type of organism is Listeria monocytogenes and what disease can it cause?

A

Gram-positive rods

Causes sepsis in the mother and the newborn

315
Q

List some investigations that may be useful in early-onset sepsis.

A

FBC

CRP

Blood culture

Deep ear swab

LP

Surface swabs

CXR

316
Q

Which antibiotic combination is often used in early-onset sepsis and why?

A

Benzylpenicillin and gentamicin

Benzylpenicillin covers Group B Streptococcus whilst gentamicin covers E. coli

317
Q

What is late-onset sepsis?

A

Sepsis that occurs more than 48-72 hours after birth

318
Q

What are the main causes of late-onset sepsis?

A

Coagulase negative staphylococci (e.g. S. epidermidis)

GBS

E. coli

Listeria monocytogenes

S. aureus

Enterococcus sp.

Gram-negatives (e.g. Klebsiella, Enterobacter, Pseudomonas)

319
Q

List some clinical features of late-onset sepsis.

A

Bradycardia

Apnoea

Poor feeding

Irritability

Convulsions

Jaundice

Respiratory distress

320
Q

Outline the treatment of late-onset sepsis.

A

Treat early with antibiotics

Guidelines differ

Example antibiotic regimen: 1st line = cefotaxime + vancomycin; 2nd line = meropenem

321
Q

What are some common non-specific symptoms of infections in childhood?

A

Fever

Abdominal pain

322
Q

List some investigations for meningitis in children.

A

Blood cultures

Throat swab

LP

Rapid antigen screen

EDTA for blood PCR

Clotted serum for serology

323
Q

What is the main bacterial cause of meningitis at the moment?

A

Meningitis B

324
Q

What type of organism is Streptococcus pneumoniae?

A

Gram-positive diplococcus

Alpha haemolytic

325
Q

Which diseases can S. pneumoniae cause?

A

Meningitis

Pneumonia

Bacteraemia

326
Q

What type of organism is Haemophilus influenzae?

A

Gram-negative cocco-bacilli

327
Q

What are the typical causes of meningitis for under 3 months

A

Neisseria meningitidis

Streptococcus pneumoniae

Haemophilus influenzae

Group B Streptococcus

Escherichia coli

Listeria monocytogenes

328
Q

What are the typical causes of meningitis for 3 months to 5 years

A

Neisseria meningitis

Streptococcus pneumoniae

Haemophilus influenzae

329
Q

What are the typical causes of meningitis for over 6 years

A

Neisseria meningitidis

Streptococcus pneumoniae

330
Q

What is the most important bacterial cause of respiratory tract infection in children?

A

Streptococcus pneumoniae

331
Q

Which children are mainly affected by Mycoplasma pneumoniae?

A

Older children (> 4 years)

332
Q

Which group of antibiotics are used to treat Mycoplasma pneumoniae?

A

Macrolides

333
Q

Describe the classical presentation of Mycoplasma pneumoniae.

A

Fever

Headache

Myalgia

Pharyngitis

Dry cough

334
Q

List some extra-pulmonary manifestations of Mycoplasma pneumoniae.

A

Haemolysis – IgM antibodies to I antigen on erythrocytes, cold agglutinins

Neurological – encephalitis, aseptic meningitis, peripheral neuropathy, transverse myelitis

Polyarthralgia

Cardiac

Otitis media

Bullous myringitis (vesicles on the tympanic membrane – pathognomonic of Mycoplasma)

335
Q

If a respiratory tract infection fails to respond to conventional treatment, which diagnoses should be considered?

A

Whooping cough

TB

336
Q

What are the main organisms responsible for UTI in children?

A

E. coli

Other coliforms (Proteus, Klebsiella, Enterococcus)

Coagulase-negative Staphylococcus (S. saprophyticus)

337
Q

List three examples of Yeast

A

Candida

Cryptococcus

Histoplasma (dimorphic)

338
Q

List three examples of Moulds

A

Aspergillus

Dermatophytes

Agents of mucormycosis

339
Q

Which systemic infections can be caused by Candida?

A

Septicaemia, endocarditis, meningitis

340
Q

List some agents that can cause candidiasis.

A

Candida albicans (MOST COMMON)

Candida glabrata

Candida krusei

Candida tropicalis

341
Q

What does generalised candidiasis in babies usually occur secondary to?

A

Seborrhoeic dermatitis

342
Q

Outline diagnostic tests used for candidiasis.

A

Swabs

Blood cultures

Beta-D glucan assay (serology)

Imaging

343
Q

What type of agar is needed for culturing Candida?

A

Sabouraud agar – impregnated with antibiotics to prevent bacteria from outcompeting the fungi

344
Q

Outline the management of candidiasis.

A

At least 2 weeks of antifungals after the last negative culture

Echo and fundoscopy to look for endocarditis/endophthalmitis

Echinocandins – empirical for non-albicans infections

Fluconazole – empirical for Candida albicans

345
Q

Which group of antifungals is Cryptococcus inherently resistant to?

A

Echinocandins

346
Q

What is the treatment of choice for Cryptococcus infection?

A

Ambisome (amphotericin B)

347
Q

What is the main aetiological agent in cryptococcosis.

A

Cryptococcus neoformans

348
Q

Why might a lumbar puncture be negative in cryptococcal meningitis?

A

Cryptococcal meningitis can cause hydrocephalus which prevents the circulation of CSF meaning that the sample taken at LP may not have been exposed to CSF within other parts of the ventricular system

349
Q

Outline the treatment options for Cryptococcus infection.

A

3 weeks amphotericin B (ambisome) +/- flucytosine

Repeat LP for pressure measurement

Secondary suppression – fluconazole

350
Q

List the diseases that can be caused by Aspergillus.

A

Mycotoxicosis

Allergic bronchopulmonary aspergillosis

Aspergilloma

Invasive/disseminated disease

351
Q

What is the mainstay of diagnosis of Aspergillus infection?

A

Microscopy – looking at fungal spores

352
Q

What is the mainstay of treatment for aspergillosis?

A

Amphotericin for at least 6 weeks

Other options: voriconazole, caspofungin, itraconazole

353
Q

List some examples of dermatophyte infections.

A

Ringworm

Tinea

Nail infections

354
Q

What is tinea pedis caused by?

A

Tricophyton rubrum

Tricophyton interdigitale

Epidermophyton floccosum

355
Q

What is tinea cruris caused by?

A

Tricophyton rubrum

Epidermophyton floccosum

356
Q

What is tinea corporis caused by?

A

Tricophyton rubrum

Tricophyton tonsurans

357
Q

What is onychomycosis caused by?

A

Tricophyton spp.

Epidermophyton spp.

Microsporum spp.

358
Q

How is onychomycosis treated?

A

Nail lacquers

If unsuccessful, systemic treatment with terbinafine

Itraconazole is also an option

359
Q

How are dermatophyte infections diagnosed?

A

Skin scrapings and microscopy

360
Q

What is pityriasis versicolor caused by?

A

Malassezia furfur

361
Q

What is the characteristic clinical manifestation of mucormycosis?

A

Cellulitis of the orbit and face which progresses with discharge and black pus from the palate and nose

NOTE: black eschars may be seen as the fungus destroys tissues

362
Q

What is the term used to describe invasion of the brain by mucormycosis?

A

Rhinocerebral mucormycosis

363
Q

List three aetiological agents that can cause mucormycosis.

A

Rhizopum spp.

Rhizomucor spp.

Mucor spp.

364
Q

How is mucormycosis managed?

A

SURGICAL EMERGENCY

Refer to ENT for debridement

May need high-dose amphotericin

365
Q

List some examples of echinocandins.

A

Caspofungin

Micafungin

Anidulafungin

366
Q

Which fungi are echinocandins active against?

A

Candida species

Aspergillus species (NOT other moulds)

IMPORTANT: it has NO coverage for Cryptococcus

367
Q

List examples of azoles along with their usual indications:

A

Fluconazole – active against Candida and Cryptococcus

Voriconazole – similar to fluconazole but better activity against Aspergillus

Itraconazole – useful against dermatophytes

Posaconazole – activity against mucor

368
Q

What is the main polyene antifungal?

A

Amphotericin B

369
Q

Amphotericin B is active against most fungi except…

A

Aspergillus terreus

Scedosporium spp.

370
Q

Which fungi are flucytosine active against?

A

Candidiasis

Cryptococcosis

371
Q

What type of virus is rubella?

A

RNA virus

Togaviridae family

372
Q

What is the role of pre-natal diagnosis of rubella?

A

All cases of symptomatic rubella infection in the 1st trimester should be considered for termination of pregnancy without prenatal diagnosis

373
Q

What is the definition of congenital CMV infection?

A

Detection of CMV from bodily fluids (normally urine and saliva) or tissues within the first 3 weeks of life

NOTE: it is the MOST COMMON congenital viral infection

374
Q

What is the main consequence of congenital CMV infection?

A

Sensorineural hearing loss

375
Q

At what stage in pregnancy does CMV infection pose a risk to the foetus?

A

At any stage in pregnancy

376
Q

What proportion of cases of congenital CMV infection are asymptomatic at birth?

A

90%

377
Q

How is congenital CMV infection treated?

A

There is NO vaccine

Congenital CMV with significant organ disease

· Valganciclovir or ganciclovir for 6 months

· Audiology follow-up until age 6 years

· Ophthalmology review

378
Q

In which scenario will the neonate be at highest risk of acquiring HSV from the mother?

A

Primary HSV infection in the 3rd trimester (particularly within 6 weeks of delivery)

C-section is recommended

379
Q

Outline the manifestations of neonatal HSV disease.

A

Skin, eyes and mouth (SEM) disease

CNS disease with or without SEM

Disseminated infection involving multiple organs (high mortality)

380
Q

Describe the clinical presentation of intrauterine HSV infection.

A

Neurological – microcephaly, encephalomalacia, intracranial calcification

Cutaneous – scarring, active lesions

Ophthlamologic – microophthalmia, optic atrophy, chorioretinitis

381
Q

Outline the features of disseminated HSV infection.

A

DIC

Pneumonia

Hepatitis

CNS involvement

NOTE: has a 30% mortality

382
Q

Outline the manifestations of HSV encephalitis.

A

Seizures

Lethargy

Poor feeding

Temperature instability

NOTE: this tends to present late – 10-28 days

383
Q

Describe the treatment of neonatal HSV infection.

A

High-dose IV aciclovir (60 mg/kg/day) in three divided doses

For 21 days minimum in disseminated disease (repeat LP and CSF PCR until PCR-negative)

For 14 days minimum in SEM disease

Monitor neutrophil count

384
Q

What type of virus is VZV?

A

DNA virus of the herpes family

385
Q

What are the risks to the mother of VZV infection during pregnancy?

A

Pneumonia

Encephalitis

386
Q

List the main features of congenital varicella syndrome.

A

LBW

Cutaneous scarring

Limb hypoplasia

Microcephaly

Chorioretinitis

Cataracts

387
Q

At what stage in pregnancy is the risk of congenital varicella syndrome highest?

A

13-20 weeks

NOTE: shingles has no risk in pregnancy

388
Q

List some complications of measles.

A

Opportunistic bacterial infection (otitis media, pneumonia, bronchitis)

Encephalitis

Subacute sclerosing panencephalitis

· Tends to occur 6-15 years after measles infection

· Present with delays motor skills and behavioural problems

389
Q

What are the risks of measles in pregnancy?

A

Foetal loss (miscarriage, intrauterine death)

Preterm delivery

Increased maternal morbidity

IMPORTANT: NO congenital abnormalities to the foetus

390
Q

How should pregnant women who have been in contact with suspected/confirmed measles be treated?

A

Measles immunoglobulin attenuates the illness if given within 6 days of exposure

391
Q

What type of virus is parvovirus B19?

A

DNA virus

Parvoviridae family

392
Q

Describe the clinical presentation of parvovirus B19 infection.

A

Erythema infectiosum (fifth disease, slapped cheek syndrome)

Transient aplastic crisis

Arthralgia

Non-immune hydrops fetalis

393
Q

At what stage in pregnancy is parvovirus B19 infection most concerning?

A

< 20 weeks gestation

394
Q

What are some consequences of Zika virus infection in pregnancy.

A

Miscarriage

Stillbirth

Congenital zika syndrome

· Severe microcephaly

· Decreased brain tissue

· Seizures

· Retinopathy/deafness

· Talipes

· Hypertonia

395
Q

Name two groups of antibiotics that inhibit cell wall synthesis.

A

Beta-lactams

Glycopeptides

396
Q

What are the three groups of beta-lactam antibiotics?

A

Penicillins

Cephalosporins

Carbapenems

397
Q

Give two examples of glycopeptides.

A

Vancomycin

Tiecoplanin

398
Q

Which type of bacteria are beta-lactams ineffective against?

A

Bacteria with no cell wall (e.g. Mycoplasma and Chlamydia)

399
Q

List four types of penicillin.

A

Penicillin

Amoxicillin

Flucloxacillin

Piperacillin

400
Q

For each of the following antibiotics, describe their coverage and mechanisms of resistance:

A

a. Penicillin

Active against Gram-positives (e.g. Streptococci, Clostridia)

Broken down by beta-lactamases (mainly produced by S. aureus)

NOTE: penicillin is the MOST ACTIVE beta-lactam antibiotic

b. Amoxicillin

Broad-spectrum penicillin

Extends coverage to Enterococci and Gram-negative organisms

Broken down by beta-lactamase produced by S. aureus and many Gram-negatives

c. Flucloxacillin

Similar to penicillin but less active

Does NOT get broken down by beta-lactamase produced by S. aureus

d. Piperacillin

Similar to amoxicillin

Extends coverage to Pseudomonas and other non-enteric Gram-negative organisms

Broken down by beta-lactamase produced by S. aureus and many Gram-negatives

401
Q

Name two beta-lactamase inhibitors. What is the benefit of giving beta-lactamase inhibitors with beta-lactams?

A

Clavulanic acid

Tazobactam

Protect penicillins from breakdown by beta-lactamases thereby increasing the coverage to include S. aureus, Gram-negatives and anaerobes

402
Q

List examples of 1st, 2nd and 3rd generation cephalosporins.

A

1st = cephalexin

2nd = cefuroxime

3rd = ceftriaxone, ceftazidime, cefotaxime

NOTE: as you go up the generations you get increasing activity against Gram-negatives and less activity against Gram-positives

403
Q

What is ceftriaxone often used to treat?

A

Bacterial meningitis

404
Q

What is a disadvantageous association of ceftriaxone?

A

Associated with C. difficile infection

405
Q

What is a benefit of ceftazidime?

A

Good anti-Pseudomonas cover

406
Q

What are extended spectrum beta-lactamases (ESBL)?

A

Type of beta-lactamase that also breaks down cephalosporins as well as penicillins

407
Q

What is the main benefit of carbapenems?

A

They are stable to ESBL enzymes

408
Q

List three examples of carbapenems.

A

Meropenem

Imipenem

Ertapenem

409
Q

List examples of bacteria that have shown carbapenem resistance.

A

Acinetobacter

Klebsiella

410
Q

Outline the key features of beta-lactam antibiotics.

A

Relatively non-toxic

Renally excreted (reduced dose in renal impairment)

Short half-life

Will not cross an intact blood-brain barrier (may cross inflamed meninges in meningitis)

Cross allergenic (penicillins have 5-10% cross-reactivity with cephalosporins and carbapenems)

411
Q

Which type of bacteria are glycopeptides effective against and why?

A

Gram-positives

They are large molecules so they cannot cross the outer membrane of Gram-negative cell walls

412
Q

What are glycopeptides often used to treat?

A

Serious MRSA infections

C. difficile infections (oral vancomycin)

413
Q

What is a major side-effect of glycopeptides?

A

Nephrotoxic

Monitor blood levels to prevent accumulation

414
Q

List some classes of antibiotics that work by inhibiting protein synthesis.

A

Aminoglycosides

Tetracyclines

Macrolides

Lincosamides (e.g. clindamycin)

Streptogramins (e.g. Synercid)

Chloramphenicol

Oxazolidinones (e.g. linezolid)

415
Q

What are some major side-effects of aminoglycosides?

A

Ototoxic and nephrotoxic

416
Q

Which aminoglycosides are particularly active against Pseudomonas aeruginosa?

A

Gentamicin

Tobramycin

417
Q

Which class of antibiotics can aminoglycosides be used in combination with to produce a synergistic effect?

A

Beta-lactams (e.g. in endocarditis)

418
Q

Which type of bacteria do aminoglycosides have no activity against?

A

Anaerobes

419
Q

Which environmental feature will inhibit the activity of aminoglycosides?

A

Inhibited by low pH so are not very effective in abscesses

420
Q

What are tetracyclines?

A

Broad-spectrum agents with activity against intracellular pathogens (e.g. Chlamydiae, Rickettsiae and Mycoplasmas) as well as most conventional bacteria

421
Q

What is a major issue with tetracyclines?

A

Widespread resistance (most Gram-negatives)

422
Q

Which groups of patients should not receive tetracyclines?

A

Children and pregnant women

Because it can deposit in bone and cause discoloration of growing teeth

423
Q

What are macrolides mainly used for?

A

Mild staphylococcal and streptococcal infections in penicillin-allergic patients

Also active against Campylobacter, Legionella and Pneumophila

424
Q

What are two major risks of taking chloramphenicol?

A

Aplastic anaemia

Grey baby syndrome – neonates have reduced ability to metabolise the drug

425
Q

Which organisms are oxazolidinones active against?

A

Gram-positives (including MRSA and VRE)

Not active against Gram-negatives

426
Q

List two groups of antibiotics that inhibit DNA synthesis.

A

Quinolones

Nitroimidazoles

427
Q

List 3 examples of quinolones.

A

Ciprofloxacin

Moxifloxacin

Levofloxacin

428
Q

List 2 examples of nitroimidazoles.

A

Metronidazole

Tinidazole

429
Q

Describe the activity of quinolones.

A

Broad antibacterial activity, especially against Gram-negatives, including Pseudomonas aeruginosa

NOTE: newer agents increased activity against Gram-negatives and intracellular organisms

430
Q

List some uses of quinolones.

A

UTIs

Pneumonia

Atypical pneumonia

Bacterial gastroenteritis

431
Q

Describe the activity of rifampicin.

A

Mainly Mycobacteria and Chlamydiae

432
Q

What should be monitored when on rifampicin?

A

LFTs (it is metabolised by the liver)

433
Q

What is a common side-effect of rifampicin?

A

Orange secretions (urine, contact lenses)

434
Q

Why should rifampicin never be used alone?

A

Resistance develops rapidly due to chromosomal mutation (single amino acid change in beta-subunit of RNA polymerase)

435
Q

Name two cell membrane toxins.

A

Daptomycin

Colistin

436
Q

Describe the activity of daptomycin.

A

Gram-positives

Likely to be used in treating MRSA and VRE

NOTE: it is a cyclic lipopeptide

437
Q

Describe the activity of colistin.

A

Active against Gram-negatives including Pseudomonas aeruginosa, Acinetobacter baumanii and Klebsiella pneumoniae

NOTE: it is a polymyxin

438
Q

Name two families of antibiotics that work by inhibiting folate metabolism.

A

Sulphonamides

Diaminopyrimidines

439
Q

What is co-trimoxazole?

A

Sulphamethoxazole + trimethoprim

440
Q

What is trimethoprim commonly used to treat?

A

Community-acquires UTIs

441
Q

Which bacteria produce beta-lactamases?

A

S. aureus and Gram-negative bacilli (coliforms)

NOTE: this is not the mechanism of resistance in pneumococcus and MRSA

442
Q

In which groups of bacteria is penicillin resistance not reported in?

A

Group A, B, C and G beta-haemolytic streptococci

443
Q

What are extended spectrum beta-lactamases?

A

Able to breakdown cephalosporins as well as penicillins

Becoming more common in E. coli and Klebsiella

NOTE: if there is > 10% resistance then empirical therapy is not advised

444
Q

What are AmpC beta-lactamases?

A

Breakdown penicillins and cephalosporins but are not inhibited by clavulanic acid

445
Q

What type of antibiotics should be used in nosocomial infections and severe sepsis?

A

Broad-spectrum

446
Q

Describe the type I pattern of antibiotic activity. Give an example of an antibiotic of this type.

A

Concentration-dependent killing

Peak above the MIC (Cmax) is the most important parameter

Example: aminoglycosides

These drugs tend to be given as one big dose

The benefits of achieving a higher Cmax must be balanced with the increased toxicity

Trough concentration should also be measured to ensure that the drug is being eliminated (this determines the frequency of drug administration)

447
Q

Describe the type II pattern of antibiotic activity. Give an example of an antibiotic of this type.

A

Time-dependent killing

Time spent above the MIC is the most important factor

Example: penicillins

Therefore, penicillins need to be given frequently

448
Q

Describe the type III pattern of antibiotic activity. Give an example of an antibiotic of this type.

A

Concentration and time-dependent

AUC above the MIC is the most important factor

Example: vancomycin

NOTE: infusions may be used to maintain an AUC above the MIC

449
Q

Outline the typical length of treatment for N. meningitidis meningitis

A

7 days

450
Q

Outline the typical length of treatment for Acute osteomyelitis

A

6 weeks

451
Q

Outline the typical length of treatment for Bacterial endocarditis

A

4-6 weeks

452
Q

Outline the typical length of treatment for Group A streptococcal pharyngitis

A

10 days

453
Q

Outline the typical length of treatment for Simple cystitis

A

3 days

454
Q

Name two common organisms that cause skin infections.

A

Streptococcus pyogenes

Staphylococcus aureus

455
Q

How are simple skin infections treated?

A

Flucloxacillin

NOTE: unless penicillin allergic or MRSA

456
Q

How should invasive group A streptococcal infection be treated?

A

Aggressive and early debridement

Early use of antibiotics (e.g. clindamycin)

Use of IVIG

457
Q

List some common organisms that cause bacterial respiratory tract infections.

A

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

Atypicals: Legionella, Mycoplasma, Chlamydia

458
Q

What is used to treat Pharyngitis

A

Benzylpenicillin (10 days)

459
Q

What is used to treat CAP (mild)

A

Amoxicillin

460
Q

What is used to treat CAP (severe)

A

Co-amoxiclav and clarithromycin

461
Q

List some treatment options for hospital-acquired pneumonia.

A

Cephalosporins

Ciprofloxacin

Tazocin

If MRSA, consider adding vancomycin

462
Q

List the main pathogens that cause meningitis.

A

Neisseria meningitidis

Streptococcus pneumoniae

Listeria monocytogenes (in the very young, elderly and immunocompromised)

463
Q

What is the mainstay of treatment for bacterial meningitis?

A

Ceftriaxone

NOTE: consider adding amoxicillin if Listeria is likely

464
Q

How is meningitis in babies < 3 months treated?

A

Cefotaxime + amoxicillin

NOTE: ceftriaxone is NOT used in neonates because it displaces bilirubin from albumin and causes biliary sludging

465
Q

What are the treatment options for N. meningitidis meningitis?

A

Benzylpenicillin

Ceftriaxone or cefotaxime

466
Q

Outline the treatment of Simple cystitis

A

Trimethoprim (3 days)

467
Q

Outline the treatment of Hospital-acquired UTI

A

Cephalexin or co-amoxiclav

468
Q

Outline the treatment of Infected urinary catheter

A

Change catheter under gentamicin cover

469
Q

How is C. difficile colitis treated?

A

Stop the offending antibiotic (usually a cephalosporin)

If severe, treat with metronidazole or vancomycin

470
Q

List the major classes of immunosuppressive drugs.

A

Glucocorticoids

Calcineurin inhibitors (cyclosporin, tacrolimus)

Anti-proliferative agents (azathioprine, mycophenolate mofetil, sirolimus)

Antibodies (e.g. rituximab)

Co-stimulation blockers

471
Q

List some iatrogenic causes of immunosuppression in order of increasing risk of opportunistic viral infection.

A

DMARDs and steroids (LOWEST RISK)

Cytotoxic chemotherapy

Monoclonal antibodies

Solid organ transplant

Advanced HIV

Allogeneic stem cell transplant (HIGHEST RISK)

472
Q

What is a feature of chronic hepatitis B infection on serology?

A

Persistent HBsAg

473
Q

What does parvovirus B19 cause in the immunocompromised?

A

Causes chronic anaemia

474
Q

What are the three main types of worms? List some examples of each.

A

Cestodes (tape worms)

· Pork/beef/fish tapeworms

· Hydatid disease

Trematodes (flukes)

· Schistosomiasis

Nematodes (roundworms)

· Hookworms

· Ascarids

· Strongyloides

475
Q

What are the two types of pork and beef tapeworms?

A

Taenia solium – pork (can invade human tissues causing cysticercosis)

Taenia saginata – beef

476
Q

How are worms treated?

A

Praziquantel

477
Q

What are the five main soil-transmitted helminths?

A

Ascaris lumbricoides

Strongyloides stercoralis

Trichuris trichiura

Enterobius vermicularis

Hookworm

NOTE: they are very well adapted to humans so cause little disease

478
Q

How can soil-transmitted helminths cause disease?

A

Migration (Ascaris and Strongyloides)

Intestinal obstruction (large worm burden)

Malabsorption and blood loss

Psychological distress

479
Q

How does Strongyloides caused damage?

A

Most are ASYMPTOMATIC

Hyperinfection

Larvae currens (itchy rash)

Malabsorption

480
Q

How is Strongyloides treated?

A

Ivermectin

481
Q

How are the nematode infections that cause filariasis spread?

A

Blackflies and mosquitoes

482
Q

Outline the classification of filariasis.

A

Based on location

Lymphatic filariasis

· Wucheria

· Brugia

Subcutaneous filariasis

· Onchocerciasis

· Mansonella

· Loa Loa

Serous cavity filariasis

· Mansonella

· Dirofilaria

NOTE: adult worms are only found in humans

483
Q

What is myiasis?

A

Parasitisation of human flesh by fly larvae

484
Q

Name two types of myiasis.

A

Bot (South America)

Tumbu (Africa)

NOTE: damage is caused by maggots eating surrounding flesh

485
Q

How is myiasis treated?

A

Removal of larvae by asphyxiation or surgery

486
Q

List some causes of eosinophilia.

A

Atopy

Drug allergy

Some malignancy (mainly Hodgkin lymphoma)

Systemic autoimmune disease (e.g. SLE)

Some forms of vasculitis (e.g. Churg-Strauss syndrome)

Cholesterol embolism

Parasites

· Soil-transmitted helminths (especially Strongyloides)

· Schistosomiasis

· Filariasis

· Leaking hydatid cyst

487
Q

Outline the components of a reasonable parasite screen.

A

Serology: Strongyloides, Schistosoma, filaria

Stool microscopy

488
Q

What is the most common cause of adult-onset seizures worldwide?

A

Brain worms

489
Q

Which organism causes cysticercosis?

A

Taenia solium

490
Q

List some CNS manifestations of cysticercosis.

A

Epilepsy

Raised ICP

Headache

Altered mental state

Stroke

Blindness

491
Q

How is the acquisition of pig tapeworm different from the acquisition of cysticercosis?

A

Ingesting cysts from undercooked pork will lead to the development of adult tapeworms in the human GI tract

Ingesting tapeworm eggs will lead to cysticercosis

492
Q

Outline the management of cysticercosis.

A

Anticonvulsants

Advice not to drive

Ventriculo-peritoneal shunt if hydrocephalus

Cestocidal drugs (e.g. praziquantel, albendazole)

This MUST be given with steroids to reduce inflammation around dying cysts

493
Q

List some risk factors for TB.

A

Malnutrition (most common)

HIV (very serious risk factor)

Poverty

Underweight

Past TB

494
Q

What is the vector for malaria?

A

Anopheles mosquito (female)

495
Q

What are the five species of Plasmodium.

A

Plasmodium falciparum

Plasmodium vivax

Plasmodium ovale

Plasmodium malariae

Plasmodium knowlesi

496
Q

Describe the clinical features of malaria.

A

Cyclical or continuous fevers with spikes

Malaria paroxysms – chills, high fever, sweats

497
Q

List some clinical features of severe malaria.

A

High parasitaemia

Altered consciousness

ARDS

Circulatory collapse

Metabolic acidosis

Renal failure

Hepatic failure

Coagulopathy

Severe anaemia

Hypoglycaema

498
Q

What is the main investigation for malaria?

A

Perform 3 thick and thin blood films

Thick – screening for parasites (sensitive)

Thin – identifying the species and quantifying the parasite (proportion of red cells that have been parasitised)

499
Q

Which stains are used for malaria?

A

Giemsa

Field’s

500
Q

Outline the treatment options for non-falciparum malaria.

A

Chloroquine – 3 days

Primaquine – 30 mg for 14 days

501
Q

What must you do before giving someone primaquine?

A

Screen for G6PD deficiency as primaquine can cause extensive haemolysis

502
Q

What counts as ‘mild’ falciparum malaria?

A

Not vomiting

Parasitaemia < 2%

503
Q

Outline the treatment options for mild falciparum malaria.

A

Oral malarone (atovaquone and proguanil)

Artemisinin combination therapy (ACT)

Oral quinine (RARELY used)

504
Q

Outline the treatment of severe falciparum malaria.

A

ABCDE approach

Correct hypoglycaemia

Cautious hydration

Organ support if necessary

IV artesunate

Daily parasitaemia monitoring

Follow on with oral antimalarials

505
Q

What is the vector for dengue?

A

Aedes mosquito

506
Q

Outline the clinical features of dengue.

A

Fever

Headache

Myalgia

Erythrodermic rash

Bleeding

Hepatitis

Severe: encephalitis, myocarditis

507
Q

What are the complications of dengue? In which circumstances does this tend to occur?

A

Dengue haemorrhagic fever and dengue shock

This occurs in individuals who have previously been infected with a different dengue serotype

508
Q

Which tropical virus is similar to dengue? What is a key difference?

A

Chikungunya

Arthralgia is more severe

509
Q

How is dengue treated?

A

Identify those at risk of severe disease

Supportive

510
Q

Outline the clinical course of dengue.

A

Fever reduces after about 4-5 days

511
Q

What is the term used to describe a high temperature with a relatively normal heart rate? List some causes.

A

Sphygmothermic dissociation

Causes: typhoid, yellow fever, brucellosis, tularaemia

512
Q

What is typhoid fever caused by?

A

Salmonella typhi and paratyphi

513
Q

What type of organism is Salmonella typhi?

A

Gram-negative rod

514
Q

Outline the clinical features of typhoid.

A

High prolonged fever

Headache

Rose spots

Constipation

Dry cough

515
Q

What is the incubation period of typhoid?

A

7-18 days

516
Q

List some complications of typhoid.

A

GI bleeding

Perforation

Encephalopathy

517
Q

Outline the treatment of typhoid.

A

Ceftriaxone 2 g IV OD

Azithromycin PO 500 mg BD 7 days

518
Q

What is a characteristic microscopic feature of mononucleosis?

A

Atypical lymphocytes

Path Laz (condensed) (COPY) (5 decks)

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