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Clinical Revision > ESA 3 Infection Clinical Conditions > Flashcards

ESA 3 Infection Clinical Conditions Flashcards

1
Q

N/A Interaction with host

A

Enters through the respiratory route normally, may either colonise the pharynx and

upper airways to cause an URTI (with conjunctivitis if it travels up the nasolacrimal duct or if they sneeze

and rub their eyes), or down the oesophagus to colonise the GI tract and cause gastroenteritis

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2
Q

N/A Mechanism(s) of infection

A

Droplet infection, direct contact, faecal-oral transmission

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3
Q

Aspergillus fumigatus Mechanism(s) of infection

A

Ubiquitious within the normal air (spores always present), inhaled constantly by a patient. Only causes disease in people with immunocompromise (immune system very good at
clearing fungal moulds before they become dangerous) – opportunistic

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4
Q

 History: Fever, chills and sweats, cycling so they occur on the 3rd or 4th day, dry cough, headache, nausea and vomiting and myalgia. Recently returned from an area where malaria is endemic (ie Sub-Saharan Africa)

Examination: Unremarkable save for splenomegaly

A

Plasmodium falciparum

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5
Q

Staphylococcus aureus Mechanism(s) of infection

A

Invasion (break of mucosa), inhalation, ingestion etc

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6
Q

Clostridium difficile Patient factors to consider

A

Age, pathological state, previous admission, physiological state, relative time

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7
Q

Staphylococcus aureus Interaction with host

A

Has a number of important virulence factors (but here are the first 3 I found):

Coagulase – converts fibrinogen to fibrin, forming a micro clot around the bacteria that protects it from phagocytosis

Hyaluronidase – breaks down hyaluronic acid (key component of ground substance in connective tissue) which leads to ability of bacteria to break down barriers and spread

DNA ribonuclease – breaks down host DNA

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8
Q

Plasmodium falciparum Treatment

A

Supportive
Antipyrexials
Anti-emetic if needed
Pain relief

Specific
Species dependant (falciparum is most common but other types exist):
 Falciparum – quinine or armitemisin
 Vivax, ovale or malariae - chloroquine

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9
Q

Hepatitis C Virus Prevention

A

Harm reduction strategies (giving clean needles to IV drug users, ensuring proper screening of all blood products), PPE when dealing with patients etc

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10
Q

Hepatitis C Virus Interaction with host

A

Travels to the liver and replicates within hepatocytes, but does not usually cause symptoms

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11
Q

Viridans Streptococci (mutans) Gram staining

A

Gram +ve cocci in chains

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12
Q

Clostridium difficile Gram staining

A

Gram +ve bacillus

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13
Q

N/A (Adenoviridae is a family, there are 60+ types) structure

A

Capsid structure: Icosahedral
Enveloped: No
DNA/RNA: dsDNA

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14
Q

N/A Treatment

A

Supportive
Mild pain relief eg paracetamol
Increase fluid intake

Specific
Only with potentially lethal strain 14 – antivirals

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15
Q

HIV Patient factors to consider

A

Age, relative time, pathological state (especially cancer, and any infections have the potential to be life-threatening), sexuality (more common in MSM), physiological state

(intravenous drug use)

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16
Q

Prevention of Staphylococcus aureus

A

Hand washing technique, decontaminating cooking surfaces etc

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17
Q

HIV Mechanism(s) of infection

A

Spread through bodily fluids (vaginal fluid, semen, blood, breast milk and pre-ejaculate), so can occur through unprotected sex, sharing of needles, vertical transmission (in-utero) or from medical proceedures (organ donation, blood transfusion etc)

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18
Q

Streptoccus Pneumonia treatment

A

Supportive

High flow O2
Correct fluid balance (IV, consider inotropes if no change to BP)
Nebulised salbutamol

Specific
Amoxycillin - Community
Co-amoxiclav - Hospital
Pneumonectomy

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19
Q

History:Typically forms skin lesions in people who are immunocompromised, such as impetigo, boils, abscesses etc. History of these before (severe, persistent, unusual and recurrent) w/ recent new formation

Examination: Evidence of large lesion, if it’s lead to sepsis can expect SIRS eg tachypnea, tachycardia, hypotension

A

Staphylococcus aureus

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20
Q

Influenza A Patient factors to consider

A

The usual factors (age, pathological state and relative time), along with calendar time (flu season is winter)

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21
Q

Influenza A treatment

A

Supportive
Pain relief
Antipyrexials (if slight fever leave it, its good for you!)

Specific
Neuraminidase inhibitor (Oseltamivir aka Tamiflu)
Antivirals (acyclovir)

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22
Q

Plasmodium falciparum Interaction with host

A

Enters host by being ejected from the salivary glands of the Anopheles mosquito, entering the bloodstream, where it then travels to the liver, colonising that until it matures and re-enters systemic circulation. Here it invades RBCs and uses Hb as a nutrient until oncosis of the RBC occurs through the intracellular multiplication of the protazoa. This leads to haemolytic anaemia

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23
Q

Prevention of HIV

A

Prevention: Avoid contact with other people’s bodily fluids (particularly blood), avoid unprotected sex (anal sex carries the greatest risk), use PPE when treating patients (which should be done anyway)

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24
Q

Varicella zoster Mechanism(s) of infection

A

Inhalation of virons that are expelled from the lungs of infected person (very contagious). Can also have direct contact with blisters/shingles

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25
Q

Coagulase negative staphylococci Gram staining

A

Gram+ve/-ve: +ve cocci in clusters

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26
Q

Viridans Streptococci (mutans) Mechanism(s) of infection

A

Normal commensal in the oral cavity, however if the oral mucosa is breached it can become an important factor in tooth decay (inoculation) and spread to the CVS (haematogenous spread)

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27
Q

N/A Prevention

A

Spreads by droplet infection so stay away from those showing symptoms, avoid enclosed spaces

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28
Q

History: A flu like illness so malaise, lethargy, fever, muscle aches,headache, nausea and vomiting etc. Following this, you would expect stages of persistent weight loss, lymph node enlargement, chronic fatigue etc

Examination: All manner of findings depending on the type of defining illness (upper lobes dull to percussion in TB, crackling in lower lobes in PCP)

A

HIV

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29
Q

Varicella zoster structure

A

Capsid structure: Icosahedral

Enveloped: Yes

DNA/RNA: dsDNA

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30
Q

Varicella zoster Treatment

A

Supportive
Pain relief
Anti itching cream

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31
Q

Aspergillus fumigatus treatment

A

Supportive

High flow O2
Pain relief
Anti-pyrexials

Specific
Antifungals
Colony stimulating factors (some cases only)

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32
Q

Norovirus Norwalk virus Treatment

A

Supportive

IV fluid bolus
ORT

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33
Q

Norovirus Norwalk virus (usually just Norovirus) structure

A

Capsid structure: Icosahedral

Enveloped: Non-enveloped

DNA/RNA: ssRNA

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34
Q

Possible sequelae of Pseudomonas aeruginosa

A

Significant cause of mortality within CF sufferers, can cause worsening of existing fibrosis

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35
Q

HIV Stages

A

Primary HIV infection – asymptomatic

Stage I – asymptomatic, CD4+ >500

Stage II – mild, CD4+

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36
Q

Hepatitis C Virus Mechanism(s) of infection

A

Blood to blood contact (primarily), classic spread of infection is sharing of needles in intravenous drug users. Blood transfusions prior to 1991 are at risk (couldn’t detect until 1991). Possibly spread by unprotected sexual contact (unknown)

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37
Q

Neisseria meningitidis treatment

A

Supportive

High flow O2
Adrenaline (inotropes)
Correct fluid balance (IV)
Measure urine output
Measure lactate
Analgesia

Specific

Blood cultures (consider source control)
Broad spectrum antibiotics (ceftriaxone)
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38
Q

Plasmodium falciparum Possible sequelae

A

Usually leads to haemolytic anaemia, can progress to cerebral malaria and therefore lead to coning. Also, jaundice, acute renal failure, shock, pulmonary oedema and of course death. Can cause stillbirth in pregnant women

 A – Assess of risk of patient (pregnant women!!) and area they’re travelling to

 B – bite prevention: DEET, nets, longs o’clock

 C – Chemoprophylaxis (antimalarials), resistance is specific to geographical locations ie doxycycline is suitable in Sub-Saharan Africa

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39
Q

Norovirus Norwalk virus Patient factors to consider

A

Age, calendar time, pathological state (diabetes, HIV, cancer treatment)

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40
Q

Possible sequelae of Coagulase negative staphylococci

A

If lines are not removed + infection not cleared, it may progress to septicaemia, septic shock and death due to multi organ failure

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41
Q

Coagulase negative staphylococci Patient factors to consider

A

Age, pathological state (in particularly their presenting surgical complaint), relative time (how long has the graft been in?)

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42
Q

Hepatitis B virus Prevention

A

Vaccinate (need to check HBsAb levels, needs to >10 for adequate protection and >100 for long-term protection), avoid infected person’s bodily fluids, use PPE with patients

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43
Q

History: Incubation period of 7 to 14 days so become unwell soon after returning from country of origin. Travel to Sub-Saharan Africa or Asia. Slowly increasing intensity of fever, headaches,
abdominal tenderness, constipation and dry cough

Examination: Fever (severe ie >40C), relative bradycardia for disease state (these two combined are known as Faget’s sign), hepatosplenomegaly

A

Salmonella typhi

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44
Q

Norovirus Norwalk virus Prevention

A

Barrier medicine, wash everything patients come in contact with (with bleach), wash handsthoroughly after any contact etc

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45
Q

Plasmodium falciparum Patient factors to consider

A

Normal ones (age, pathological state and relative time – incubation period) along with calendar time (how long they’ve been back)

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46
Q

HIV Treatment

A

Supportive
Treat the AIDS defining illness

Specific
CD4+ count checked on a regular basis and action taken if it falls below a certain level (

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47
Q

Influenza A structure

A

Capsid structure: Circular

Enveloped: Yes

DNA/RNA: non-sense ssRNA

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48
Q

Hepatitis B virus Patient factors to consider

A

Age, pathological state (HIV, cancer etc), physiological state (IV drug use),relative time

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49
Q

Streptoccus Pneumonia Actions on host

A

Pneumonia occurs when the bacteria colonise the lungs, due to their thick capsule they are not easily phagocytosed. The pus from dead neutrophils quickly accumulates and consolidates in the lungs, producing most of the symptoms in the patient. If left unchecked it may cause bacteraemia and potential meningitis with an atypical pathogen

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50
Q

History: Fever, aches and pains, dry cough, malaise, myalgia (beginning a day or two agp)

Examination: Fever, tachypnea, maybe tachycardia

A

Influenza A

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51
Q

Salmonella typhi Patient factors to consider

A

Patient factors to consider: The standard ones (age, pathological state, relative time – incubation period) along with calendar time (how long since they got back?)

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52
Q

Influenza A Possible sequelae

A

Chest infection, sinusitis, in VERY severe cases can get meningitis

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53
Q

Neisseria meningitidis Interaction with host

A

Lives harmlessly in the upper respiratory tract (naso/oropharynx) of 1/10 individuals, but a few individuals are susceptible to this. It colonises and attacks the meninges (the lining of the brain), which causes some of the well known symptoms. It quickly progresses to the blood, causing a non-blanching rash. Due to the extremely potent endotoxin on it’s outer cell membrane, it causes a severe immune overreaction and due to this a drastic fall in TPR, leading rapidly to septic shock, disseminated intravascular coagulopathy, both causing multi organ failure and quickly death. If the meninges become significantly inflamed, the ICP rises to the point the patient cones and death is imminent.

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54
Q

History: Fever, shortness of breath, productive cough

Examination: Tachypnea, high grade fever, bibasal crepitations of lungs, SpO2 of

A

Legionella pneumophilia

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55
Q

Viridans Streptococci (mutans) Interaction with host

A

Initially colonises the tooth surface, where it converts ingested sucrose into lactic acid, which lowers the pH of the tooth enamel and leaves it vulnerable to breakdown. After this, if the oral mucosa is breached by this low pH or any kind of abrasion (eg. vigorous brushing) then the bacteria have a route into systemic circulation. This causes harmless bacteraemia, but they can get stuck on the heart valves due to turbulent flow, which leads to them colonising these as a ‘vegetation’ – this is infective endocarditis

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56
Q

Staphylococcus aureus Patient factors to consider

A

Age, pathological state (are they immunocompromised eg neutropenic)

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57
Q

Legionella pneumophilia treatment

A

Supportive

Serum lactate measure
High flow O2
Analgesia

Specific
Clarithromycin

58
Q

Prevention of Legionella pneumophilia

A

Keep water below 20 degrees or above 60 degrees, keep water moving (don’t let it stagnate)

59
Q

Hepatitis C Virus Treatment

A

Supportive Specific

Lifestyle changes
 Stop drinking and smoking
 Eating a healthy diet
 Regular exercise

Specific
Pegylated interferon (stimulates immune system)
Ribavirin (antiviral, stops replication)

60
Q

Norovirus Norwalk virus Possible sequelae

A

Very unlikely to cause death, especially if fluid balance is restored, most patients make

a full recovery

61
Q

Salmonella typhi treatment

A

Supportive

Oral rehydration therapy
Antipyrexials (paracetamol)
Pain relief (paracetamol)

Specific
Ceftriaxone or azithromycin

62
Q

Legionella pneumophilia Gram staining

A

Gram -ve rods

63
Q

Possible sequelae of Viridans Streptococc

A

Heart failure (left or right depends on the valve that is defective, if tricuspid or pulmonary then right, if mitral or aortic then left), valvular dysfunction (stenosis or regurgitation), cardiogenic shock

64
Q

History: Most patients will be asymptomatic, but in ~20% of patients you may see fatigue, nausea,anorexia, dark urine and RUQ abdo pain

Examination: RUQ abdominal pain, possibly hepatomegaly

A

Hepatitis C Virus

65
Q

Possible sequelae of C Diff

A

Severe diarrhoea can lead to acute renal failure and cognitive impairment in severe dehydration, perforated/toxic megacolon leading to peritonitis leading septic shock

66
Q

Salmonella typhi Gram staining

A

Gram -ve rod

67
Q

Hepatitis B virus structure

A

Capsid structure: Icosahedral

Enveloped: Yes

DNA/RNA: dsDNA non-sense

68
Q

N/A Possible sequelae

A

Almost always resolves, but can lead to epiglottitis (dysphagia and aspiration of food common so life threatening) or quinsy (see GI, clinical conditions ESA 3)

69
Q

Hepatitis B virus Treatment

A

Supportive

Nothing specific, just treat symptoms as and when they occur (paracetamol for fever and pain etc)
Hepatitis B serology (assesses state of infection/immune response)

Specific
Vaccinate if you catch it early enough (ie if youknow they’ve been exposed within 24 hours of it happening)
Peginterferon-alfa-2a to stimulate immune system to destroy virus
Antiretroviral drugs (in chronic infection)

70
Q

Pseudomonas aeruginosa Mechanism(s) of infection

A

Inhalation of bacteria which then begin to colonise the respiratory tract/lungs (Can also enter through other routes at other sites eg up urethra in cystitis)

71
Q

Aspergillus fumigatus Possible sequelae

A

Resolution, progression to chronic pulmonary aspergillosis, death

72
Q

Coagulase negative staphylococci Interaction with host

A

Usually a commensal as a part of the normal skin flora. It can form biofilms onsurgical equipment that bypasses the primary defences of the innate immune system (intubation bypasses mucociliary escalator, catheters bypass periodic flushing etc), and so has a route to cause local infection. If biofilms are sheared off this can provide a route into systemic circulation and cause extremely rapid sepsis and shock. Can also cause rejection of prosthetics such as artificial knees or hip replacements if It infiltrates at the time of surgery.

73
Q

Pseudomonas aeruginosa treatment

A

Supportive

High flow O2
Ventilation if needed
Nebulised salbutamol

Specific
Tobamycin (IV or inhalation, not absorbed from GI)

74
Q

Salmonella typhi Possible sequelae

A

Normally resolves with no long term complications if ORT and antibiotics are administered, but if left untreated may progress to intestinal haemorrhage, intestinal perforation, encephalitis, metastatic abscesses (endocarditis)etc

75
Q

Norovirus Norwalk virus Mechanism(s) of infection

A

Directly from person to person, or indirectly from contimated water or food

76
Q

Legionella pneumophilia Interaction with host:

A

Undergoes phagocytosis but inhibits formation of phagolysosome, so instead multiply within the macrophage until it bursts (so both depletes WBC count and uses this to bolster its own numbers)

77
Q

Legionella pneumophilia Patient factors to consider

A

Normal ones (age, pathological state, relative time), particularly concerned about co-morbidities ie HIV

78
Q

Coagulase negative staphylococci Mechanism(s) of infection

A

Inoculation onto prosthetic surfaces during surgery

79
Q

Hepatitis C Virus Possible sequelae

A

Can lead to cirrhosis due to chronic liver damage, liver failure (requiring a transplant) or liver cancer (which is almost always fatal)

80
Q

Streptoccus Pneumonia Mechanism of Infection

A

Direct contact, is part of the normal flora of the upper respiratory tract but can colonise the lungs under the right conditions if they are not cleared in time

81
Q

Mechanism(s) of infection Neisseria meningitidis

A

Direct contact with respiratory secretions

82
Q

Plasmodium falciparum Mechanism(s) of infection

A

Vector spread by the female Anopheles mosquito (travels in their saliva, and is ingested from human’s blood)

83
Q

HIV Interaction with host

A

Enters the bloodstream, then infects the CD4+ T cells (along with other cells of the immune system), where the ssRNA is converted to DNA by reverse transcriptase and inserted into the genome of the T cells. Following this, it is transcribed and translated, which eventually results in budding of immature viral proteins (and genetic material), and they exit by causing lysis of the T cell. Eventually, a viral protease cuts the proteins, which converts it into an active virus, with ssRNA genetic material again. As this happens over and over the number of CD4+ T cells declines, which leads to a loss of the cell mediated (active) immune system. As this progresses, infections the body would be able to fight off with a healthy immune system take hold. These are known as ‘AIDS defining infections’, the key ones are as follows:

 Opportunistic oral candida albicans – oral thrush, occurs as a direct result of lack of immunity

 Extrapulmonary mycobacterium tuberculosis (eg brain)

 Pneumocystis pneumonia/PCP (caused by Pneumocystis jerovecii, an opportunistic yeast like fungi)

 Kaposi’s sarcoma (rare tumour of the skin caused by infection with HHV8 (human herpes virus 8), an opportunistic virus)

84
Q

Hepatitis B virus Mechanism(s) of infection

A

Spread through bodily fluids (vaginal fluid, semen, blood, breast milk and pre-ejaculate), so can occur through unprotected sex, sharing of needles, vertical transmission (in-utero) or from medical proceedures (organ donation, blood transfusion etc)

85
Q

History: Fit and well in last 24 hours, suddenly feeling non-specifically ill (fever, chills). Within next 12 hours neck pain, fever, photophobia, nausea, malaise, abdo pain, severe headache, non-blanching (purperic) rash

Examination: Raised temp, tachypnea, tachycardia, low BP, pale cold extremeties

A

Neisseria meningitidis

86
Q

Possible sequelae of Staphylococcus aureus

A

Chronic abscess formation, scar tissue formation, resolution, sepsis

87
Q

Prevention of Viridans Streptococc

A

Good dental hygiene (dentist every 6 months)

88
Q

History: At least a week (can be chronic) long hx of SOB, productive cough, fatigue, weight loss etc

Examination: Tachypnea, tachycardia, hypotension, cyanotic, wheeze etc

A

Aspergillus fumigatus

89
Q

Hepatitis B virus Interaction with host

A

Enters the bloodstream and replicates within hepatocytes, which leads to host damage by inflammation when the active immune system recognises the viral molecules (cytotoxic T lymphocytes)

90
Q

Staphylococcus aureus treament

A

Supportive

If septic needs the sepsis six (see Neisseria meningitidis)

Specific

Antibiotics
Drain abscess

91
Q

Neisseria meningitidis Prevention

A

Vaccine available for ACWY and B strains, stop kissing people! At risk individuals ie in close contact with people who show meningitis symptoms given prophylactic antibiotics, particularly those that are immunocompromised

92
Q

Norovirus Norwalk virus Interaction with host

A

Multiplies within the small intestine and irritates the lining of the GI tract, causing vomiting, nausea etc (gastroenteritis)

93
Q

Staphylococcus aureus (in context of the immunocompromised patient) Gram staining

A

Gram+ve/-ve: G+ve coccus

94
Q

Neisseria meningitidis investigations

A

Investigation: FBCs, U and Es, BM, LFTs, CRP, clotting studies, ABG, MCS (microscopy, culture, sensitivity), EDTA for PCR

95
Q

Legionella pneumophilia Mechanism(s) of infection

A

Aerosolisation of water and soil infected with the bacteria. Held in reservoirs with amoebae in water (even water such as that circulating in vapour in air conditioning systems)

96
Q

HIV Possible sequelae

A

Some people can live for years without the illness becoming too severe or taking over (maintain a good CD4+ count and low viral load) because they have the right Class I MHCs to present the virus to the CD8+ T cells that can destroy it. Most individuals when on HAARTs have an average life expectancy and good quality of life. However, some people are not as lucky and deteriorate (average life expectancy without any treatment is 10 years after first infection) into AIDS where the opportunistic infections kill them

97
Q

Viridans Streptococci (mutans) Patient factors to consider

A

Age, pathological state (immunocompromised), relative time, physiological state (dental hygiene and phobia of dentists in particular)

98
Q

Influenza A Interaction with host

A

Droplets inhaled into the respiratory tract, where the virus begins to enter the cells of the upper respiratory tract. Virulence is determined by the levels of haemagglutinin and neuraminidase expressed on the outer envelope of the virus (these determine the strain of virus depending on their type of toxins ie H1N1). Haemagglutinin helps facilitate the entrance of the virus into a cell by binding the envelope to the CSM (the virus can only affect the URT because the enzymes to cleave haemaggulutinin to its active form are only present there – exception is H5N1 which is diffuse across the whole lung).
Neuraminidase cleaves glycoproteins to allow viral release from a cell following replication. Cytokine overreaction is the cause for most of the symptoms

99
Q

Hepatitis B virus possible sequelae

A

If HBsAg persists for 6 months, then patient has chronic Hep B. 25% of chronic cases result in cirrhosis and 5% result in hepatocellular carcinoma. Most patients make a full recovery

100
Q

Streptoccus Pneumonia Case History

A

Age, pathological state (smoking, obesity, diabetes, HIV, chemo), relative time, calendar time (more common in winter)

101
Q

Clostridium difficile treatment

A

Supportive

IV fluid bolus
ORT

Specific

Faecal transplant
Metronidazole
Discontinue causative antibiotics

102
Q

Human Immunodeficiency Virus structure

A

Capsid structure: Roughly circular

Enveloped: Yes

DNA/RNA: ssRNA (sense)

103
Q

Viridans Streptococci (mutans) treatment

A

Supportive

Measure urine output (if U and E elevated)
O2 to address tachypnea

Specific
Replace defective valve in surgery
Penicillin and gentamicin

104
Q

Clostridium difficile Interaction with host

A

Exotoxin A causes inflammation that leads to the intracellular spaces widening (due to the excessive release of histamine), whilst exotoxin B exits through these gaps and kills the healthy cells of the host (both contribute to disease)

105
Q

Salmonella typhi prevention

A

Food and water hygiene increase ie proper hand washing, those who are sick don’t prepare food, vaccine (high risk travellers) and chlorinate water

106
Q

Varicella zoster Prevention

A

Not really preventable, apart from treating any cause of immunocompromise that is modifiable (obviously chemotherapy isn’t as destroying the cancer is more important)

107
Q

Hepatitis C Virus

A

Capsid structure: Icosahedral

Enveloped: Yes

DNA/RNA: ssRNA (sense)

108
Q

Coagulase negative staphylococci treatment

A

Supportive

Manage symptoms such as fever
Physiotherapy for affected joint
Replace prosthesis to restore normal function
(after antibiotics have worked)

Specific

Surgical exploration of infected joint, possible removal of the prosthesis
Extensive antibiotic regime (flucloxacillin, switch to vancomycin/doxycycline if MRSA detected – minimum of 14 days)
Removal of infected line

109
Q

History: Pain in site of implant/prosthesis (eg hip) and unsteadiness on the affected joint (eg hip again). Can also have tenderness at site of insertion of line etc (central venous lines are the most common)

Examination: Malaise, fever, possible myalgia, reduced power in affected limb (if joint replacement), infection tends to be localised so SIRS symptoms tend to be absent

A

Coagulase negative staphylococci

110
Q

Hepatitis C Virus Patient factors to consider

A

Age, pathological state (HIV, cancer etc), physiological state (IV drug use),

111
Q

Salmonella typhi Mechanism(s) of infection

A

Mechanism(s) of infection: Faecal-oral transmission (contaminated food and water)

112
Q

History: Fatigue, abdominal pain, anorexia, nausea, vomiting, arthralgia, malaise, myalgia etc. Can develop anywhere from 1 to 5 months after initial infection (previous history of unprotected sex/intravenous drug use to be expected)

Examination: Hepatomegaly, jaundice (particularly of the sclera)

A

Hepatitis B virus

113
Q

Salmonella typhi Interaction with host

A

Interaction with host: Enters GI tract and hits SI, where it interacts with Peyer’s patches (part of the RE system) – adheres with fimbriae. If lysis occurs, it will release endotoxins. Also, secrets invasin to allow intracellular growth. Eventually enters the blood through the Peyer’s patches, causing bacteraemia, which rarely advances to sepsis

114
Q

Pseudomonas aeruginosa Interaction with host

A

Opportunistic pathogen that requires a disease state to take hold eg. HIV, CF, neutropenia etc. Is a facultative anaerobe, which is essential when it is trapped in the sputum of a CF sufferer (low O2 diffusion). Enters through the URT, where it begins to colonise the brochi, leading to bronchopneumonia. Blocks eukaryotic protein synthesis leading to oncosis. Has a mucopolysaccharide
capsule that makes it hard to phagocytose, so even more disastrous for immunocompromised eg neutropenic

115
Q

History: Poor access to dental care, systemic response (fever, chills etc) for 6 weeks at least, lack of energy, breathlessness, toothache, anorexia, cahexia

Examination: Poor dentition/dental abscess, heart murmur, tachypnea, possible tachycardia, possible hypotension (slight), peripheral oedema (due to decreased CO reducing hydrostatic pressure)

A

Viridans Streptococci (mutans)

116
Q

Influenza A Mechanism(s) of infection

A

Droplet infection

117
Q

Aspergillus fumigatus Patient factors to consider

A

Key one is pathological state (immunocompromised eg chronic granulomatous disease)

118
Q

Clostridium difficile Mechanism(s) of infection

A

Appears as an opportunistic infection when the normal microbiota of the gut is eliminated by antibiotics (ceftriaxone) for an unrelated infection (the flora that are removed usually outcompete the C diff, which is a normal albeit minor component of gut flora)

119
Q

Aspergillus fumigatus Interaction with host

A

Cleared by mucociliary escalator/internalised by alveolar macrophages in most
patients (healthy). In those that have a phagocyte deficiency eg CGD, a switch to hyphae and active multiplication is seen in the alveoli/alveolar epithelium

120
Q

Hepatitis B virus Stages

A

HBsAg – surface antigen, virus recognised, first to appear

HBeAg – e-antigen, signals highly infectious period, symptoms at this point

IgM – core antibody (can’t detect core antigen) – first antibody to appear, immune system is mounting challenge)

HBeAb – e-antibody, signals end of infectious period and viral inactivity (immune system is winning)

HBsAb – surface antibody, last antibody to appear, virus is cleared and patient has recovered

IgG – core antibody – persists for life

121
Q

History: 2 days of severe diarrhoea, rarely vomiting, abdo discomfort, previous antibiotic treatment

Examination: Generalised tenderness over the abdomen (particularly umbilicus), BP down slightly,

slightly tachy

A

Clostridium difficile

122
Q

Neisseria meningitidis Gram staining

A

Gram -ve

123
Q

Prevention of C diff

A

Isolation, responsible prescribing, good barrier medicine (throw away gowns/gloves, wash hands thoroughly)

124
Q

History: ~3 day history of pain in pharynx, cough, sinus pain (in some cases), temperature, malaise etc

Examination: Red, inflamed pharynx. Enlarged tonsils, lymphadenitis (in neck) etc

A

N/A

125
Q

Neisseria meningitidis Patient factors to consider

A

Age, pathological state (smoking, obesity, diabetes, HIV, chemo), relative time, physiological state, social factors (kissing disease?)

126
Q

Pseudomonas aeruginosa Patient factors to consider

A 
Age, pathological state (CF!!!), relative time, physiological state (how are they managing their condition?),
social factors (do they smoke?)
127
Q

Possible sequelae of Legionella pneumophilia

A

Can lead to septic shock  multi organ failure and death

128
Q

Prevention of Coagulase negative staphylococci

A

Silver coated IV lines (act as antibacterial agent), good ANTT used when inserting cannulas, sterile surgical environment when performing joint operations, antibiotic prophylaxis when anaesthetised (co-amoxiclav 1.2g IV)

129
Q

Presents in a similar fashion to regular pneumonia e.g. productive cough (very dry mucus),fever and SOB. Obviously are known to have CF

Examination: Tachycardic, tachypnic, cyanotic, dullness to percussion, pulmonary crackles etc

A

Pseudomonas aeruginosa

130
Q

Prevention of Pseudomonas aeruginosa

A

Don’t let CF sufferers meet (risk of cross infection), pulmonary physiotherapy, prophylactic antibiotics

131
Q

Varicella zoster Interaction with host

A

Normal adaptive immune response (presentation of Class I MHCs activating CD8+ T cells  cytotoxic T cells) followed by lifelong persistence of IgG antibodies, conferring lifelong immunity.
Varicella zoster lies dormant in dorsal ganglion of sensory nerves. Reactivation leads to rash that’s known as Shingles

132
Q

Aspergillus fumigatus Prevention

A

Avoid areas where Aspergillus spores are abundant eg rotting plants, soil, compost. Air purifiers in the home (but very expensive)

133
Q

Influenza A Prevention

A

Flu vaccine (changes every year as virus tends to mutate) and good hygiene (hands, cooking surfaces etc)

134
Q

Varicella zoster Possible sequelae

A

Resolution (by far the most common), can lead to chronic nerve pain in a small number of patients

135
Q

Varicella zoster Patient factors to consider

A

Age (childhood disease is almost a rite of passage), pathological state (immunocompromised)

136
Q

History: 3 days of dyspnea and malaise, 4 or 5 days of productive yellow sputum

Examination: Crackles and bronchial breathing over area of lung, tachypnea, tachycardia, mild hypotension, decreased O2 sats

A

Streptoccus Pneumonia

137
Q

History: Previous exposure and case of chickenpox (almost always in childhood). Sudden appearance of rash that usually roughly corresponds to a dermatome. Some type of immunocompromise

Examination: Red, raised rash at a localised area of the body

A

Varicella zoster

138
Q

Streptoccus Pneumonia gram staining

A

Gram +ve

139
Q

Pseudomonas aeruginosa (discussed in context of CF sufferer only) Gram staining

A

Gram Gneg bacillus (rods)

140
Q

History: Vomiting under 2 days after first exposure, diarrhoea, usually in contact with someone with the virus, classic symptoms of dehydration (sunken eyes, dry hair, pale, reduced urine output, headache, tiredness, dry lips etc)

Examination: Usually wouldn’t examine the patient as those with norovirus are advised to stay at home, but would expect abdominal tenderness along with dec BP and inc HR if the dehydration got

very bad

A

Norovirus Norwalk virus

Clinical Revision (6 decks)

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