ESA 3 Infection Clinical Conditions Flashcards
N/A Interaction with host
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
N/A Mechanism(s) of infection
Droplet infection, direct contact, faecal-oral transmission
Aspergillus fumigatus Mechanism(s) of infection
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
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
Plasmodium falciparum
Staphylococcus aureus Mechanism(s) of infection
Invasion (break of mucosa), inhalation, ingestion etc
Clostridium difficile Patient factors to consider
Age, pathological state, previous admission, physiological state, relative time
Staphylococcus aureus Interaction with host
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
Plasmodium falciparum Treatment
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
Hepatitis C Virus Prevention
Harm reduction strategies (giving clean needles to IV drug users, ensuring proper screening of all blood products), PPE when dealing with patients etc
Hepatitis C Virus Interaction with host
Travels to the liver and replicates within hepatocytes, but does not usually cause symptoms
Viridans Streptococci (mutans) Gram staining
Gram +ve cocci in chains
Clostridium difficile Gram staining
Gram +ve bacillus
N/A (Adenoviridae is a family, there are 60+ types) structure
Capsid structure: Icosahedral
Enveloped: No
DNA/RNA: dsDNA
N/A Treatment
Supportive
Mild pain relief eg paracetamol
Increase fluid intake
Specific
Only with potentially lethal strain 14 – antivirals
HIV Patient factors to consider
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)
Prevention of Staphylococcus aureus
Hand washing technique, decontaminating cooking surfaces etc
HIV Mechanism(s) of infection
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)
Streptoccus Pneumonia treatment
Supportive
High flow O2
Correct fluid balance (IV, consider inotropes if no change to BP)
Nebulised salbutamol
Specific
Amoxycillin - Community
Co-amoxiclav - Hospital
Pneumonectomy
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
Staphylococcus aureus
Influenza A Patient factors to consider
The usual factors (age, pathological state and relative time), along with calendar time (flu season is winter)
Influenza A treatment
Supportive
Pain relief
Antipyrexials (if slight fever leave it, its good for you!)
Specific
Neuraminidase inhibitor (Oseltamivir aka Tamiflu)
Antivirals (acyclovir)
Plasmodium falciparum Interaction with host
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
Prevention of HIV
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)
Varicella zoster Mechanism(s) of infection
Inhalation of virons that are expelled from the lungs of infected person (very contagious). Can also have direct contact with blisters/shingles
Coagulase negative staphylococci Gram staining
Gram+ve/-ve: +ve cocci in clusters
Viridans Streptococci (mutans) Mechanism(s) of infection
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)
N/A Prevention
Spreads by droplet infection so stay away from those showing symptoms, avoid enclosed spaces
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)
HIV
Varicella zoster structure
Capsid structure: Icosahedral
Enveloped: Yes
DNA/RNA: dsDNA
Varicella zoster Treatment
Supportive
Pain relief
Anti itching cream
Aspergillus fumigatus treatment
Supportive
High flow O2
Pain relief
Anti-pyrexials
Specific
Antifungals
Colony stimulating factors (some cases only)
Norovirus Norwalk virus Treatment
Supportive
IV fluid bolus
ORT
Norovirus Norwalk virus (usually just Norovirus) structure
Capsid structure: Icosahedral
Enveloped: Non-enveloped
DNA/RNA: ssRNA
Possible sequelae of Pseudomonas aeruginosa
Significant cause of mortality within CF sufferers, can cause worsening of existing fibrosis
HIV Stages
Primary HIV infection – asymptomatic
Stage I – asymptomatic, CD4+ >500
Stage II – mild, CD4+
Hepatitis C Virus Mechanism(s) of infection
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)
Neisseria meningitidis treatment
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)
Plasmodium falciparum Possible sequelae
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
Norovirus Norwalk virus Patient factors to consider
Age, calendar time, pathological state (diabetes, HIV, cancer treatment)
Possible sequelae of Coagulase negative staphylococci
If lines are not removed + infection not cleared, it may progress to septicaemia, septic shock and death due to multi organ failure
Coagulase negative staphylococci Patient factors to consider
Age, pathological state (in particularly their presenting surgical complaint), relative time (how long has the graft been in?)
Hepatitis B virus Prevention
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
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
Salmonella typhi
Norovirus Norwalk virus Prevention
Barrier medicine, wash everything patients come in contact with (with bleach), wash handsthoroughly after any contact etc
Plasmodium falciparum Patient factors to consider
Normal ones (age, pathological state and relative time – incubation period) along with calendar time (how long they’ve been back)
HIV Treatment
Supportive
Treat the AIDS defining illness
Specific
CD4+ count checked on a regular basis and action taken if it falls below a certain level (
Influenza A structure
Capsid structure: Circular
Enveloped: Yes
DNA/RNA: non-sense ssRNA
Hepatitis B virus Patient factors to consider
Age, pathological state (HIV, cancer etc), physiological state (IV drug use),relative time
Streptoccus Pneumonia Actions on host
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
History: Fever, aches and pains, dry cough, malaise, myalgia (beginning a day or two agp)
Examination: Fever, tachypnea, maybe tachycardia
Influenza A
Salmonella typhi Patient factors to consider
Patient factors to consider: The standard ones (age, pathological state, relative time – incubation period) along with calendar time (how long since they got back?)
Influenza A Possible sequelae
Chest infection, sinusitis, in VERY severe cases can get meningitis
Neisseria meningitidis Interaction with host
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.
History: Fever, shortness of breath, productive cough
Examination: Tachypnea, high grade fever, bibasal crepitations of lungs, SpO2 of
Legionella pneumophilia
Viridans Streptococci (mutans) Interaction with host
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
Staphylococcus aureus Patient factors to consider
Age, pathological state (are they immunocompromised eg neutropenic)
Legionella pneumophilia treatment
Supportive
Serum lactate measure
High flow O2
Analgesia
Specific
Clarithromycin
Prevention of Legionella pneumophilia
Keep water below 20 degrees or above 60 degrees, keep water moving (don’t let it stagnate)
Hepatitis C Virus Treatment
Supportive Specific
Lifestyle changes
Stop drinking and smoking
Eating a healthy diet
Regular exercise
Specific
Pegylated interferon (stimulates immune system)
Ribavirin (antiviral, stops replication)
Norovirus Norwalk virus Possible sequelae
Very unlikely to cause death, especially if fluid balance is restored, most patients make
a full recovery
Salmonella typhi treatment
Supportive
Oral rehydration therapy
Antipyrexials (paracetamol)
Pain relief (paracetamol)
Specific
Ceftriaxone or azithromycin
Legionella pneumophilia Gram staining
Gram -ve rods
Possible sequelae of Viridans Streptococc
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
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
Hepatitis C Virus
Possible sequelae of C Diff
Severe diarrhoea can lead to acute renal failure and cognitive impairment in severe dehydration, perforated/toxic megacolon leading to peritonitis leading septic shock
Salmonella typhi Gram staining
Gram -ve rod
Hepatitis B virus structure
Capsid structure: Icosahedral
Enveloped: Yes
DNA/RNA: dsDNA non-sense
N/A Possible sequelae
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)
Hepatitis B virus Treatment
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)
Pseudomonas aeruginosa Mechanism(s) of infection
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)
Aspergillus fumigatus Possible sequelae
Resolution, progression to chronic pulmonary aspergillosis, death
Coagulase negative staphylococci Interaction with host
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.
Pseudomonas aeruginosa treatment
Supportive
High flow O2
Ventilation if needed
Nebulised salbutamol
Specific
Tobamycin (IV or inhalation, not absorbed from GI)
Salmonella typhi Possible sequelae
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
Norovirus Norwalk virus Mechanism(s) of infection
Directly from person to person, or indirectly from contimated water or food
Legionella pneumophilia Interaction with host:
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)
Legionella pneumophilia Patient factors to consider
Normal ones (age, pathological state, relative time), particularly concerned about co-morbidities ie HIV
Coagulase negative staphylococci Mechanism(s) of infection
Inoculation onto prosthetic surfaces during surgery
Hepatitis C Virus Possible sequelae
Can lead to cirrhosis due to chronic liver damage, liver failure (requiring a transplant) or liver cancer (which is almost always fatal)
Streptoccus Pneumonia Mechanism of Infection
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
Mechanism(s) of infection Neisseria meningitidis
Direct contact with respiratory secretions
Plasmodium falciparum Mechanism(s) of infection
Vector spread by the female Anopheles mosquito (travels in their saliva, and is ingested from human’s blood)
HIV Interaction with host
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)
Hepatitis B virus Mechanism(s) of infection
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)
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
Neisseria meningitidis
Possible sequelae of Staphylococcus aureus
Chronic abscess formation, scar tissue formation, resolution, sepsis
Prevention of Viridans Streptococc
Good dental hygiene (dentist every 6 months)
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
Aspergillus fumigatus
Hepatitis B virus Interaction with host
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)
Staphylococcus aureus treament
Supportive
If septic needs the sepsis six (see Neisseria meningitidis)
Specific
Antibiotics
Drain abscess
Neisseria meningitidis Prevention
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
Norovirus Norwalk virus Interaction with host
Multiplies within the small intestine and irritates the lining of the GI tract, causing vomiting, nausea etc (gastroenteritis)
Staphylococcus aureus (in context of the immunocompromised patient) Gram staining
Gram+ve/-ve: G+ve coccus
Neisseria meningitidis investigations
Investigation: FBCs, U and Es, BM, LFTs, CRP, clotting studies, ABG, MCS (microscopy, culture, sensitivity), EDTA for PCR
Legionella pneumophilia Mechanism(s) of infection
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)
HIV Possible sequelae
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
Viridans Streptococci (mutans) Patient factors to consider
Age, pathological state (immunocompromised), relative time, physiological state (dental hygiene and phobia of dentists in particular)
Influenza A Interaction with host
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
Hepatitis B virus possible sequelae
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
Streptoccus Pneumonia Case History
Age, pathological state (smoking, obesity, diabetes, HIV, chemo), relative time, calendar time (more common in winter)
Clostridium difficile treatment
Supportive
IV fluid bolus
ORT
Specific
Faecal transplant
Metronidazole
Discontinue causative antibiotics
Human Immunodeficiency Virus structure
Capsid structure: Roughly circular
Enveloped: Yes
DNA/RNA: ssRNA (sense)
Viridans Streptococci (mutans) treatment
Supportive
Measure urine output (if U and E elevated)
O2 to address tachypnea
Specific
Replace defective valve in surgery
Penicillin and gentamicin
Clostridium difficile Interaction with host
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)
Salmonella typhi prevention
Food and water hygiene increase ie proper hand washing, those who are sick don’t prepare food, vaccine (high risk travellers) and chlorinate water
Varicella zoster Prevention
Not really preventable, apart from treating any cause of immunocompromise that is modifiable (obviously chemotherapy isn’t as destroying the cancer is more important)
Hepatitis C Virus
Capsid structure: Icosahedral
Enveloped: Yes
DNA/RNA: ssRNA (sense)
Coagulase negative staphylococci treatment
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
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
Coagulase negative staphylococci
Hepatitis C Virus Patient factors to consider
Age, pathological state (HIV, cancer etc), physiological state (IV drug use),
Salmonella typhi Mechanism(s) of infection
Mechanism(s) of infection: Faecal-oral transmission (contaminated food and water)
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)
Hepatitis B virus
Salmonella typhi Interaction with host
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
Pseudomonas aeruginosa Interaction with host
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
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)
Viridans Streptococci (mutans)
Influenza A Mechanism(s) of infection
Droplet infection
Aspergillus fumigatus Patient factors to consider
Key one is pathological state (immunocompromised eg chronic granulomatous disease)
Clostridium difficile Mechanism(s) of infection
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)
Aspergillus fumigatus Interaction with host
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
Hepatitis B virus Stages
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
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
Clostridium difficile
Neisseria meningitidis Gram staining
Gram -ve
Prevention of C diff
Isolation, responsible prescribing, good barrier medicine (throw away gowns/gloves, wash hands thoroughly)
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
N/A
Neisseria meningitidis Patient factors to consider
Age, pathological state (smoking, obesity, diabetes, HIV, chemo), relative time, physiological state, social factors (kissing disease?)
Pseudomonas aeruginosa Patient factors to consider
Age, pathological state (CF!!!), relative time, physiological state (how are they managing their condition?), social factors (do they smoke?)
Possible sequelae of Legionella pneumophilia
Can lead to septic shock multi organ failure and death
Prevention of Coagulase negative staphylococci
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)
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
Pseudomonas aeruginosa
Prevention of Pseudomonas aeruginosa
Don’t let CF sufferers meet (risk of cross infection), pulmonary physiotherapy, prophylactic antibiotics
Varicella zoster Interaction with host
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
Aspergillus fumigatus Prevention
Avoid areas where Aspergillus spores are abundant eg rotting plants, soil, compost. Air purifiers in the home (but very expensive)
Influenza A Prevention
Flu vaccine (changes every year as virus tends to mutate) and good hygiene (hands, cooking surfaces etc)
Varicella zoster Possible sequelae
Resolution (by far the most common), can lead to chronic nerve pain in a small number of patients
Varicella zoster Patient factors to consider
Age (childhood disease is almost a rite of passage), pathological state (immunocompromised)
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
Streptoccus Pneumonia
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
Varicella zoster
Streptoccus Pneumonia gram staining
Gram +ve
Pseudomonas aeruginosa (discussed in context of CF sufferer only) Gram staining
Gram Gneg bacillus (rods)
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
Norovirus Norwalk virus
