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Specific Infections (Sources: Revision notes) Flashcards

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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?

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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?

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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
What is Pneumocystis jiroveci?
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
How is Pneumocystis jiroveci treated?
Co-trimoxazole is first line Primaquine is an alternative Steroids (normally prednisolone) should be given to all patients with PJP on the ICU
27
Describe Cryptococcal meningitis
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
How is Cryptococcal meningitis treated?
First-line treatment is with amphoteici B plus flu cytosine for the initial phase
29
What is toxoplasmosis encephalitis?
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
What is botulism?
The clinical manifestation of Clostridium botulinum infection Classically a consequence of ingesting contaminated food
31
What is Clostridium botulinum?
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
What is the pathophysiology of botulism?
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
How is botulism investigated?
Primarily supportive No specific antibiotic for botulism Anti-toxin exists which may be effective if given early - risk of anaphylaxis
34
What is tetanus?
A disease secondary to infection with Clostridium tetani
35
Describe Clostridium tetani
Gram-postive, anaerobic, spore-forming bacteria Commonly found in soil and human faeces Incubation period 7-10 days
36
What are the pathophysiological features of tetanus?
Tetanus toxin inhibits neurotransmitter release from presynaptic GABA inhibitory interneurons - leading to uninhibited motor and sympathetic nerve activity
37
What are the clinical features of tetanus?
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
How do you investigate for tetanus?
No specific diagnostic tests available
39
How is tetanus treated?
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
What is necrotising fasciitis?
A life-threatening, fulminant infection of the soft tissues
41
How is necrotising fasciitis classified?
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
What are the risk factors for necrotising fasciitis?
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
How is NF diagnosed?
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
How do cellultits and NF differ?
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
How is NF treated?
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
What are multi drug resistant organisms?
Micro-organisms that are resistant to antimicrobial agents to which they would be expected to be responsive
47
What is contamination?
Microbial attachment without proliferation
48
What is colonisation?
microbial attachment and proliferation within the host but no inflammatory response
49
What is infection?
an inflammatory response to the presence of microorganisms
50
Which patients are most vulnerable to multi drug resistant organisms?
Those with severe underlying disease esp those which impair the immune system and those with in dwelling medical devices
51
What measures do the CDC recommend for reducing the transmission of MDROs?
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
What is MRSA?
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
What is VRE?
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
What are the risk factors for VRE?
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
What are multidrug-resistant Gram-negative bacilli?
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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