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2a > Infection > Flashcards

Infection Flashcards

1
Q

What is MRSA? What abx are used to treat it?

A
  • Staph aureus bacteria that have become resistant to beta-lactam abx
  • Doxycycline, vancomycin, clindamycin, teicoplanin, linezolid
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2
Q

What causes TB? Shape? Gram staining?

A
  • Mycobacterium tuberculosis
  • Rod shaped
  • Zeihl-Neelsen stain (bright red against blue background)
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3
Q

What is MDR-TB?

A
  • Multidrug-resistant TB
  • Strains resistant to more than one TB drug
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4
Q

How is TB spread? What are possible outcomes of infection?

A
  • Saliva droplets
  • Immediate clearance
  • Primary active TB
  • Latent TB
  • Secondary TB
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5
Q

What normally causes reactivation of latent TB? What is this then called?

A
  • Immunosuppression
  • Secondary TB
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6
Q

What is a cold abscess? How does it present?

A
  • Abscess caused by TB
  • Firm, painless abscess in the neck
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7
Q

What is the BCG vaccine?

A

Live attenuated Mycobacterium bovis bacteria (close relative of M tuberculosis)

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8
Q

What tests are used to detect an immune response to TB?

A
  • Mantoux test
  • Interferon-gamma release assay
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9
Q

What is check before someone is given a BCG vaccine?

A
  • Mantoux test
  • HIV status
  • Possibility of immunosuppression
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10
Q

What investigations are useful where active TB infection is suspected?

A
  • CXR
  • Cultures
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11
Q

What is involved in the Matoux Test? What is a positive result? What does this indicate?

A
  • Tuberculin (a collection of tuberculosis proteins isolated from the bacteria) is injected into the intradermal space on the forearm. This creates a bleb under the skin which is measured 72 hrs later
  • An induration of 5mm or more
  • Immune response to TB caused by active, latent or previous TB infection
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12
Q

What is involved in the Interferon-Gamma Release Assays? What is a positive result? Why does this occur?

A
  • Mixing a blood sample with antigens from the M. tuberculosis bacteria
  • When interfon-gamma is released
  • After previous contact with M. tuberculosis, white blood cells becomes sensitised to the bacteria antigens are will release interferon-gamma on further contact
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13
Q

What indicated primary TB on CXR
?

A
  • Patchy consolidation
  • Pleural effusions
  • Hilar lymphadenopathy
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14
Q

What indicated reactivated TB on CXR?

A
  • Patchy/nodular consolidation
  • Cavitation (gas filled spaces) typically in the upper zones
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15
Q

What indicates disseminated miliary TB on CXR?

A
  • ‘Millet seeds’ (small 1-3mm nodules) disseminated throughout the lung fields
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16
Q

Why are culture samples required in TB? When are the collected? How long do the results take to come back?

A
  • Cultures are used for testing drug resistance
  • Ideally collected before starting treatment
  • Can take several months - tx is normal started while waiting for culture results
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17
Q

What is the treatment of active TB?

A
  • Rifampicin (6 months)
  • Isoniazid (6 months)
  • Pyrazinamide (2 months)
  • Ethambutol (2 months)
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18
Q

What is the treatment of latent TB?

A

Either:
- Rifampicin and Isoniazid for 3 months
- Isoniazid for 6 months

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19
Q

What can rifampicin cause? What drugs can it interact with?

A

Red/orange discolouration of secretions (‘red-an-orange-pissin’’)

Contraceptive pills

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20
Q

What can isoniazid cause?

A

Peripheral neuropathy (‘I’m-so-numb-azid’)

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21
Q

What can pyrazinamide cause?

A

Hyperuricaemia resulting in gout

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22
Q

What can ethambutol cause?

A

Colour blindness and reduced visual acuity (‘eye-thambutol’)

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23
Q

What type of virus is HIV?

A

RNA retrovirus

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24
Q

What are the two types of HIV? Which is more common?

A
  • HIV-1 (more common)
  • HIV-2
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25
Q

What is AIDS? When does it occur?

A

Acquired immunodeficiency syndrome

  • Occurs when HIV is not treated -> disease progression -> person becomes immunocompromised
  • This leads to opportunistic infections and AIDS-defining illnesses
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26
Q

What is the basic pathophysiology of HIV?

A
  • The virus enters and destroys CD4 T-helper cells
  • This causes progressive immunocompromise resulting in a number of AIDS defining conditions
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27
Q

What are examples of AIDS-defining illnesses?

A
  • Kaposi’s sarcoma
  • Pneumocystitis jirovecii pneumonia
  • CMV infection
  • Candidiasis (oesophageal/bronchial)
  • Lymphomas
  • TB
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28
Q

What are the stages of HIV infection?

A
  1. Acute seroconversion: 2-6 wks following infection, 50% develop flu like symptoms (sore throat, fever, malaise, maculopapular rash, lymphadenopathy)
  2. Asymptomatic: can last 8-10 years, may have generalised lymphadenopathy
  3. Symptomatic: as the immune system fails and the virus mutates, the pt becomes more susceptible to common pathogens (colds/gastroenteritis), constitutional symptoms inc. wt loss/fatigue
  4. AIDS - diagnosis with an AIDS defining illness
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29
Q

How can HIV be transmitted?

A

Blood borne;
- Mother to child
- Sexual intercourse
- IVDU
- Needle stick injuries
- Blood products

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30
Q

What is an example of vertical HIV transmission?

A

Mother to child at any stage of pregnancy, birth or breastfeeding

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31
Q

What screening tests are used for HIV?

A
  • Fourth-generation laboratory test
  • Point of care test
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32
Q

What does the fourth generation laboratory test involve? When is a negative test unreliable?

A
  • Tests for antibodies to HIV and the p24 antigen
  • A negative result within 45 days of exposure is unreliable
  • This is because it had a window period of 45 days
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33
Q

What is involved in the point-of-care test for HIV? Any window period?

A
  • Test for HIV antibodies
  • Gives a result within minutes
  • 90 day window period
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34
Q

Who has a bigger willy, Maddie or Emma

A

Maddie

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35
Q

What tests are used to monitor and plan treatment in HIV?

A
  • CD4 count
  • Viral load
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36
Q

What is the CD4 count used to assess?

A

Risk of opportunistic infection

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37
Q

What is the normal CD4 count? What would indicate patients are at high risk of opportunistic infections?

A
  • 500-1200 cells/mm3
  • Under 200 cells/mm3
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38
Q

What is measured to determine the viral load in HIV? What level indicates an undetectable viral load?

A
  • HIV RNA per ml of blood
  • <20 copies/ml
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39
Q

What is the aim of HIV treatment?

A

To achieve and normal CD4 count and an undetectable viral load

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40
Q

What is the treatment of HIV?

A

A combination of antiretroviral therapy (ART) medications

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41
Q

What are the classes of ART medications?

A
  • Protease inhibitors (PI)
  • Integrase inhibitors (II)
  • Nucleoside reverse transcriptase inhibitors (NRTI)
  • Non-nucleoside reverse transcriptase inhibitors (NNRTI)
  • Entry inhibitors (EI)
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42
Q

What is the usual starting regime in HIV management?

A

Two NRTIs (e.g. tenofovir plue emtricitabine) PLUS a tri agent (e.g. bictegravir)

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43
Q

What are all HIV positive patients with a CD4 count <200/mm3 treated with?

A

Prophylactic co-trimoxazole to protect against pneumocystis jirovecii pneumonia

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44
Q

What are the recommendations surrounding cervical smears for HIV positive people?

A

Yearly cervical smears due to increased risk of HPV and cervical cancer

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45
Q

What are the recommendations surrounding vaccinations for HIV positive people?

A
  • Ensure vaccinations are up to date
  • Yearly influenza vaccine
  • Avoid live vaccines e.e. BCG and typoid
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46
Q

What viral load would indicate VD vs CS in HIV positive pregnant women?

A
  • <50 copies/ml = normal VD
  • > 50 copies/ml = consider CS
  • > 400 copies/ml - recommend CS
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47
Q

What is the management of HIV positive women in labour with a viral load >1000 copies/ml?

A
  • CS
  • IV zidovudine during labour and delivery
48
Q

What indicates a newborn is low-risk of HIV? What is given as HIV prophylaxis to low-risk vs his-risk babies?

A
  • Low-risk if the mother’s viral load is <50 copies/ml
  • Low-risk prophylaxis = zidovudine for 2-4 weeks
  • High-risk prophylaxis = zidovudine, lamivudine and nevirapine for 4 weeks
49
Q

Is breast feeding recommended in HIV positive mothers?

A
  • No
  • HIV can be transmitted during breastfeeding
50
Q

What is PEP? What does it consist of? When should it be taken? How long for?

A
  • Post exposure prophylaxis
  • A combination of ART
  • PEP should be commenced within a short window of opportunity (<72 hrs)
  • Current regime is for 28 days
51
Q

What is PrEP?

A
  • Pre-exposure prophylaxis
52
Q

Kapsoi’s sarcoma:
1. What is it caused by?
2. How does it present?
3. What is the management?

A
  1. HHV-8
  2. Purple papules/plaques on the skin or mucosa (GI/resp tract). Lesions may ulcerate. Resp involvement can lead to pleural effusion and massive haemoptysis
  3. Radiotherapy + resection
53
Q

Is HIV a notifiable disease?

A

No

54
Q

What causes malaria? Which is the most severe subtype?

A

Malaria is caused by members of the Plasmodium family of protozoan parasites

  • Plasmodium falciparum (most severe)
  • Plasmodium vivax
  • Plasmodium ovale
  • Plasmodium malariae
  • Plasmodium knowlesi
55
Q

What is malaria spread by?

A

Female Anopheles mosquito

56
Q

What is the life cycle of malaria?

A
  • Feeding mosquito sucks up parasites
  • Parasite reproduce in mosquito producing sporozoites
  • These are injected into human when bitten by mosquito
  • Sporozoites travel to the liver where they lie dormant as hypnozoites (this can be for 4 yrs if P. ovale / P. vivax)
  • In the liver the parasites mature into merozoites which infect red blood cells -> reproduce -> rupture -> merozoites released into blood -> haemolytic anaemia
  • The rupture and release of merozoites is responsible for fever spikes
57
Q

What are the patterns of fever spikes for different malaria causing parasites?

A
  • Every 48 hrs = P. vivax, P. ovale (tertian malaria)
  • More frequent, irregular fever spikes = P. falciparum (subtertian)
  • Every 72 hrs = P. malariae (quartan)
58
Q

What is the typical incubation period for malaria?

A

1-4 weeks

59
Q

Give some symptoms and signs of malaria

A

Symptoms:
- Fever (up to 41)
- Fatigue
- Myalgia
- Headache
- N+V

Signs:
- Pallor (due to anaemia)
- Hepatosplenomegaly
- Jaundice (rupture of RBC -> bilirubin release)

60
Q

How is malaria diagnosed?

A
  • Malaria blood film
  • Will show the parasites, the concentration (as percentage) and the type
61
Q

What is required to exclude a diagnosis of malaria?

A
  • Three negative samples taken over three consecutive days
  • This is because the parasites are released into the blood every 48-72 hrs meaning they may be missed
62
Q

When should patients with malaria be admitted?

A
  • Any patients with P. falciparum malaria
  • Severe/complicated malaria
63
Q

What is the first line oral and first and second line IV treatment for malaria?

A

Oral:
- Artemether with lumefantrine

IV:
- Artesunate (first)
- Quinine dihydrochloride

64
Q

What is a side effect of IV artesunate for malaria?

A

Haemolysis

65
Q

What are possible complications of P. falciparum malaria?

A
  • Cerebral malaria
  • Seizures
  • Reduced consciousness
  • AKI
  • Pulmonary oedema
  • DIC
  • Severe haemolytic anaemia
  • Multi-organ failure and death
66
Q

What are the most common medications used for malaria prophylaxis? Include potential side effects

A
  • Proguanil with atovaquone (Malarone)
  • Doxycycline (diarrhoea/thrush/photosensitivity)
  • Mefloquine (anxiety/depression/abnormal dreams)
67
Q

What are protective factors against malaria?

A
  • Sickle cell trait
  • GP6D deficiency
  • HLA-B53
  • Absence of Duffy antigens
68
Q

What is clostridium difficile?

A

A gram positive, rod-shaped, anaerobic bacteria

69
Q

What are the main causes of C. diff?

A
  • Antibiotics
    • Clindamycin
    • Ciprofloxacine
    • Cephalosporins
    • Carbapenems
  • PPIs
70
Q

C. diff produces toxins which cause symptoms and complications. What are the main two?

A
  • Toxin A (enterotoxin)
  • Toxin B (cytotoxin)
71
Q

How do you test for C. diff?

A

Stool sample:
- C. diff antigen (screening test)
- A and B toxins (diagnostic)

72
Q

What is the first and second line management of C. diff?

A
  1. Oral vancomycin
  2. Oral fidaxomicin
73
Q

What are complications of C. diff?

A
  • Pseudomembranous colitis
  • Toxic megacolon
  • Bowel perforation
  • Sepsis
74
Q

What are ddx for intra-abdominal infections?

A
  • Acute diverticulitis
  • Acute cholecystitis
  • Ascending cholangitis
  • Appendicitis
  • SBP
  • Intra-abdominal abscess
75
Q

Intra-abdominal infections are caused by a range of different bacteria. They require broad-spectrum abx whilst awaiting culture results. 2/3 broad spec abx are often used to cover for gram +ve, gram -ve, anaerobic and atypical bacteria. What abx covers for all three of these apart from atypical bacteria?

A

Co-amoxiclav

76
Q

What is cellulitis?

A

An infection of the skin and the soft tissues underneath

77
Q

What feature of cellulitis indicates a staph aureus infection?

A

Golden yellow crust

78
Q

What are the most common causes of cellulitis?

A
  • Staph aureus
  • Group A strep
  • Group C strep (strep dysgalactiae)
79
Q

What classification system can be used to assess the severity of cellulitis?

A

Eron classification
- Class 1-4
- Class 4 = sepsis or life threatening infection

80
Q

Which cellulitis pts require admission for IV abx?

A
  • Class 3/4 cellulitis
  • Frail
  • V young
  • Immunocompromised
  • Facial, periorbital or orbital cellulitis
81
Q

What is the first line abx for cellulitis? What is favoured for cellulitis near the eyes of nose?

A
  • Flucloxacillin
  • Co-amoxiclav
82
Q

What is the pathophysiology of sepsis?

A
  • Macrophages, lymphocytes and mast cells recognise pathogens -> release cytokines (interleukins/TNF) -> activate immune system -> systemic inflammation
  • Cytokines -> endothelial lining of blood vessels -> more permeable -> fluid leaks out into extracellular space -> oedema and reduced intravascular volume -> decreased oxygen supply to tissues -> anaerobic respiration -> serum lactate rises + metabolic acidosis occurs
  • Activation of the coagulation system -> formation of blood clots throughout the body -> platelets and clotting factors used up -> thrombocytopenia + haemorrhage = DIC
83
Q

What happens in septic shock?

A

The arterial blood pressure drops despite adequate fluid resuscitation -> organ hypo perfusion

84
Q

How is septic shock diagnosed?

A
  • Low mean arterial pressure despite fluid resuscitation (<65mmHg)
  • Raised serum lactate (>2mmol/L)
85
Q

What is the management of septic shock?

A
  • Aggressive treatment with IV fluids
  • Escalate to HDU/ICU for treatment with vasopressors (e.g. noradrenaline) to increase systemic vascular resistance and MAP
86
Q

What is the sepsis 6?

A

3 test:
- Serum lactate
- Blood cultures
- Urine output

3 treatments:
- Oxygen
- Broad spec abx
- IV fluids

87
Q

What is neutropenic sepsis?

A

Sepsis in someone with a neutrophil count below 1x10^9/L

88
Q

What medications can cause neutropenia?

A
  • Chemotherapy
  • Clozapine
  • DMARDs
  • Biologics
89
Q

What is treated as neutropenic sepsis until proven otherwise?

A

Temp >38 in pts on chemo or meds that may cause neutropenia

90
Q

What is the treatment of neutropenic sepsis?

A
  • Broad spec abx e.g. Piperacillin with tazobactam (tazocin is name for both together)
  • Refer to local guidelines
91
Q

What is infectious mononucleosis? What is it aka?

A
  • Condition caused by infection with EBV
  • Glandular fever
92
Q

What are the features of infectious mononucleosis?

A
  • Fever
  • Sore throat
  • Fatigue
  • Lymphadenopathy
  • Tonsillar enlargement
  • Splenomegaly
93
Q

What antibiotics cause an itchy maculopapular rash in patients with infectious mononucleosis?

A
  • Amoxicillin
  • Cefalosporins
94
Q

How can you investigate IM?

A
  1. Test for heterophile antibodies:
    - Monospot test
    - Paul-Bunnell test
    - These tests are not 100% sensitive as not everyone with IM produces heterophile antibodies
  2. Test for EBV antibodies:
    - IgM rises early suggesting acute infection
    - IgG persists after the condition suggesting immunity
95
Q

What is the management of IM?

A
  • Self limiting - acute illness lasts 2-3 weeks
  • Avoid alcohol - EBV affects livers ability to process alcohol
  • Avoid contact sports - risk of splenic rupture
96
Q

How does scabies present?

A
  • Itchy small red spots
  • Track marks where the mites have burrowed
  • The classic location is between the finger webs
  • Can take up to 8 weeks for symptoms to appear after the initial infection
97
Q

What is the management of scabies?

A
  • Permethrin cream - apply to whole body and leave on for 8-12 hours, repeat a week later to kill the eggs that survived
  • Oral ivermectin as a single dose can be repeated a week later for difficult to treat/crusted scabies
  • Wash all clothes etc on a hot wash to destroy mites, hoover carpets and furniture
  • Note itching can continue for 4 weeks after successful treatment
98
Q

What is crusted scabies?

A
  • A serious infestation with scabies in patients that are immunocompromised
  • Rather than individual spots they have patches of red skin that turn into scaly plaques (misdiagnosed as psoriasis)
  • Immunocompromised patients may not have an itch as they do not mount an immune response to infestation
  • Tx = oral ivermectin
99
Q

What causes Lyme disease?

A

The spirochaete Borrelia burgdorferi which is spread by ticks

100
Q

What are early features of Lyme disease? (within 30 days)

A
  • Erythema migrant (build eye rash at the site of tick bite)
  • Systemic features - headache, lethargy, fever, arthralgia
101
Q

What are late features of Lyme disease? (after 30 days)

A
  • Cardiovascular - heart block, peri/myocarditis
  • Neurological - facial nerve palsy, radicular pain, meningitis
102
Q

What is the first line test for Lyme disease?

A
  • Enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelial burgdoferi
  • If -ve test and within first 4 weeks of symptoms onset, retest in 4-6 weeks
103
Q

When can you commence abx for Lyme disease without antibody testing?

A

If erythema migrans is present

104
Q

What is the management of Lyme disease?

A
  • Doxycycline if early disease
  • Ceftriaxone if disseminated disease
105
Q

What reaction can be seen after commencing abx therapy for Lyme disease?

A
  • Jarisch-Herxheimer reaction
  • Fever, rash, tachycardia after first dose of abx
106
Q

What is toxic shock syndrome?

A
  • A severe systemic reaction to bacterial toxins
  • Toxins are produced by staph aureus or Group A strep
107
Q

What can cause toxic shock syndrome?

A
  • Tampons
  • Soft tissue infections
  • Post-surgical infections
  • Burns
  • Retained foreign objects e.g. nasal packing, dialysis catheters
108
Q

What is the diagnostic criteria for toxic shock syndrome?

A
  • Fever - temp >38.9
  • Hypotension - systolic <90
  • Diffuse erythematous rash
  • Desquamation of rash - especially palms and soles
  • Involvement of 3 or more organ systems - e.g. CNS involvement (confusion), mucous membrane erythema, D+V, hepatitis, renal failure, thrombocytopenia
109
Q

What is the management of toxic shock syndrome?

A
  • Removal of infection focus
  • IV fluids
  • IV antibiotics
110
Q

How can necrotising fasciitis be classified?

A
  • Type 1 - caused by mixed anaerobes and aerobes (often post-surgery in diabetics) (more common)
  • Type 2 - caused by strep pyogenes
111
Q

What are RF for necrotising fasciitis?

A
  • Skin factors - recent trauma, burns, soft tissue infections
  • DM - particularly if treated with SGLT-2 inhibitors
  • IVDU
  • Immunosuppression
112
Q

What is the most commonly affected site in necrotising fasciitis?

A

Perineum

113
Q

How does necrotising fasciitis present?

A
  • Acute onset
  • Pain, swelling, erythema of affected site
  • Skin necrosis is a late sign
  • Fever and tachycardia may occur late in the presentation
114
Q

What is the management of necrotising fasciitis?

A
  • Urgent surgical referral for debridement
  • IV abx
115
Q

What is the prognosis of necrotising fasciitis?

A

Average mortality = 20%

116
Q
A

2a (12 decks)

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