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Infection > Specific Infections (Sources: Revision notes) > Flashcards

Specific Infections (Sources: Revision notes) Flashcards

1
Q

What is influenza?

A

An acute respiratory illness caused by the influenza A, B or C virus

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2
Q

How is influenza transmitted?

A

By large droplets or prolonged close contact

Average incubation period is 2 days

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3
Q

Which influenza strain is responsible for epidemics and pandemics?

A

A as it’s more transmissible than B and C

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4
Q

What are the clinical features of influenza?

A

Respiratory - coryzal symtpoms, breathlessness, cough

Constitutional - fever, myalgia, headache

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5
Q

What complications occur secondary to influenza?

A

Secondary bacterial infection esp with Staphylococcus aureus
Direct viral pneumonitis
Rhabdomyolysis

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6
Q

Who is most susceptible to complications from influenza?

A 
The elderly
Pregnant women
Obese
Immunocompromised
Those with chronic illness
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7
Q

How is influenza managed?

A

Primarily supportive
Neuramidase inhibitors are used to treat the underlying infection
First line treatment of influenza A on ICU is oseltamivir 75mg BD, higher dose may be considered for B
Patients should be isolated and barrier-nursed

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8
Q

Which patient with influenza should be treated with oseltamivir?

A

Any patient with confirmed or suspected influenza A or B in who

  • admission to critical care is required
  • Evidence of lower respiratory tract infection
  • Evidence of CNS infection
  • Significant exacerbation of underlying disease
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9
Q

In the returned traveller what is the most common cause of fever?

A

Malaria

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10
Q

Which of the malaria strains causes the most severe clinical presentations?

A

Plasmodium falciparum

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11
Q

What are the different malarial strains

A

P.ovale
P.vivax
P.malaraie
P.falciparum

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12
Q

How is malaria diagnosed?

A

Thick and thin blood films

Thick films have a high sensitivity and thin films are more specific and allow quantification for paraitaemia

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13
Q

According to the WHO, what are the clinical markers of severe malaria infection?

A

Cerebral malaria - impaired consciousness, coma, convulsions
ARDS
Circulatory collapse
Jaundice in the setting of other organ dysfunction
Haemoglobinuria
Abnormal spontaneous bleeding

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14
Q

What are the laboratory features of severe falciparum infection?

A 
Hypoglycaemia < 2.2
Severe anaemia (Hb < 50)
Metabolic acidosis (bicarb < 15, pH < 7.35)
Hyperparasitaemia 
Hyperlactataemia (>5)
AKI (Cr > 265 micro mols per litre)
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15
Q

Why do patients with malaria get admitted to ICU?

A

Cerebral malaria
AKI
ARDS

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16
Q

What are the side-effects of IV quinine?

A

Tinnitus, blurred vision
Hypoglycaemia
Prolonged QT

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17
Q

What supportive measures are used in the management of malaria?

A

Restricted fluid strategy - to minimise risk of lung injury and cerebral oedema
Lung protective ventilation strategies

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18
Q

What is the natural progression of HIV?

A 
Viral transmission
Seroconversion
Chronic infection 
-asymptomatic, latent period
-AIDS CD4 < 200 or AIDS defining illness
Advanced HIV/AIDS
-CD4 < 50
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19
Q

What are the AIDS defining illnesses? (as per the WHO)

A 
HIV wasting syndrome
Pneumocystis jirovecii pneumonia
Recurrent severe bacterial pneumonia
Chronic herpes simplex infection of > 1 months duration
Oesophageal candidiasis
Extra pulmonary tuberculosis
Kaposi's sarcoma
Cytomegalovirus infection
CNS toxoplasmosis
HIV encephalopathy
Extra pulmonary cryptococcosis
Disseminated non-tuberculosis mycobacterial infection
Progressive multifocal leukoencephalopathy
Chronic cryptosporidiosis
Chronic isoporiasis
Disseminated mycosis
Recurrent non-typhoids Salmonella bacteraemia
Lymphoma
Invasive cervical carcinoma
Atypical disseminated leishmaniasis
Symptomatic HIV-associated nephropathy or symptomatic HIV - associated cardiomyopathy
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20
Q

How is HIV treated?

A

Highly active antiretroviral treatment (HAART)
A combination of at least 3 drugs to suppress HIV replication
The timing of initiation is debated
Those with CD4 < 200 are considered to benefit
Treating those with higher CD4 counts has a public health advantage and reduces the rate of progression of HIV-related cardiovascular and neurological disease
The disadvantages to early treatment are the costs, side-effects and lack of trial data demonstrating benefit

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21
Q

What are the different classes of antiretroviral agents?

A

Entry inhibitors e.g. enfuvirtide
Nucleoside and nucleotide reverse transcriptase inhibitors e.g. zidovudine
Non-nucleoside reverse transcriptase inhibitors e.g. efavirenz
Integrase inhibitors e.g. raltegravir
Protease inhibitors e.g. lopinavir

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22
Q

What is the immune reconstitution inflammatory syndrome?

A

An inflammatory process, associated with worsening of existing infectious processes, occurring on initiation of antiretroviral therapy
Most commonly associated with TB, Cryptococcus, Pneumocystis, or CMV infection
A rise in CD4 count occurring on starting treatment leads to a sudden increase in natural inflammatory reposes, leading to systemic inflammatory symptoms

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23
Q

What are the risk factors for the immune reconstitution inflammatory syndrome?

A

Low CD4 count on initiation of treatment
Significant response to antiretroviral treatment
Presence of opportunistic infection

24
Q

What considerations with antiretroviral therapy are important in ICU?

A

Timing tof initiation of antiretrovirals (and associated risk of IRIS)
Drug interactions - there are many
Difficultly with enteral access and absorption - most antivirals are enteral only

25
Q

What is Pneumocystis jiroveci?

A

An opportunistic infection
Classified as a fungus
One of the most commonly encountered opportunistic infections on the ICU
Patients with a CD4 count of < 200 are at risk
Presents as progressive dyspnoea and cough
Classical CXR appearance of diffuse bilateral infiltrates
Beta D gluten levels are typically elevated
Diagnosis is based upon immunofluorescence staining +/- PCR

26
Q

How is Pneumocystis jiroveci treated?

A

Co-trimoxazole is first line
Primaquine is an alternative
Steroids (normally prednisolone) should be given to all patients with PJP on the ICU

27
Q

Describe Cryptococcal meningitis

A

Cryptococcus neoformans can produce an invasive fungal infection in the meninges
Presents with a headache and general decline
Definitive diagnosis is with culture of Cryptococcus in CSF, it also normally shows low WCC, low glucose and moderately increased protein

28
Q

How is Cryptococcal meningitis treated?

A

First-line treatment is with amphoteici B plus flu cytosine for the initial phase

29
Q

What is toxoplasmosis encephalitis?

A

Toxoplasmosis may occur in up to 30% of patient s with a CD4 count < 100
Presents with confusion, headache and fever
Patients will be Toxoplasmosis gondii IgG antibody positive
Neuro imaging shows multiple ring enhancing lesions
Initial treatment is with pyrimethamine, sulfadiazine and calcium foliate
Dexamethasone is given if there is evidence of raised ICP

30
Q

What is botulism?

A

The clinical manifestation of Clostridium botulinum infection
Classically a consequence of ingesting contaminated food

31
Q

What is Clostridium botulinum?

A

A spore forming Gram-postive anaerobic rod
Heat resistant
Found in soil, vegetables, fish, putrid food
Produces toxins - A,B and E are associated with human disease
Denatured at > 80 degrees C
Very potents - 1g of toxin could kill millions of humans
Absorbed via the mucous membranes and spread in blood

32
Q

What is the pathophysiology of botulism?

A

Botulinum toxin binds to a specific receptor at the acetylcholine transmission site, leaving to an irreversible blockade of acetylcholine release - leading to impaired transmission at the neuromuscular junctions
This results in progressive descending paralysis with no sensory involvement, respiratory compromise, CNS involvement - diplopia, dysarthria, dysphonia
Autonomic ganglia and paprasypathetic terminals also involved - causing nausea and vomiting, abode distension, ileum, dry mouth, urinary retention, absent pupillary reflexes, hypotension with normal heart rate

33
Q

How is botulism investigated?

A

Primarily supportive
No specific antibiotic for botulism
Anti-toxin exists which may be effective if given early - risk of anaphylaxis

34
Q

What is tetanus?

A

A disease secondary to infection with Clostridium tetani

35
Q

Describe Clostridium tetani

A

Gram-postive, anaerobic, spore-forming bacteria
Commonly found in soil and human faeces
Incubation period 7-10 days

36
Q

What are the pathophysiological features of tetanus?

A

Tetanus toxin inhibits neurotransmitter release from presynaptic GABA inhibitory interneurons - leading to uninhibited motor and sympathetic nerve activity

37
Q

What are the clinical features of tetanus?

A

Progress over 2-3 weeks
Locked jaw
Tonic contractions of the skeletal muscles, spasmodic episodes
- rigid abdomen, intermittent apnoea/airway obstruction, dysphagia
Autonomic instability - tachycardia, labile blood pressure, sweating, irritability
Differential diagnosis includes dystonic syndromes e.g. NMS, or strychnine poisoning

38
Q

How do you investigate for tetanus?

A

No specific diagnostic tests available

39
Q

How is tetanus treated?

A

Antibiotics - metronidazole, widely recommended but no proven benefit
debridement of the infected wound
Antitoxin - human tetanus immune toxin should be administered by the subcutaneous or intramuscular route, and some should be infiltrated around the wound. It will only affect the unbound toxin and not that already bound to the nerves
Supportive measures - benzodiazepines for spasms, anaesthesia, muscle relaxants. magnesium and beta blockers for autonomic dysfunction

40
Q

What is necrotising fasciitis?

A

A life-threatening, fulminant infection of the soft tissues

41
Q

How is necrotising fasciitis classified?

A

Classified on the basis of microbe
Type 1 - accounts for the majority. Slower progression, therefore more opportunity for better outcomes
Typically a combination of Gram-positive e.g. Streptococcus, Gram negative e.g. Enterobacter, E.coli, Klebsiella, Proteus and anaerobic organisms .g. Clostridium, Baceteriodes
Type 2 - group A strep infection +/- Staph
Typically affects the extremities, associated with toxin shock syndrome
Type 3 - related to Vibrio app and type 4 related to Candida are very uncommon and have a high mortality

42
Q

What are the risk factors for necrotising fasciitis?

A

Relative immunocompromised - diabetes, steroids, underlying malignancy, malnutrition
Chronic disease - renal failure, peripheral vascular disease
Disruption of skin integrity- IV drug use, trams, surgery, childbirth

43
Q

How is NF diagnosed?

A

Diagnosis is clinical, but may be retrospectively confirmed by histological samples
Imaging may show gas in the tissues particularly type I NF - specific but insensitive

44
Q

How do cellultits and NF differ?

A

Cellulitis begins at the junction between the dermis and epidermis
NF begins between subcutaneous fat at deep dermis
Erythema and oedema are earlier signs in celultis, NF may be associated with a purple-blue appearance of the skin
NF is more painful, disproportionate pain is one of the cardinal symptoms of NF

45
Q

How is NF treated?

A

Supportive
Early and adequate surgical debridement, multiple debridements may be required
Antibiotics - piptaz or a carbapenem provide good Gram-positive, Gram neg and anaerobic cover.
Clindamycin provides additional group A step cover with additional benefit of an anti-toxin effects
Hyperbaric oxygen is reported to benefit Clostridium app but limited availability with significant logistical difficulties

46
Q

What are multi drug resistant organisms?

A

Micro-organisms that are resistant to antimicrobial agents to which they would be expected to be responsive

47
Q

What is contamination?

A

Microbial attachment without proliferation

48
Q

What is colonisation?

A

microbial attachment and proliferation within the host but no inflammatory response

49
Q

What is infection?

A

an inflammatory response to the presence of microorganisms

50
Q

Which patients are most vulnerable to multi drug resistant organisms?

A

Those with severe underlying disease esp those which impair the immune system and those with in dwelling medical devices

51
Q

What measures do the CDC recommend for reducing the transmission of MDROs?

A

Organisational-wide response with infection control part of the organisational ethos
Education
Judicious use of antimicrobial agents
-narrow spectrum when feasible, limiting duration, optimising pharmacokinetics
MRDO surveillance
Infection control measures - hand hygiene, aprons, gloves, side rom for those with MRDO
Environmental measures - robust cleaning of equipment and surfaces
Decolonisation - successful for MRSA - chlorhex, nasal mucopuricin

52
Q

What is MRSA?

A

The most common MDRO in hospitals
A genetic alteration within MRSA leads to a change in the penicillin-binding protein - beta lactic antibiotics cannot effectively bind the bacterium

53
Q

What is VRE?

A

Vancomycin resistant enterococcus
Increasingly commonResistance occurs due to modification of the glycopeptide-binding sites on enterococci
Multiple subtypes of resistance, which vary in sensitivity to alternative antibiotics

54
Q

What are the risk factors for VRE?

A

Previous antibiotics exposure esp vancomycin and cephalosporins
Prolonged hospitalisation and ICU in particular
Co-morbidities - particularly transplant, ESRF and cancer
Long-term IV access and enteral tubes
Prevalence in the hospital/ICU
Low staff to patient ratio

55
Q

What are multidrug-resistant Gram-negative bacilli?

A

Defined as Gram-negative bacilli resistant to more than two antimicrobial agents
Typically resistant to penicillins, cephalosporins, fluroquinolones and aminoglycosides
Acinetobacter baumannii is resistant to most antimicrobials
Carbapenem-resistant enterobacteriaceae include Klebsiella and E.coli, produce carbapenemase enzymes, deactivating the antibiotic. These are also known as extended-spectrum beta-lactamase (ESBL)- producing enterobacteriaceae

Infection (4 decks)

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