Public Health Microbiology - 4th Ed

PUBLIC HEALTH &
MICROBIOLOGY NOTES
FOURTH EDITION
PRE-SUMMARIZED FOR THE TIME-POOR
READY-TO-STUDY MEDICAL, PRE-MED,
HIGH-YIELD NOTES USMLE OR PA STUDENT
199 PAGES

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Table Of Contents:

What’s included: Ready-to-study notes of various population health & infectious disease topics presented in
succinct, intuitive and richly illustrated downloadable PDF documents. Once downloaded, you may choose to either
print and bind them, or make annotations digitally on your iPad or tablet PC.

Clickable Hyperlinks Below:

- PUBLIC HEALTH OVERVIEW
- MEASURING HEALTH CONCEPTS
- HEALTH BEHAVIOUR
- CHANGING BEHAVIOUR
- CHRONIC DISEASE & RISK FACTORS
- PANDEMICS
- VACCINATION/IMMUNIZATION
- BASIC CONCEPTS OF INFECTIOUS DISEASES
- MICROBIOLOGY: PRIONS
- MICROBIOLOGY: VIRUSES
- MICROBIOLOGY: PARASITES
- MICROBIOLOGY: BACTERIA
- NOTABLE INFECTIVE DISEASES
o INFECTIVE ENDOCARDITIS
o LYMPHANGITIS
o MYOCARDITIS – VIRAL & TOXIC
o PERICARDITIS
o IMPETIGO (SCHOOL SORES)
o ERYSIPELAS
o CELLULITIS
o SCABIES
o LICE (PEDICULOSIS)
o HERPES SIMPLEX
o CHICKEN POX (VARICELLA ZOSTER)
o HERPES ZOSTER (SHINGLES)
o MEASLES VIRUS
o RUBELLA VIRUS (“GERMAN MEASLES)
o HUMAN PARVOVIRUS B19 (“5TH DISEASE”)
o SCARLET FEVER
o DERMATOPHYTOSIS - “RINGWORM”/“TINEA”
o PARASITIC GUT INFECTIONS
o POLIOMYELITIS
o MENINGITIS
o ENCEPHALITIS
o COMMON COLD (ACUTE RHINITIS)
o PHARYNGITIS (SORE THROAT)
o ACUTE LARYNGOTRACHEOBRONCHITIS (CROUP)
o ACUTE EPIGLOTTITIS
o PERTUSSIS - WHOOPING COUGH
o Q-FEVER
o LEPTOSPIROSIS
o MELIOIDOSIS
o PNEUMONIAS (“Infections of the Lung”)
o BRONCHIOLITIS
o SEASONAL FLU (INFLUENZA A & B)
o BIRD FLU (H5N1)
o SWINE FLU (H1N1)
o SARS & COVID – SEVERE ACUTE RESPIRATORY SYNDROME
o GENITAL HERPES SIMPLEX
o HUMAN PAPILLOMA VIRUS
o SYPHILIS
o CHLAMYDIA
o GONORRHOEA
o DONOVANOSIS
o HEPATITIS C
o HUMAN IMMUNODEFICIENCY VIRUS
o TRACHOMA
o PULMONARY TUBERCULOSIS
o INTESTINAL TUBERCULOSIS
o LEPROSY
o WHIPPLES DISEASE
o METAZOAN PARASITES
o LYMPHATIC FILARIASIS
o MALARIA
o LEISHMANIASIS
o ARBOVIRUSES
o ROSS RIVER VIRUS (RRV)
o DENGUE VIRUS
o YELLOW FEVER
o MURRAY VALLEY ENCEPHALITIS

PUBLIC HEALTH OVERVIEW:

PUBLIC HEALTH OVERVIEW:

Definitions:
- Population Health:
o Relates the health of certain groups of people to their health-determinants, health-trends, and
health-inequalities
o May be dependent upon:
§ Physical factors
§ Biological factors
§ Social factors
§ Environmental factors
§ Economic factors
§ Personal health behaviours
§ Available health services
- Public Health:
o The programs/policies instituted by a society to protect, promote, and restore individual’s health and
prevent morbidity and mortality
o Includes:
§ Practices
§ Programs
§ Policies
§ Institutions
- Epidemiology:
o The study of the distribution and determinants of disease in a population
- Preventative Medicine:
o The arm of medicine devoted to addressing health problems at the risk-factor level in order to
minimise the manifestation of disease in a population
- Aetiology (Etiology):
o The Cause of disease or study of factors involved in development of disease
- Risk factor:
o Something associated with an increased risk of developing a particular disease or condition
§ Demographic
§ Behavioural
§ Biomedical
§ Genetic
§ Environmental
§ Social
§ Other factors which may interact to increase or reduce effect

Common Goals of Public Health Services:
- Health Protection:
o Addressing potential health risks at the population level (Eg: Safe water / food regulation)
- Surveillance:
o Monitoring and early identification of epidemics or events/behaviours likely to cause negative health
outcomes
- Disease/Injury Prevention:
o Eg: Vaccination
o Eg: Mandating PPE in certain workplaces
- Population assessment:
o Studying & engaging with a community to better understand their needs
- Promoting health:
o Promote improved health via policy, interventions, community organizing etc
- Preparedness & Response Planning
o Eg: For natural disasters
o Eg: For pandemics
o Eg: For man-made disasters

People Have Different Concepts of Health:
- Wellness:
o State of dynamic physical, mental, social, and spiritual well-being that enables a person to achieve
full potential and have an enjoyable life
- Disease:
o Abnormal, medically-defined changes in the structure or function of the human body
- Illness:
o An individual’s experience or subjective perception of a lack of physical or mental well-being and
consequent inability to function normally in social roles
- Sickness:
o Views the individual and their society hold towards a health condition, affecting their thoughts and
actions
- Impairment:
o Any loss or abnormality of psychological, physiological, or anatomical structure or function
- Disability:
o Any restriction or lack of ability to perform an activity within the range considered normal for a
human being

Disease Prevention Measurements:
- DALY = Disability Adjusted Life Years:
o An indicator of the time lived with a disability and the time lost due to premature mortality
- YLL = (years of life lost):
o Years Lost due to premature death
- YLD = Years Lost to Disability

https://nccid.ca/publications/understanding-summary-measures-used-to-estimate-the-burden-of-disease/

- Risk Factor Contribution to DALYs:

Why Prevent Disease?:
- Beneficial for patient
- Prevents disability/mortality
- Some diseases aren’t curable (Eg: AIDs), but are preventable
- Cheaper than treating chronic disease – Some 70% of all GP visits are due to Chronic Disease:

Types of Prevention:
- Primary Prevention:
o Preventing the disease from developing in the first place by modifying removing risk factors
§ Eg: Changing eating habits to prevent obesity
§ Eg: Immunisation
§ Eg: Fitting vehicles with seat-belts
- Secondary Prevention (Screening):
o Prevent disease progression by early detection of disease & Early Intervention
§ Eg: Identifying someone with hypertension → early treatment to prevent CVD
§ Eg: Mammography
§ Eg: Routine pap smears
- Tertiary Prevention:
o Interventions to prevent or minimise complications with an Established disease
§ Eg: Bariatric surgery for morbidly obese people with poor diabetic control to avoid needing
insulin therapy
§ Eg: Monitoring diabetes with HbA1c, eye exams, foot exams
§ Eg: Medications

Screening:
- “Identifying individuals who are More Likely To Be HELPED THAN HARMED by further tests/treatment”
- Criteria for Selecting Diseases to Screen for:
o 1: It should be an obvious burden for the Individual/Community
§ Deaths
§ Suffering
§ Economic/Social Costs
o 2: It should have an initial Latent Stage, or be determined by risk factors, which can be detected by
tests
o 3: The Tests should be simple, safe, precise, socially-acceptable & validated
o 4: Treatment/Intervention is crucial to prognosis
o 5: Early intervention must provide a BETTER prognosis (Mortality/Morbidity/QOL)

Prevention Strategies:
- 1: “High Risk” Prevention Strategies:
o Selecting individuals at high risk of a disease → Medical Intervention
o Opportunistic Screening
o Advantages:
§ Appropriate for the individual
§ Cost-Effective
§ Good Risk-Benefit Ratio
o Disadvantages:
§ Problems with screening
• Who
• How
• When
• Borderline Cases
• Behaviourally Inappropriate (Eg: Pap smears)
• $Costs$
§ Difficult to predict the Absolute Risk of disease in an individual:
• Some people with risk factors don’t get the disease
• Many people with the disease, don’t have the risk factors
- 2: “Population” Prevention Strategies:
o Where you attempt shift the whole distribution of an exposure in a favourable direction by
controlling the determinants of the disease (Environmental/Behavioural/etc)
o Ie: Trying to reduce the underlying causes of a disease across an entire population
o Advantages:
§ A small change can make a huge difference when it occurs across an entire population
o Disadvantages:
§ Low Benefit-Risk ratio:
• Limited benefit to the individual (Eg: Immunisation – even @ low risk of disease)
• Poor motivation

Commonplace Disease Prevention Practices:
- Pregnancy:
o Folic Acid (Folate) Supplementation – Prevents Neural Tube Defects (Eg: Spina Bifida)
o Get Genetic Testing for Fragile X
o Check Rubella Immunity
o Stop Smoking
o Stop Drinking
o Prevent Listeriosis – A bacterial infection typically contracted from ‘Deli-foods’
§ Unpasteurised Dairy Products
§ Soft Cheeses
§ Cold Meets
§ Raw Seafood
§ Maintain good Personal/Food-Hygiene

https://www.mymumnbaby.com/pregnancy-your-age/
- Breast Cancer:
o Screening not necessary until 50yrs
o If 50+, screen every 2 years – Mammogram & Breast Examination

https://healthtools.dhw.idaho.gov/products/copy-of-cancer-infographic-poster-breast-cancer-2-max-10-per-order

- Cervical Cancer:
o Screen 2yrly
o Pap-smear
o Immunisation (Gardasil)

- Overweight & Obesity:
o Screen 12mthly for:
§ Blood Pressure
§ Cholesterol & Lipids
§ Diabetes
o Screen 6mthly for:
§ Nutritional Advice
o Ideal Waist Circumference = <94cm

Source: WHO via www.healthbuzz.asia

- Alcohol:
o Reduce consumption as much as possible
o Ensure 2x ‘Alcohol-Free Days’ per week

https://www.finlandia.edu/news/sophomore-nursing-class-hosting-events-alcohol-awareness-month/

- Falls:
o Common in elderly due to:
§ Vision Problems (Eg: Glaucoma – screen @ 55+yrs)
§ Inner Ear Problems → ↓Balance
§ Multiple Meds → Nauseating
§ Gait
o Screening Procedures:
§ Check all of above
§ Suggest Installation of handles/non-slip surfaces in their home
§ Suggest having a carer

https://www.finlandia.edu/news/sophomore-nursing-class-hosting-events-alcohol-awareness-month/
- Prostate Cancer:
o Risk Factors:
§ #1 – Family History (The closer the affected relatives, the more likely one is to be affected)
§ Age – Typically seen in men over 50yrs (40% of men over 50yrs have prostate cancer)
§ Race: Highest = African American; Lowest = Chinese
o Screen 2yrly for 50+yrs
o Note: 85% of cases have a 20yr survival rate with no treatment → Most die with it, not of it
o Note: Early surgery only saves 1:12 (NNT=12)
o Screening Procedures:
§ Digital Rectal Exam (DRE)
§ Prostate Specific Antigen (PSA) blood test
o PSA Screening:
§ ↑PSA occurs with:
• Carcinoma – (The purpose of the test)
• However, also with:
o Benign prostatic hypertrophy
o Prostatitis/UTI
o Recent Ejaculation
o Bike Riding
§ Sensitivity = Relatively Sensitive (A Few false negatives)
• Ie: ≈99% of Normal PSAs are Not Cancer
§ Specificity = Poorly Specific (Many false positives)
• Ie: ≈33% of Abnormal PSAs Are Cancer
• Note: False positives → Anxiety, further tests & possible treatment → ↓QOL
o Best Treatment:
§ Uncertain; Can’t predict who will benefit from early treatment (Ie: No way of knowing which
cancers are fatal)
§ Options:
• Wait & Watch
• Radical Prostatectomy
• Radiation Therapy
• Hormone Therapy
§ Side Effects:
• Infection
• Urinary Incontinence (Very Common)
• Chronic Diarrhoea & Rectal Bleeding (From radiation)
• Impotence

https://www.guidelines.co.uk/cancer/phe-psa-prostate-cancer-test-guideline-/252826.article
- Cardiovascular Risk Calculators:

https://www.summithealth.org.au/wp-content/uploads/2013/03/chronic-disease-referral-pathways.pdf

Disease Prevention Success Stories:
- Vaccination →
o Eradication of Smallpox/Polio
o Control of Measles/Rubella/Tetanus/HiB

- Car Safety →
o Personal Behaviour Change (Seat-belts/Helmets/Drink-Driving)
o ↑Engineering of Roads & Vehicles
o → Large Reduction in Deaths

- Occupational Hazards →
o Injury reductions due to legislation (Health & Safety at all sites/Smoking Ban)
o → ↓ “Black Lung”/Asbestosis/Workplace Deaths/etc

- Communicable Disease Control →
o Clean Water & sanitation
o Antibiotics
o Vector control

- Cardiovascular Disease →
o Risk factor reduction
o BP Control
o Smoking Cessation
o Earlier Detection
o Safer, more-effective treatment

- Food Safety →
o ↓Microbial Content (Eg: Pasteurisation)
o ↑Nutritional Content (Eg: Food fortification – Eg: Iodised Table Salt)
o Food safety legislation for handlers
o Elimination of major nutritional deficiency diseases (Rickets, Goitre, Pellagra)

- Mothers’ & Babies’ Health →
o Hygiene & Nutrition
o Antibiotics
o Access to healthcare
o Technology
o → Infant & maternal mortality decreased by 90%+

- Fluoridation of Water →
o Entire population benefits
o 40% Reduction in adult tooth-loss
o 60% Reduction in Child Tooth Decay

- Antismoking Campaigns →
o Recognition of tobacco as a health hazard
o Legislation – Sales to minors, Advertising banned, No Smoking in Public/Work-Places
o Smoking reduced from 40% → 20%

MEASURING HEALTH CONCEPTS:

MEASURING HEALTH CONCEPTS:

Sensitivity Vs Specificity:
- Sensitivity:
o The ability of a test to pick up people who truly have the disease of interest
o Ie: Few/No False Negatives
o Calculating Sensitivity:

𝑁𝑢𝑚𝑏𝑒𝑟 𝑜𝑓 𝑇𝑟𝑢𝑒 𝑇𝑒𝑠𝑡_𝑃𝑜𝑠𝑖𝑡𝑖𝑣𝑒𝑠
𝑆𝑒𝑛𝑠𝑖𝑡𝑖𝑣𝑖𝑡𝑦 =
𝐴𝑐𝑡𝑢𝑎𝑙 𝑃𝑜𝑠𝑖𝑡𝑖𝑣𝑒𝑠

Ie: The % of the diseased people that the test recognised as diseased

- Specificity:
o The ability of a test to weed out people who are truly Free of the disease of interest
o Ie: No False Positives
o Calculating Specificity:

𝑁𝑢𝑚𝑏𝑒𝑟 𝑜𝑓 𝑇𝑟𝑢𝑒 𝑇𝑒𝑠𝑡_𝑁𝑒𝑔𝑎𝑡𝑖𝑣𝑒𝑠
𝑆𝑝𝑒𝑐𝑖𝑓𝑖𝑐𝑖𝑡𝑦 =
𝐴𝑐𝑡𝑢𝑎𝑙 𝑁𝑒𝑔𝑎𝑡𝑖𝑣𝑒𝑠

Ie: The % of the healthy people that the test recognised as healthy

Why can’t some tests be both 100% Sensitive AND Specific?:
- Certain diseases have a distribution in a population

- So where do you draw the line? Answer – Depends on the disease in question
- Note: When ‘drawing the line’, you trade Sensitivity for Specificity and vice versa:
o Eg: If the disease has extreme morbidity/mortality, and the treatment is cheap and harmless, then
you want a highly Sensitive test to pick up every possible case
o Eg: However, if the consequences of the disease are minor, but the treatment is extremely
costly/invasive/risky, you want a highly Selective test so you only treat actual cases

Positive Predictive Value (PPV):
- Tells us how likely a Positive Test will be a True Positive
o Ie: The % of Positives that were True
- Calculating PPV:

𝑇𝑟𝑢𝑒 𝑃𝑜𝑠𝑖𝑡𝑖𝑣𝑒𝑠
𝑃𝑃𝑉 =
𝑇𝑟𝑢𝑒 𝑃𝑜𝑠𝑖𝑡𝑖𝑣𝑒𝑠 + 𝐹𝑎𝑙𝑠𝑒 𝑃𝑜𝑠𝑖𝑡𝑖𝑣𝑒𝑠

Relative Risk: “The risk of getting a disease when comparing one group to another”
- Eg: Relative risk of lung-cancer in smokers is 2x that of non-smokers
- Rate Ratio:
o Derived from Cohort Studies
o Compares the incidence rates of a disease in 2 groups of people (With/Without Exposure)
o Calculating Rate Ratio:

𝐼𝑛𝑐𝑖𝑑𝑒𝑛𝑐𝑒 𝑅𝑎𝑡𝑒 𝑖𝑛 𝐸𝑥𝑝𝑜𝑠𝑒𝑑
𝑅𝑎𝑡𝑒 𝑅𝑎𝑡𝑖𝑜 =
𝐼𝑛𝑐𝑖𝑑𝑒𝑛𝑐𝑒 𝑅𝑎𝑡𝑒 𝑖𝑛 𝑈𝑛𝑒𝑥𝑝𝑜𝑠𝑒𝑑

- Odds Ratio:
o Supposedly tells you what your Odds are of getting a disease if you are exposed to a certain risk
factor
o Calculating Odds Ratio:

𝑇ℎ𝑒 % 𝑜𝑓 𝑝𝑒𝑜𝑝𝑙𝑒 𝑤𝑖𝑡ℎ 𝑡ℎ𝑒 𝑑𝑖𝑠𝑒𝑎𝑠𝑒 𝑤ℎ𝑜 ℎ𝑎𝑑 𝐸𝑥𝑝𝑜𝑠𝑢𝑟𝑒
𝑂𝑑𝑑𝑠 𝑅𝑎𝑡𝑖𝑜 =
𝑇ℎ𝑒 % 𝑜𝑓 𝑝𝑒𝑜𝑝𝑙𝑒 𝑤𝑖𝑡ℎ𝑜𝑢𝑡 𝑡ℎ𝑒 𝑑𝑖𝑠𝑒𝑎𝑠𝑒 𝑤ℎ𝑜 ℎ𝑎𝑑 𝐸𝑥𝑝𝑜𝑠𝑢𝑟𝑒

Absolute Risk:
- The actual risk of getting the disease, over a period of time
- Eg: Assuming you live to 90, your risk of getting breast cancer is ≈12%
- This is based on the prevalence of that specific disease in that population

Numbers Needed to Treat (NNT):
- The number of patients you need to treat to prevent one additional bad outcome
- Gives insight to the effectiveness & cost of a treatment
- Ideal NNT = 1 Ie: Everyone treated improves
- Eg: A drug with an NNT of 5 → you have to treat 5 people with the drug to get 1 cure

Validity & Reliability:
- Validity = The ability of a test to test what it’s meant to be testing
o (Eg: How well IQ measures intelligence)
- Reliable = The degree of consistency of results despite changes in external factors
o (Eg: Different testers, different times, different places)

HEALTH BEHAVIOUR

HEALTH BEHAVIOUR

Health Promotion:
• Promote healthy behaviours through education
• Monitor individual wellbeing and risk-taking behaviours
• Doctor’s Role:
o Advise the most effective way to a healthy lifestyle
o Monitor patient’s behaviour
o Skill training
o Reinforcement of behaviour
o Role modelling
o Provision of information
o Give “expert” opinions
• Psychologist’s Role:
o Develop interventions at individual & community levels
• Mass Media’s Role:
o Educate people about health risks (AIDs, smoking, alcohol)
• Role of Legislation:
o Rules enforcing healthy behaviour (seatbelts/drink-driving/smoking)

Role of Behavioural Factors in Disease & Disorder:
• Health Behaviours:
o Behaviours that promote/maintain individual wellbeing
(Eg: Exercise/healthy diet)
o Either Habitual or Intentional
o Health Habits:
§ Seatbelt/cleaning teeth etc
• Risk Behaviours:
o Behaviours which are proven to increase susceptibility to a specific disease/illness

Primary Prevention:
• Instilling good health habits & changing poor ones
• Strategies:
o Change current health behaviour
o Prevent the uptake of poor health habits in the first place

Obstacles to Changing Health Behaviours:
• Pleasure (being high)
• Addiction (drugs)
• Behaviour is now habitual
• Relapse
• Factors influencing behaviour (stress → smoking)

Unrealistic Optimism & Irrational Risk Perception:
• Inaccurate perceptions of risk
• Inaccurate perceptions of susceptibility
• Lack of personal experience with problem
• There’s no problem now so there won’t be in the future
• Belief that problem is infrequent

Components of Motivation:
• Patient must be…
o Willing
§ Perceived importance of change
o Able
§ Self-efficacy
o & Ready
§ Motivations to change outweigh motivations not to change

Health Belief Model (Factors determining health behaviour):
1. Perceived Threat:
a. Perceived Susceptibility: One’s perceived risk of contracting a health condition
b. Perceived Severity: One’s opinion of the seriousness of getting/having the condition
2. Perceived Benefits: The believed effectiveness of preventative measures
3. Perceived Barriers: Potential negative consequences of taking the preventative measures
4. Cues To Action: Events (symptoms/media/social) that motivate people to take action
5. Self-Efficacy: One’s confidence in being able to undertake the preventative measure successfully

Theory of Planned Behaviour
• Assumes that behaviour is a direct result of a person’s intentions
• 3 Behavioural Intentions:
1. Attitude Toward Behaviour
§ Evaluation of outcomes: Positive / Negative
§ “If I diet, I’ll lose weight, improve my health & be more attractive
• Being healthy & looking good are desirable
2. Subjective Norms
§ The individual’s perception of social standard pressures
§ Pressures of significant others (family/friends/girlfriend) to change behaviour
3. Perceived Behavioural Control
§ One’s perceived confidence in being able to change their behaviour
§ “I think I can diet”
o Results in an Intention:
§ Change behaviour
§ Or Continue behaviour
§ Results in Behaviour

Cognitive-Behavioural Therapy
• Behaviour = the outcome of an interaction between the way one thinks and environmental events
• Behaviour is governed by the individual’s expectations about the outcomes of engaging in it
o Eg: Hot Stove Vs Smoking
• Focus on:
o The behaviour itself: Ie: The conditions that elicit/maintain/& reinforce it
o Individual’s Beliefs about their health habits: “I will never be able to quit smoking”
o Self-observation & monitoring: Record & chart behaviour

Classical Conditioning
• Where a natural stimulus acquires the ability to be evoked by another stimulus
o Ie: Unacquiring a ‘taste’ for something
o Eg: Using ‘antabuse’ to treat alcoholism:

Operant (‘Instrumental’) Conditioning
• Assumes that an individual’s behaviour is a consequence of positive or negative reinforcement
• If positive, the behaviour is more likely to occur again
• If negative, it is less likely

CHANGING BEHAVIOUR

CHANGING BEHAVIOUR

How People Change:
- Note: Patients don’t change just because you say so
o Ambivalence, Resistance & Defence Mechanisms are Normal
o Intentional Change Occurs Gradually
- Requirements for Change:
o Change in Thinking/Feeling about an Issue
o Planned Steps
o Time

“SNAP”: – Guidelines for Managing Lifestyle Risk Factors:
- What are the Risk Factors?
o Smoking
o Nutrition
o Alcohol
o Physical Exercise
- 5 A’s Approach to SNAP:
o 1: Ask:
§ Ask which Risk Factors apply to Patient
§ Eg: Do you Smoke/Eat Healthily/Drink/Exercise?
o 2: Assess:
§ Assess Level of Risk & Relevance to Patient’s Health
• Ie: Behaviour History (Smoking/Diet/Drinking/Exercise History)
• BMI
• *Cardiovascular Risk Calculator – Work out absolute risk level for CVD
§ Assess Readiness to Change
o 3: Advise:
§ Advise with Written Information (Eg: Pamphlets)
§ Advise with a Lifestyle Prescription (Life Script)
§ Advise with a Brief Intervention & Motivational Interviewing
o 4: Assist:
§ Assist with Pharmacotherapy
§ Assist with Self-Monitoring (Suggest Keeping a Diary)
o 5: Arrange:
§ Arrange Referral to:
• Specialist Services (Eg: Dietician/Exercise Physiologist/‘ATODs’)
o Note: ATODs = Alcohol, Tobacco & Other Drugs
• Support Groups
• Helplines
• Counselling
§ Arrange Follow-Up

A Useful Tool: “The 5 Stages of Change Model”:
- 1: Precontemplation:
o No intention to change behaviour
o Precontemplation → Contemplation:
§ Make the patient aware of the problem (Link their Behaviour to their Health)
§ Encourage them to take ownership of the problem
§ Explain the Negative Aspects of Problem (Convince patient that the behaviour Is a problem)
- 2: Contemplation:
o Person is thinking about changing behaviour
o Contemplation → Preparation:
§ Get patient to Think How the Behaviour is Affecting Others
§ Change how they think & feel about the Issue
§ Note: Pushing People to Change can be Counterproductive → Resentment
§ 3 Strong Motivators:
• Health
• Money
• Relationships
- 3: Preparation:
o Person prepares to make the change:
o Preparation → Action:
§ Gathers information
§ Finds out how to achieve the change
§ Set Firm Goals & Priorities
§ Acquiring Skills Necessary for change
- 4: Action:
o Person makes changes (may be small steps at first)
o Action → Maintenance:
§ Self-Efficacy is very important
§ Keep focussed
§ Acknowledge that Change is Difficult & Potential Relapse is Normal
- 5: Maintenance:
o Consistently practices new/altered behaviour
o Acknowledge that Change is Difficult & Potential Relapse is Normal
- //Relapse:
o Person relapses back to original behaviour
o Move back to Contemplation if Relapse Occurs

Relapse Prevention
• Common with addictive disorders (smoking, drinking, gambling, etc)
• More likely to occur in times of stress, anxiety, depression
• Once relapse has occurred, it is just as hard to ‘quit’ the 2nd time as it was for the 1st

CHRONIC DISEASE & RISK FACTORS

CHRONIC DISEASE & RISK FACTORS

Chronic Disease:
- Definition:
o A Disease with One/More of the Following Characteristics:
§ It is Permanent (Ie: Incurable) and Leaves Residual Disability (Morbidity)
§ Caused by Non-Reversible Pathological Alteration
§ Requires long-term Observation/Management /Care
- Biggest Contributors to Burden of Chronic Disease:
§ Cardiovascular Disease
§ Anxiety/Depression
§ Diabetes
§ Chronic Kidney Disease
- Causes of Chronic Disease:
o Patients Presenting to Doctors:
§ ≈20% are Smoking (Decreasing)
§ ≈55% are Overweight/Obese (Increasing)
§ ≈65% Do Less than Recommended Levels of Exercise (30mins x 5days/week)
§ ≈25% Drink at Risky Levels
o Risk Factors:
§ Risk Factors are often Associated with Many Diseases
§ Risk Factors shouldn’t be considered in Isolation
• Risk Factors Interact → Multiplies Risk
§ Most Risk Factors are Completely Avoidable

https://dhss.alaska.gov/dph/Chronic/Pages/Publications/Default.aspx

Overweight & Obesity:
- Trend:
o ≈55% are Overweight/Obese
o Rates are Increasing in first world countries
- BMI:
o Calculation:
§ Kg/Height in m2
o Ranges:
§ Underweight <18.5
§ Normal 18.5 – 25
§ Overweight 25 – 30
§ Obese >30
o Limitations:
§ Limited Sensitivity – Some people who are clearly overweight may be tall → False Negatives
§ Limited Specificity – Extremely muscular people will have a high BMI → False Positives
§ Hence, should be used in Conjunction with Waist Circumference

- Waist Circumference:
o Males:
§ > 94cm → Increased Risk
§ > 102cm → High Risk
o Females:
§ >80cm → Increased Risk
§ >88cm → High Risk

Physical Inactivity:
- Ie: Sedentary Lifestyle
- Recommended Levels of Exercise (30mins x 5days/week)
- It’s estimated ≈65% of people don’t do enough exercise
- Note: Sedentary Lifestyle increases with Age
- Associated with higher cholesterol levels and risk of type 2 diabetes

*No, not literally equivalent to a pack of cigarettes; but illustrates risk*
https://mobile.twitter.com/avonhmo/status/1022838331053432832

Poor Diet:
- Inadequate Fruit & Vegetable Intake
- Most prevalent in Low Socioeconomic Status groups

Tobacco Smoking:
- Smoking rates are ≈20% spread evenly across all age groups
- Most prevalent in Low Socioeconomic Status groups

Excessive Alcohol:
- Approximately ≈25% Drink at Risky Levels
- Rates among adults are consistent with age
- Most prevalent in Rural & Remote Areas

High Blood Pressure:
- Approximately 30% of Adults over 25yrs
- Most prevalent in Males
- What is High?
o Systolic above 140mmHg
o Diastolic above 90mmHg

High Blood Cholesterol:
- Approximately 50% of Population have High Cholesterol (Rates are stagnant)
- ≈60% of Indigenous (Rates are stagnant)
- What is High?
o LDL:HDL Ratio

Social Determinants of Health:
- Socioeconomic Status:
o High SES people tend to live longer
o Why? – They can Afford Better:
§ Nutrition
§ Medical Care
§ Education → ↓Risky behaviours
- Early Life:
o Eg: Low Birth Weight (Ie: From maternal smoking)
o Eg: Poor Nutrition
o Eg: Neonatal Infections
o Eg: Breastfed Vs Non-Breastfed
- Stress:
o Money
o Family
o Relationship
o Job Security
- Employment:
o Eg: Occupational Hazards
o Eg: Bad influences of Workmates (Eg: Drinking/Smoking)
o Eg: Fast foods for lunches
- Social Networks:
o Or Lack of → Depression
o Social Exclusion (Eg: Minorities – Racial/SES/Sexuality/Weight/etc)
- Drug Addiction:
o Direct impact on health (Eg: Hep-B/HIV/Substance-Dependence)
o Indirect impact through:
§ Crime
§ Compromise on nutrition etc. To save money for drugs

https://mobile.twitter.com/avonhmo/status/1022838331053432832

Prevention of Chronic Diseases You Will See as a Doctor:
- Hypertension:
o Primary Prevention:
§ ↑Exercise
§ Lose weight
§ ↓Salt intake
§ ↓Saturated Fats
§ ↓Stress
§ Coping Strategies
o Secondary Prevention:
§ Screening for Hypertension
§ Early Diagnosis
§ Review for other risk factors
§ Lifestyle Counselling
o Tertiary Prevention:
§ Antihypertensive Drug Interventions
§ Follow-up Monitoring

Source: WHO

- Depression:
§ Address Social Isolation/Greif/Family Problems
§ Strategies for Coping with Stress
§ Build good support networks
§ Physical Exercise → ↓Stress
§ Screening for signs of depression
§ Early Diagnosis
§ Early Intervention
§ Appropriate Therapy/Counselling
§ Monitoring & Support
§ Refer to Therapist

- Diabetes:
§ Physical Activity
§ Weight Control & Diet
§ Find out Family History
§ Screening blood tests in At-Risk patients
§ Referral to Diabetes Educator
§ Initiation of Treatment
§ Ongoing Monitoring

- Lipid Disorder:
§ Diet
§ Exercise
§ Family History
§ Screening
§ Risk Factor Profile
§ Dietary Counselling
§ Start Treatment (Monitor Effects & Side-Effects)

- Osteoarthritis:
§ Avoidance of Injuries in Early Life
§ Diagnose from Other Rheumatological Disorders
§ Provide Early Intervention
§ Medication
§ Physical Therapies
§ Devices & Aids
§ Surgical Referral

PANDEMICS

PANDEMICS

What is a Pandemic?
• World Health Organization (WHO) – 3 Criteria:
o Disease is New to a population; (Ie: NO Existing Human Immunity)
o Agents infect Humans, causing serious illness; and
o Agents Spread Easily and among humans
• It is not a pandemic just because it is widespread or kills many people; it must also be infectious
o Eg: Cancer kills many people, but is not a pandemic because it is not infectious or contagious
• Excludes “seasonal influenza” –not a new disease

Pandemic Management:
• Potential Solutions Depend on phase of pandemic
• One example of a pandemic management model:
o ALERT:
§ A novel zoonotic virus with pandemic potential causes severe disease in humans
§ There is no Human-Human Transmission
§ Novel virus has not arrived in the home country
o DELAY:
§ Novel virus still not in the home country
§ OS4 Small cluster of cases in one country overseas
§ OS5 Large cluster(s) of cases in only one or two countries overseas
§ OS6 Large cluster(s) of cases in more than two countries overseas
o CONTAIN:
§ Pandemic Virus Arrives in the home country
§ Small Number of Cases
o SUSTAIN:
§ Pandemic virus Established in the home country and Spreading in the community
o CONTROL:
§ Customised Vaccine widely available
§ Beginning to bring the Pandemic under control
o RECOVER:
§ Pandemic controlled in the home country but further waves may occur if the virus drifts
and/or is re-imported

Who do you treat?
• Depends on phase-
o Early phase, treat everyone → Reduce disease transmission
o Later phases, treat at risk groups
• Who pays for it?
o If you treat everyone, it gets very expensive

Vaccine Prophylaxis: Theoretically Becomes Available At “Control” Phase:
• Who Gets it?
o High Risk Individuals (Eg: old, debilitated, chronic heart/respiratory/renal disease)
o People in closed institutions (Eg: Prisons/nursing homes)
o Groups in community service (Eg: Doctors/Hospital Staff)
• Types:
o Inactivated Vaccines are prepared from the appropriate strain of virus
o Subunit Vaccines are prepared to reduce the content of extraneous proteins
o Live Attenuated Vaccines:
§ These vaccines could be administered as a nasal spray
§ This would encourage the development of appropriate immune responses based on mucosal
immunity
o Recombinant Vaccines:
§ Based on Recombinant DNA Technologies

Ethical Allocation Of Scarce Resources:
• Single biggest question is how to ration scarce lifesaving resources:
o “who shall live when not all can?”
• WHO GETS IT? (Fleming, BMJ 2005)
o Blind Justice?
§ (1st come or lottery)
o High risk given priority?
§ (old, chronic disease)
o Healthcare workers?
o Essential services?
§ (Policemen/Firemen)
o Children?
o Global allocation of resources
• Eg: In the Recent Covid-19 Outbreak:
o Massive access block (Where there are insufficient beds for new patients)
§ →ED overcrowding
§ → Not enough ICU beds
o →More beds were created by:
§ →Cancellation of elective surgery
§ →Especially cancellation of elective major surgery needing ICU
§ → Erecting Field Hospitals

2 Arms of Countermeasures in a Pandemic:
• Therapeutic countermeasures
o stockpiling of resources
§ vaccines
§ antiviral medications
o access to care
o health care workers
• Non therapeutic countermeasures
o infection control
o surveillance and contact tracing
o social separation
o quarantine and containment
o international boundaries, duties and foreign nationals

Isolation And Quarantine – Essential In Early Phase:
• Isolation:
o Separation (for the period of communicability) of known infected persons to prevent or limit the
spread of infection
• Quarantine:
o Restriction of activities of healthy persons who have been exposed, to prevent disease transmission
during the incubation period

https://www.matherhospital.org/wellness-at-mather/isolation-vs-quarantine-whats-the-difference/

Surveillance & Contact Tracing:
• Contact Tracing = Identification of cases by Name
• Surveillance is more intrusive than simply reporting names:
o daily temperatures, health questionnaires
o complete daily certificates

https://www.cdc.gov/coronavirus/2019-ncov/global-covid-19/contact-tracing-workflow.html

Conflicts of Interest:
• Clinical Medicine:
o Doctors Promote best interests of a Patient
§ (Respect patients Liberty & Autonomy)
• Public Health:
o Promotes best interest of the Population
o Liberty and Autonomy of the Patient may be Overridden for the good of the public
§ Quarantine
§ Isolation
§ Closing International Borders

What will the future hold?
• Will there be another pandemic – Yes!!
• What serotype of virus will be responsible - ??
• How well are we prepared ?? - NOT
• How much warning will we get??
• What should I be doing to prepare ?

VACCINATION/IMMUNIZATION

VACCINATION/IMMUNIZATION

WHO: “The most successful & cost-effective public health intervention in history”

How Vaccines Work:
- Individual Protection:
o They stimulate the immune system to create Antibodies/Memory-Cells in the absence of Disease
Symptoms
o Once immune, if the body is subjected to the actual pathogen, it mounts an even stronger attack
(Secondary Immune Response) against it
- Herd Immunity:
o Protects those who aren’t vaccinated in the community, providing there is a high rate of vaccination
within the population

Principals of Vaccine Development & Use:
- 1: Separate the Disease-Causing effects from the Immune-Generating effects in an organism
- 2: Give it to susceptible individuals to provoke an immune response
- 3: Result is non-susceptible, immune individuals
- 4: Eventually results in herd immunity

Contraindications to Vaccination:
- Absolute:
o Anaphylactic response to vaccine or component
- Relative: (Ie: Risks Vs Benefits)
o Immunocompromised (Live Vaccines)
o Pregnant or Suspected Pregnancy (Live Vaccines
o Fever of >38.5oC
o Recent Live Vaccine (4 weeks)
o Recently received blood/blood products
o Guillain Barre Syndrome (GBS)
o Influenza
- Note: All other excuses are not good reasons not to vaccinate!
- Note: All patients should have the freedom to choose whether or not to receive a vaccine

Types of Vaccines:
• Live Attenuated vaccines:
o Live organisms that have been de-pathogenised
o Advantages:
§ Robust Immune Response
§ Lifetime Immunity with 1 or 2 doses
o Disadvantages:
§ Potential to cause disease (can’t give to immunocompromised or pregnant women)
§ Potential for Adverse Events/Side-Effects

• Inactivated/killed vaccines:
o Dead organisms containing relevant proteins but unable to replicate
o Advantages:
§ No Ability to cause disease
§ Fewer Adverse Events/Side-Effects
o Disadvantages:
§ Less robust immune response
§ Waning Immunity → Requires multiple doses & may require booster

• Acellular/Toxoid/Subunit:
o Artificially synthesised non-toxic antigens
o Advantages:
§ No Ability to cause disease
§ Fewer Adverse Events/Side-Effects
o Disadvantages:
§ May require Adjuvants or Conjugation
§ Less robust immune response
§ Waning Immunity → Requires multiple doses & may require booster

• Recombinant Protein Vaccines:
o Made using bacterial or yeast cells to manufacture surface proteins from the pathogen
o Advantages:
§ No ability to cause disease
§ Can be highly targeted
o Disadvantages:
§ Needs to be supplemented with adjuvants to stimulate generation of antibodies

• Nucleic Acid Vaccines (Eg: RNA Vaccines):
o Inoculating the body with a synthetic RNA strand, which gets into body’s own cells → translated into
antigen proteins → stimulates immune response to antigen
o Advantages:
§ Can be highly targeted
§ No risk of disease
o Disadvantages:
§ Expensive
§ Labour intensive
§ Delicate
§ Highly sensitive to cold chain

Pollard, A.J., Bijker, E.M. A guide to vaccinology: from basic principles to new developments. Nat Rev
Immunol 21, 83–100 (2021). https://doi.org/10.1038/s41577-020-00479-7

2 Important Vaccine-Preventable Diseases:
- Measles:
o Extremely Virulent: – One of the most infectious (easily Spread) Diseases known to man
o Genus: – Morbillivirus
o Occurrence:
§ Prior to Immunisation = >100Million cases/year → 6 Million Deaths/year (Worldwide)
§ Post-Immunisation = 99% drop in cases
o Transmission: - Airborne Droplet Spread
o Incubation Period:
§ ≈10 days to onset of fever
§ ≈14 days to onset of rash
o Period of Communicability:
§ From ‘Prodrome’ (Time before symptoms) to 4 days after onset of rash
o Susceptibility:
§ Everyone un-sensitised people
§ Survival of Illness → Lifetime immunity
§ 1st Vaccine → 95% Immune
§ 2nd Vaccine → 99% Immune
§ Maternal Antibodies protect infant for 6-9 months
§ Malnutrition is a problem – as measles causes diarrhoea in children
o Symptoms:
§ Fever
§ Malaise
§ Cough
§ ‘Coryza’ – (“Overflowing Head”)
§ Conjunctivitis
§ Rash – starting on face → Spreading to rest of body
§ Koplic Spots (Unique to Measles) – White/Blueish spots on buccal mucosa
o Complications:
§ Otitis Media (Middle ear infection)
§ Pneumonia
§ Diarrhoea
§ Acute Encephalitis (Rare)
o Measles Vaccine:
§ Type: - Live Attenuated Vaccine (Given in combination with Mumps, Rubella & Varicella)
§ Note: It interferes with other live vaccines
§ NOT given during Pregnancy
§ Adverse Reactions:
• Fevers – common
• Faint red rash
• Local swelling
• Local Knot in muscle
§ Dosing:
• 1st Dose @ 12mths
• 2nd Dose @ 18mths

Photo Credit:Content Providers(s): CDC/Dr. Heinz F. Eichenwald, Public domain, via Wikimedia Commons

CDC, Public domain, via Wikimedia Commons

Public domain: CDC

Julius Senegal, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons

- Rubella:
o Genus: - Rubivirus
o Occurrence:
§ Pre-Vaccine = Worldwide Endemic
• Epidemics every 5-9yrs
§ Post-Vaccine = Elimination of Rubella
o Transmission:
§ Airborne Droplet Spread
§ Contact with Mucus Membranes
o Incubation Period:
§ 14-21 Days
o Period of Communicability:
§ 1 Week Before & 4 Days after Rash
o Susceptibility:
§ Universal Without Vaccine/Prior Infection
§ Immunity after single dose (95-100%)
§ Maternal Antibodies protect infant for 6-9mths
o Symptoms:
§ 50% Asymptomatic
§ Low-Grade Fever
§ Headache
§ Malaise
§ Coryza (“Overflowing Head”)
§ Conjunctivitis
§ Lymphadenopathy
§ Arthralgia
§ Rash
o Complications:
§ Post Viral Encephalitis (Uncommon)
§ **Congenital Rubella Syndrome (CRS)
• Occurs in 90% of babies whose mother had Rubella during 1st Trimester
• Multiple Defects are common (Eg: Blindness, Deafness, many more...)
• Hence ALL WOMEN OF CHILD-BEARING AGE MUST BE IMMUNISED
o Rubella Vaccine:
§ Type: - Live Attenuated Vaccine (Given in combination with Measles, Mumps & Varicella)
§ Note: It interferes with other live vaccines
§ NOT given during Pregnancy
§ Adverse Reactions:
• Fevers – common
• Faint red rash
• Local swelling
• Local Knot in muscle
§ Dosing:
• 1st Dose @ 12mths
• 2nd Dose @ 18mths
§ ALL WOMEN OF CHILD-BEARING AGE MUST BE IMMUNISED

commons.wikimedia.org, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons

https://www.cdc.gov/rubella/about/photos.html

http://phil.cdc.gov/phil_images/20030724/28/PHIL_4284_lores.jpg

Other Notable Vaccines & the Diseases They Prevent:
- Hep B:
o Hepatitis B:
§ An Infectious illness caused by Hep-B-Virus
§ Infects the Liver
§ Causes Vomiting, Jaundice, Liver Cirrhosis & Liver Cancer (Rarely death)
- DTP:
o Diphtheria:
§ Upper Respiratory Tract illness
§ Characterised by sore throat, low fever & a pseudomembrane on tonsils/pharynx/nasal
cavity
o Tetanus:
§ Gram-Positive anaerobic bacteria infection – occurs through skin wound
§ Bacteria secrete a neurotoxin → Prolonged contraction of skeletal muscle fibres (“Tetany”)
o Pertussis:
§ Whooping Cough – A highly contagious disease spread by droplet transmission
§ Bacterial Infection
§ Droplet Transmission
- Hib:
o Haemophilus Influenzae B:
§ Actually a Bacteria (Despite the ‘viral’ name)
§ Cause opportunistic infections
§ Leads to Bacteraemia, Pneumonia, Bacterial Meningitis
- IPV:
o Inactivated Poliomyelitis (Polio):
§ AKA: Infantile Paralysis
§ An acute viral infection
§ Faecal-Oral Transmission
§ 90% of infections are asymptomatic
§ If the virus enters the CNS, it preferentially destroys motor neurons → Muscle Weakness,
Paralysis & Muscle Wasting
- 7vPCV:
o Pneumococcal Conjugate:
§ Bacterium →
• Pneumonia, Sinusitis, Otitis Media
• Meningitis (Most common cause of bacterial meningitis)
• Bacteraemia → Sepsis
• Endocarditis
• Pericarditis
- Rotavirus:
o Leading cause of Severe Diarrhoea among infants & young children
§ Also causes gastroenteritis & dehydration
o Known as Stomach Flu (But no relation to influenza)
o Faecal-Oral Route
- MMR:
o Measles: See Above
o Mumps:
§ Viral Disease
§ Droplet Transmission
§ Typically presents as painful swelling of the Salivary Glands, fever & headache
§ Can also cause painful testicular swelling & rash
o Rubella: See Above
- MenCCV:
o Meningococcal C:
§ Bacterium
§ Typically causes Meningitis & Fever, but is most dangerous when infection becomes septic

The Cold Chain:
1. What is the cold chain?
• Is the transport and storage of a vaccine at or below a certain temperature
• It includes the vaccine equipment, people and the procedures

2. What are the stages in the cold chain?
• Manufacture
• Supply
• Distribution
• Clinic
• Fridge
• Patient

3. Name 5 Vaccines that are damaged or destroyed by freezing?
• Tetanus
• DTP
• Hib
• Hep A & B
• Influenza
• Pneumococcal

Which vaccines are damaged by exposure to heat or light?
• BCG
• Oral polio
• MMR

4. What is the main requirement for vaccine fridge thermometers?
• Can measure max & min temperature for the previous 24 hrs

5. Which are the best types of thermometers?
• Mercury and digital thermometers

6. Where in the fridge would you place the temperature probe?
• In the centre of the fridge
• In the case of a multiple purpose fridge (Eg: If food is stored with it), then is best located with the
immunisations in the foam box within the fridge

7. What monitoring device is included in vaccine transportation of vaccine supplies?
• Temperature monitors → heat & freeze cards (charts)

8. How would you pack vaccines for transport and what other precautions would you take for
transportation?
• Vaccine package
- Good icebox with a tight fitting lid
- Store immunisations with ice block that is “sweating”
- Shredded newspaper is recommended to allow air to circulate around vaccines
- Layers: ice block - shredded newspaper – immunisations – shredded newspaper – piece foam – ice
block
• Transport
- Whenever being transported don’t place in direct sunlight
- Minimise duration of journey
- Record temperature whenever vaccines are put in/ taken out
- Place securely in boot
- Only deliver to surgery if someone is there
- Check the temperature of the fridge at surgery before put new immunisations in

9. What are the requirements of a surgery vaccine fridge?
• Have a safe lockable fridge
• Try to keep immunisations in a proper immunisation fridge – if not possible separate the immunisation
from the other things that are being stored in the fridge (Eg: Have separate shelf for immunisation and
separate shelf for medications)
• Check the temperature of the immunisation fridge daily
• When placing new vaccines in fridge, rotate stock
• Use older vaccines first, don’t use the most recent – will prevent vaccines going out of date
• Use only 50% of available space in fridge – allow air to circulation around the vaccines in the fridge
• Place immunisation in correct location in fridge – the bottom shelf and door shelves should not be used
- recommended to place salty water in these draws to prevent shelves from being used and the water
from being drank
• Don’t co-store non-vaccine items in the fridge (eg food) – this will ↑ fridge door opening and may
interfere with temperature

• If it is thought that cold chain may have been broken or vaccine has been tampered with contact supplier
1st before throwing out. Isolate in the fridge in with clear label stating “do not use” until ascertained
whether should be thrown out

BASIC CONCEPTS OF INFECTIOUS DISEASES

BASIC CONCEPTS OF INFECTIOUS DISEASES

The Birth of ‘Germ Theory’:
- People recognised that meat broth became cloudy and overgrown with microbes
- But where did these microbes come from? – 2 Schools of Thought:
o 1: Spontaneous Generation
o 2: Formed from Seeds/Germs
- Pasteur Proved that Microbes exist In the Air through his Swan-Necked Flask experiment

https://www.medassureservices.com/getting-to-know-germs-and-hand-sanitizers/

- Robert Koch Proved that Specific Microbes caused Specific Diseases through ‘Koch’s Postulates’:

[mike jones], CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
Revision of Microbial Diversity:
- Some bugs are good (even essential) and some bugs are bad
- Organisms capable of causing disease are pathogens

Normal Flora (commensals)
• Heavily colonise skin – armpit, perineum, interdigital areas
o Nose and oropharynx
o GI Tract
o Uro-genital tract
• Are normal at certain places where they are not harmful
o However when they colonise an area where they shouldn’t, they cause disease (nosocomial
infection)

Pathogenesis
• The biochemical mechanisms whereby microbes (bacteria, fungi, parasites & viruses) causes disease
• Virulence: the propensity of a microbe to cause infection → disease

Steps to disease:
I. Entry
• Oral
• Skin
• Trans-placental
• Inhalation
• Inoculation (wound/skin penetration)
• Sexual
II. Colonisation
• Breach of skin/epithelia/conjunctiva
• Attachment
III. Persistence + avoiding host defences
• Beat natural barriers – flushing, mucous + cilia, stomach pH, Lysosomes in saliva, etc
IV. Replication
• Mucosal (GI tract)/systemic (blood)/nerves (viruses)/cerebrospinal fluid (meningitis)
V. Dissemination – (Host-Host)
• Faecal-oral (diarrhoea), Aerosols (sneezing), Sexual (intercourse)
• Depends on:
o Organism size
o Ability to survive in external environment
VI. Cause Disease
• Can release toxins – either local effects / or systemic
• Can cause unusual cellular activity
• Can cause tissue damage

Host-Parasite Interactions:
1) Colonised, no disease, no illness (asymptomatic)
Eg: Helicobacter – in stomach
2) Colonised, disease, no illness (asymptomatic)
Eg: Chlamydia & other genital tract infections
3) Colonised, disease, illness (symptomatic)

The Organism Classifications:
• Prokaryotes:
o Viruses
§ Very small
§ Nucleic acid inside protein coat (DNA or RNA)(ss or ds)
§ Complete parasitic dependency
§ Replicates inside cell - but metabolically inert in external environment
§ Need close/direct contact
§ Need a moist environment
§ Lyses host cells and then infects more
§ Respiratory route / oral / inoculation / sexual transmission

User:YK Times, CC BY-SA 3.0 <http://creativecommons.org/licenses/by-sa/3.0/>, via Wikimedia Commons

o Bacteria
§ Larger than viruses
§ Visible under light microscope
§ Living → replicate by binary fission
- Can be killed
§ Intracellular or extracellular
§ Motile
§ Can produce toxins
§ Contain DNA, Ribosomes + Inclusions – no true nucleus
§ Resulting disease often more severe

CNX OpenStax, CC BY 4.0 <https://creativecommons.org/licenses/by/4.0>, via Wikimedia Commons
• Eukaryotes:
o Protozoa
§ Single-Celled Animals
§ Larger than bacteria – still small enough to live intracellularly
• Can also live extracellularly
§ Vectors / faecal-oral route →most infections occur tropically


o Helminths
§ Multi-celled, often macroscopic organisms
§ Complex body organisation and reproduction (some have sexual dimorphism)
§ Difficult for immune system to destroy – too big
§ Cause inflammation
§ Are often never eliminated

https://upload.wikimedia.org/wikipedia/commons/b/bf/Hookworms.JPG
o Fungi
§ Thousands of species
§ Few are pathogenic to humans
• 20ish are fatal
§ Resulting Mycoses (disease) either:
• Superficial
• Cutaneous
• Subcutaneous
• Systemic
• Opportunistic – seen in compromised hosts
-Depending on site of infection
§ Exist as branched filamentous forms, or yeasts
§ Asexual spores (conidia)
§ Spores commonly inhaled & cause infection

https://aspergillusproject11.wordpress.com/2013/04/18/life-cycle/amp/

Host-Parasite Relationships:
- Commensalism:
o Colonised; But No Disease
o (Eg: E-Coli in stomach)
- Mutualism:
o Colonised; No Disease; Mutually Beneficial
o (Eg: Digestive Bacteria in Colon; Lactobacillus in Vaginal → Acidity)
- Parasitism:
o Colonised; With Disease/Damage
o (Eg: Hookworm; Plasmodium Malariae)

- Differential Features Of Microbes:

Pathogen: Visible Via: Cellular? Nuclear Nuclear Structural Outer Surface:
Material: Organisation: Constituents:
Prions No Nucleic No Membrane.
Acid – Just No Membrane
Electron Acellular Protein. No Cellular
Microscope Machinery.
Viruses No Nucleus No Cytoplasm. ‘Enveloped’
DNA or RNA Or
‘Non-
Enveloped’
Bacteria No Distinct Bi-lipid
(Prokaryotes) Nucleus. membrane is
covered by a
Single, Circular thick Cell Wall.
Chromosome.
Gram Pos =
Light Single Cell Simultaneous Membrane- Peptidoglycan
Microscope Transcription & Bound. Gram Neg =
Translation. Lipopolysacchar
DNA Cellular ide
Protozoan Distinct Machinery.
Parasites Nucleus.
(Eukaryotes) Cytoplasm.
Several Linear
Chromosomes
Simple Bi-lipid
Metazoan Transcription in Membrane.
(Eukaryotic) the Nucleus.
Parasites
(Helminths) Naked Eye Multi-Cell Translation on
Ribosomes in
the Cytoplasm.

Normal Flora Vs Pathogens:
- Normal Flora (Commensals):
o Can be Beneficial:
§ Can be Protective by outcompeting potential pathogens for Space/Nutrients
§ If they are washed away (Eg: Vaginal Antibiotics), pathogens can colonise the area → Disease
o Heavily Colonise Skin:
§ Armpit, Perineum, Interdigital areas
§ Nose and oropharynx
§ GI Tract
§ Uro-genital tract
o Heavily Colonise the GIT:
§ Density of Microbes Increases Towards the Rectum (Stomach Acid → Low Numbers)
§ Species of Microbes change throughout due to different environments
o Some Areas are Sterile:
§ Bladder
§ Blood
§ Organs
o Location depends on Aerobic/Anaerobic Species:
§ Aerobic – Likes Oxygen (Eg: In Respiratory Tract)
§ Anaerobic – Cannot stand Oxygen (Eg: Found in Bowel/Necrotic Tissue/Etc)
o Nosocomial Infection (Opportunism):
§ If Commensals Colonise somewhere they shouldn’t, they cause disease
§ Often occurs in Hospitals → Typically Highly Resistant to Antibiotics

Unattributable
- Pathogens (4 Features of a “Pathogen”):
o Pathogens = Organisms capable of causing disease
o *They MUST do ALL 4 of the Following:
§ 1: Gain Entry to Host
§ 2: Attach & Multiply
§ 3: Evade Host Defences
§ 4: Cause Damage to Cells/Tissues
o Primary Vs Secondary Pathogens:
§ 1o Pathogens:
• Can produce an Infection without the help of other organisms
• →Also Encourage 2o Pathogens
• (Eg: HIV → Immunocompromise)
§ 2o Pathogens (Aka: Opportunistic Pathogens):
• Only produce an Infection due to damage caused by 1o Pathogens

Virulence:
- Short Definition: The propensity of a microbe to cause infection → disease in a Definitive Host
- Long Definition: The degree of pathogenicity of an infectious agent, indicated by:
o Case-fatality rates
o Ability of the agent to invade and damage tissues of the host
o Toxicity
o Ability to overcome/evade body defences
- (‘Avirulence’ = Antonym)
- Virulence Factors:
o Molecules Expressed/Secreted by Pathogens that enable them to achieve the following:
§ Colonization of a Niche in the host (this includes adhesion to cells)
§ Immunoevasion, evasion of the host's immune response
§ Immunosuppression, inhibition of the host's immune response
§ Entry into & Exit out of cells (if the pathogen is an intracellular one)
§ Obtain nutrition from the host
o Eg: Endotoxin (LPS) – Potent antigen
o Eg: Exotoxins (Eg: Tetanus Toxin) → Tetanus
o Eg: Fungal Mycotoxins (Eg: Aspergillus) → Severe Liver Damage
o Eg: Ig-Proteases (Eg: Strep Pyogenes) → Break down Antibodies
o Eg: Capsules (Eg: Bacterial cell walls) → Inhibits Phagocytosis

Pathogenesis (4 Stages to Infection):
- Pathogenesis = The biochemical sequence of events whereby microbes (bacteria, fungi, parasites & viruses)
causes disease
- 4 Stages to Infection:
o 1: Gain Entry to Host:
§ Needs a Portal of Entry & Exit. Egs:
• (For Exogenous Organisms) - Oral/Skin/Trans-placental/Inhalation/Inoculation
(wound/skin penetration)/Sexual
• (For Endogenous Organisms) – Organisms already present On/In Body – Requires
Immunocompromise
o 2: Attach & Multiply:
§ Attachment Via:
• Adhesion Receptors (Eg: Glycoproteins on Viruses)
• Cellular Extensions (Eg: Fimbriae/Pili on Bacteria)
• Physical Structures (Eg: Hooks/Suckers on Helminths)
§ Multiplication/Spread of Infection:
• Local (Abscesses/Mucosal/Nerves/CSF)
• Systemic (Blood/Sepsis)
§ Factors Affecting Spread:
• Organism Factors:
o Virulence Factors
• Host Factors:
o Genetic Susceptibility
o Immune Status
o (Age, Pregnancy, Nutrition, Etc)
o 3: Evade Host Defences:
§ Beat Physical Barriers (Eg: Flushing, Mucous + Cilia, Stomach pH, Lysosomes)
§ Beat Innate Cellular Defences (Eg: Inflammation, Phagocytosis, NK Cells)
§ Beat Adaptive Defences (Eg: Antibodies, Cell-Mediated Immunity)
o 4: Cause Damage to Cells/Tissues:
§ Physical Disruption
§ Toxic Damage
§ Aberrant Cell Activity
§ Immune-Mediated Damage

Transmission - (Exiting the infected host & Spread of Infection):
- Successful Microbes Must Exit the Body →Transmit to a new host. They are Either:
o Shed in Secretions/Excretions
o Taken up by Vectors (Eg: Mosquitoes) from the blood
- Transmission Depends On:
o Number of Organisms Shed (High Numbers Needed)
o Activities of the host (Eg: Coughing, Sneezing, Diarrhoea, Intercourse)
o Stability in the Environment (Eg: Amoebic Cysts resist drying & heat →Survive)
o # Required for Infective Dose (Depends on organism & route)
o Virulence/Pathogenicity
- Types of Transmission: - (Requires a “Vehicle”)
o Airborne – (Must survive outside the host & in Dry Conditions)(Eg: Influenza)
o Waterborne – (Eg: Cholera)
o Food-borne – (Spoilage, Preformed Toxins, Faecal-Oral)

Unattributable

- Vertical Transmission: Parent →Offspring
- Horizontal Transmission: Person → Person
- Zoonotic Transmission: Animal → Human (Via Contact/Inhalation/Ingestion/Bites/Scratches)

Epidemiology:
- Epidemiology = “The relationship between factors determining the frequency & distribution of infectious
disease in a population”
- Factors Influencing Epidemiology (Eg: ∆ in # of susceptible/environment/organism/new organism):
o The Organism:
§ ∆ in Properties of the Endemic Organism (Eg: Persistence; Transmissibility)
§ New Organism
o The Host:
§ ∆ in # of Susceptible Hosts
§ ∆ in Concentration Of Susceptible Hosts
§ ∆ in Behaviour
o The Environment:
§ ∆ in Climate (Eg: Cold → People crowd indoors → ↑Droplet Transmission)
§ ∆ in # of Vectors (Eg: Rainy season → ↑Mosquitoes)

Immune Evasion Strategies:
- Viruses:
o Persist as Latent Infections →Reactivation/Recrudescence following Immunosuppression/Stress
o Superantigens → Inappropriate Immune Response
o Inhibition of MHC-I Synthesis/Assembly/Ag-Loading
- Bacteria:
o Depression of phagocytosis by neutrophils
o Depress cellular immunity
o Induction of apoptosis
o Killing of alveolar macrophages
o Superantigens → Inappropriate Immune Response
o Produce superoxide dismutase, catylase or oxidase → protect it from the hydrogen peroxide of the
respiratory burst of Neutrophils
o Intracellular bacterial evasion:
§ Travel b/w cells without being exposed to extracellular fluid
§ Escape into vacuole in the cytoplasm
§ Prevent fusion of lysosomes with phagosomes
- Parasites:
o Protozoan Parasites:
§ Antigenic Variation
§ Antigenic Drift
§ Molecular Mimicry (Expression of Host Proteins)
§ Intracellular Localisation
§ Self-Isolation in Membrane-bound Vesicle
§ Prevent fusion of lysosomes with phagosomes
§ Sequestration in privileged sites
§ Regulation of host functions
o Helminth Parasites:
§ Antigen Shedding
§ Protease production → Neutralise some immune components (Eg: Antibodies)
§ Superoxide Dismutase → Neutralise Respiratory Burst by Neutrophils
§ Regulation of host functions (Immunosuppression/Maladaptive Response)
§ Skew the T-Helper Response to Favour Th1-Cells:
• Favouring Th1→ Reduced class-switching to IgE, the AntiParasitic Antibody
§ Use Host Cytokines as Parasitic Growth Factors

MICROBIOLOGY: PRIONS

MICROBIOLOGY: PRIONS

Prions; What are they?
- Abnormally folded Host-Proteins that accumulate in the brain → Spongiform Encephalopathies
- Note: All known Prion Diseases affect the Brain and are currently Untreatable & Universally Fatal
- The precise structure of the Prion is Unknown
- Derivation of the term “prion”: Proteinaceous, Infectious + ‘on’

TSE’s – (Transmissible Spongiform Encephalopathies):
- EG: CREUTZFELDT JACKOB DISEASE, GERTSMANN-STRAUSSLER SYNDROME, KURU KURU:
o Aetiology:
§ Prion Infection of the Brain
§ “Prions” = Proteinaceous, Infectious + ‘on’
• = Abnormally folded Host-Proteins that accumulate in the brain
• NO DNA or RNA!! (Important for Exams)
§ Prion Proteins (PrP):
• Normal Form = PrPc (Cellular)
o Normal α-Helix form (Functional & Denaturable)
o Found throughout the body (Also in mammals)
• Abnormal Form = PrPsc (Scrapie)
o Abnormal β-Sheet form (Non-Functional & Non-Denaturable)
o Accumulates in plaques in the brain → Tissue Damage & Cell Death
o EXTREMELY STABLE – Resists denaturation :. Difficult disposal
o Pathogenesis:
§ Prions cause Neurodegenerative Disease by aggregating Extra-Cellularly in the CNS → form
amyloid plaques → Plaques are Internalised → Vacuole formation in Neurons → Spongy
Architecture
§ Accumulation in Neurons → Death of Neurons
§ Propagation: Conversion of Normal Proteins (α-helix → β-sheet):
• Prions propagate by transmitting a Mis-Folded Protein State, not replicating
• Ie: They convert Pre-Existing, Normal forms of the protein to the Abnormal Form

Unattributable
o Morphology:
§ Macro:
• Empty cystic lesions in the brain → Spongiform Encephalopathy
§ Micro:
• Neuronal Vacuolation & Plaque Formation
o Clinical Features:
§ Initially Subtle Memory & Behavioural Changes → Then Rapidly Progressive Dementia
§ Convulsions (Myoclonus)
§ Dementia
§ Ataxia, Dysarthria, Dysphagia, Nystagmus
§ Behavioural/Personality Changes
o Prognosis:
§ All known Prion Diseases affect the Brain and are currently Untreatable & Universally Fatal
§ 7mths life expectancy

Source: https://joelwattslab.org/prions/

Transmission:
- Acquired, Familial, or Sporadic
- Current Theory – Primarily infected through ingestion. Prions may be deposited in the environment through
Animals Carcases, Urine, Saliva, other body fluid; and may linger in the soil.

MICROBIOLOGY: VIRUSES

MICROBIOLOGY: VIRUSES

Virus Nomenclature:
- Virion – A Complete Viral Particle
- Capsid – The Protein Coat made up of smaller structural Subunits (Capsomeres)
- Capsomeres – The Subunits of the Capsid
- Nucleocapsid – The Capsid + Nucleic Acid + Associated Nucleoproteins
- Envelope – Lipid Bilayer of Host-Cell Origin, imbedded with Viral Lipoproteins

https://microbeonline.com/virus/

Properties Distinguishing Viruses from other Microorganisms:
- Acellular
- No Cell Membrane
- No Cytoplasm
- Can have a DNA or RNA Genome (All others only have DNA)
- No Cellular Synthetic Machinery (Metabolically Inert)
- Can Only Replicate in Living Cells

Viral Envelopes - (Construction/Origin/Proteins):
- Origin: Some viruses envelop themselves in a modified piece of host cell membrane (Either the Plasma
Membrane, or Organelle Membranes)
- Construction: This membrane is studded with Viral & Host Proteins. Most enveloped viruses depend on the
envelope for infection.
- Proteins: Viral envelopes are studded with Glycoproteins – Serve to identify and bind to receptor sites on
the host's membrane. The viral envelope then fuses with the host's membrane, allowing the capsid and viral
genome to enter and infect the host.

Emmanuel Boutet, CC BY-SA 2.5 <https://creativecommons.org/licenses/by-sa/2.5>, via Wikimedia Commons
Structural Vs Non-Structural Proteins:
- Structural Proteins:
o Proteins Encoded by a Virus that form Structural Components of the end Viral Particle
- Non-Structural Proteins:
o Proteins Encoded by a Virus, but NOT part of the Viral Particle

Symmetry:
- Helical Symmetry:
o Composed of a single type of capsomere stacked around a central, coiled Nucleic Acid →form a
helical structure
o Results in rod-shaped or filamentous virions: (Short and Rigid, or Long and Flexible)
- Cubic (Icosahedral/Polyhedral) Symmetry:
o Icosahedron = a regular polyhedron with 20 identical equilateral triangular faces
- Spherical Symmetry:
o Membranous envelope forms spherical shape. (Eg. Influenza virus)
- Complex Symmetry:
o Capsid is neither purely helical, nor purely icosahedral, and that may possess extra structures such as
protein tails or a complex outer wall
o Some have a Cubic head bound to a Helical tail, with protruding protein tail fibres that attach to the
host cell and then injecting the viral genome into the cell

Artasensi, A.; Mazzotta, S.; Fumagalli, L. Back to Basics: Choosing the Appropriate Surface
Disinfectant. Antibiotics 2021, 10, 613. https://doi.org/10.3390/antibiotics10060613

Requirements for Viability & Culturing Viruses:
- Viability Requires:
o 1: Must Retain an Intact Protein Coat
§ (Note: Enveloped Viruses are Inactivated by Detergents → Disperses Lipid Bilayer)
o 2: Must Retain an Intact Genome
- Culturing Viruses Requires:
o Living Cells – (Because Viruses lack the cellular machinery for replication)

“Shedding” & Disease:
- Viral Shedding:
o The Successful Reproduction, Expulsion & Host-Cell Infection caused by Virus Progeny
o (Typically Accompanied by Illness/Disease)

- Examples of Shedding Mechanisms:
o Shedding Via Budding:
§ “Budding” through the cell membrane, using it to form the viral Envelope
§ Primarily Enveloped Viruses
o Shedding Via Apoptosis:
§ Forcing cell into Apoptosis → Release of progeny into Extracellular Space within apoptotic
bodies. Macrophages phagocytose the apoptotic bodies → Become Infected
§ Primarily Non-Enveloped Viruses
o Shedding Via Exocytosis:
§ Exocytotic release of Viral Progeny into the Extracellular Space
§ Primarily Non-Enveloped Viruses
o Others:

Egress of non-enveloped enteric RNA viruses, Owusu, Quaye, Passalacqua, et al; Journal of General Virology; DOI:
https://doi.org/10.1099/jgv.0.001557
Innate Immunity Against Viruses:
- ***Interferons (IFNs):
o (Four Major Classes):
§ IFNα – Produced by virally-infected WBCs
§ IFNβ – Produced by virally-infected Fibroblasts
§ IFNγ – Produced by Ag-Stimulated Effector T-Cells (Helper & Cytotoxic)
§ IFNω – Secreted by Embryonic Trophoblasts
o Early, non-specific Anti-Viral Proteins (Particularly IFN-γ)
§ Secreted by Virally Infected Cells to protect nearby cells that haven’t yet been infected
o Mechanism of Action → IFN results in Synthesis of Gene Products:
§ **Ribonuclease:
• Cleaves Viral mRNA → Inhibits Viral Protein Synthesis & Reproduction
• Allows time for Adaptive Immunity to destroy infected cells
§ Nitric Oxide Synthase:
• Prevents viral growth in Macrophages
§ Protein Kinase:
• Prevents Elongation of Viral dsRNA
§ Mx Protein:
• Can inhibit the Transcription & Translation of some viral mRNA
o Also Activates Natural Killer-Cells


- **Natural Killer Cells:
o (Activated by IFN-γ)
o Lyse some Virally-Infected Cells
o Altered/Missing MHC-I → NK cell lyses cell


- **Compliment Activation (Alternate Pathway) & Phagocytosis of Extracellular Viruses:
o C3b opsonisation → Phagocytosis
- Lysozyme:
o (in Tears/Saliva/Mucus/Neutrophils)
o Some viruses are susceptible
- Stomach Acid:
o Denatures some viruses
- Intestinal Enzymes:
o Degrade some viruses

Adaptive Immunity Against Viruses:
- **Helper CD4 T-Cells:
o →Secretion of IFN-γ (→ Further activates NK Cells)
o → Activates Macrophages → Kill intracellular contents
o → Activates CD8-T-Cells → Proliferate
- **Cytotoxic CD8 T-Cells:
o Recognition of Viral Peptide:MHC-I → Cytotoxic Granules line up @ site of cell contact
§ → Apoptosis of Virally Infected Cells
o (also →Secretion of IFN-γ) (→ Further activates NK Cells)


- **Antibodies:
o Antibodies → Neutralise Extracellular Viruses
§ (By Blocking Viral Absorption & causing Agglutination)
o Antibodies → Opsonisation of Virus for Phagocytosis (Macrophages)
o Antibodies → Opsonisation of Virus for Antibody-Dependent Cell-Mediated Cytotoxicity
§ (ADCC – Fc Receptors on Cytotoxic cells bind to Antibody → Lysis of Virus)
o Antibodies + Complement → Opsonisation of Virus for Phagocytosis (Macrophages)
o Antibodies + Complement → Virolysis (NK Cells/Tc-Cells)
o Antibodies + Viral Ags on Cells → Initiate Compliment →CD8-mediated Lysis of infected cell
o Antibodies + Viral Ags on Cells → Cell-Mediated Cytotoxicity → Lysis of infected cell

Neutralisation

Opsonisation

Agglutination

Antibody-dependent cell-mediated cytotoxicity (ADCC)


- Activated Macrophages:
o (Via CD4 T-Helper Cells)
o → Phagocytosis & destruction of Extracellular Viruses

Latency (Recurrence & Recrudescence):
- Latency = The Ability of a Pathogenic Virus to lie Dormant within a cell
- Virus Production Ceases:
o NO active Viral Shedding
o NO Pathologies/Symptoms
- However, Latency is still an Active Process:
o Maintaining latency requires expression of viral genes which may function to:
§ Keep the viral genome from being digested by cellular Ribozymes
§ Downregulate MHC-I to hide from the immune system
§ Inhibit Apoptosis
§ Induce Cell Growth/Division
- 2 Types of Latency:
o Episomal Latency:
§ Viral genes are left floating in the Cytoplasm or Nucleus
§ (Eg: Herpes Virus)
o Proviral Latency:
§ Virus genome Integrates into the Host Genome → Becomes a Provirus
§ (Eg: HIV)
- Reactivation/Recrudescence:
o A Latent Virus can Reactivate
o Triggers include Stress, Sunlight
Classification of Viruses:
- The ICTV Classification:
o Family (“-viridae”)
§ Genus (“-virus”)
• Species
o (Ie: Binomial Nomenclature isn’t used)
- The Baltimore Classification:
o (7 Groups of viruses based on DNA/RNA, Strandedness (Single/double), Sense/Nonsense, & Method
of Replication)
o 1: dsDNA Viruses (double-stranded DNA Viruses)
§ Eg: Herpesvirus, Poxvirus, Adenovirus
o 2: ssDNA Viruses (single-stranded DNA Viruses)
§ Eg: Parvovirus
o 3: dsRNA Viruses (double-stranded RNA Viruses)
§ Eg: Reovirus
o 4: (+)ssRNA Viruses (positive [sense] single-stranded RNA Viruses)
§ Eg: Picornavirus, Togavirus
o 5: (-)ssRNA Viruses (negative [nonsense] single-stranded RNA Viruses)
§ Eg: Orthomyxovirus, Rhabdovirus
o 6: ssRNA-RT Viruses (single-stranded RNA Reverse Transcriptase Viruses)
§ Eg: Retroviruses (HIV)
o 7: dsDNA-RT Viruses (double-stranded DNA Reverse Transcriptase Viruses)
§ Eg: Hepadnavirus (Hep-B Virus)

Revision of DNA Replication/Transcription/Translation & Enzymes (For Viral Replication Cycles):
- DNA Replication:
o DNA Replication DNA → DNA (Via DNA Polymerase)


- Protein Synthesis:
o 1: Transcription: DNA → mRNA (Via RNA Polymerase)
§ mRNA Exits the Nucleus → Cytosol
o 2: Translation: mRNA → Protein (Via Ribosomes)
§ Occurs in the Cytosol

Public Domain: https://www.cancer.gov/publications/dictionaries/genetics-dictionary/def/transcription

- Enzymes: (Host Enzymes) (Viral Enzymes):
o DNA Polymerase – Synthesizes new DNA from DNA
o (DNA-Dependent) RNA Polymerase – Synthesizes mRNA from DNA
o RNA-Dependent RNA Polymerase (Transcriptase) – Synthesizes new mRNA from mRNA
o RNA-Dependent DNA Polymerase (Reverse Transcriptase) – Converts mRNA back to dsDNA
o Retroviral Integrase – Allows viral DNA to be integrated into the DNA
Viral Replication Cycles:
- 1: dsDNA Viruses (double-stranded DNA Viruses)
o Eg: Herpesvirus, Poxvirus, Adenovirus
o Replication Features: (In the Nucleus (As with all DNA Viruses))
§ Requires Host-Cell DNA Polymerase (& hence Host-Cell Division) to Replicate its Genome
§ Also Requires Host-Cell RNA Polymerase to transcribe dsDNA → mRNA for Protein Synthesis

Public Domain: https://www.ogtr.gov.au/sites/default/files/2021-06/dir180-
full_risk_assessment_and_risk_management_plan.pdf

- 2: ssDNA Viruses (single-stranded DNA Viruses)
o Eg: Parvovirus
o Replication
o Replication Features: (In the Nucleus (As with all DNA Viruses))
§ Requires Host-Cell DNA Polymerase (& hence Host-Cell Division) to form a dsDNA
Intermediate & Replicate its Genome

Human Parvovirus B19: https://www.researchgate.net/figure/Schematic-life-cycle-of-B19_fig3_11279270
- 3: dsRNA Viruses (double-stranded RNA Viruses)
o Eg: Reovirus
o Replication Features: (In the Cytoplasm (As with all RNA Viruses))
§ Supplies its Own RNA-dependent-RNA-Polymerase for RNA Replication
• (As opposed to RNA Polymerase which transcribes DNA → RNA)
§ Have Segmented Genomes – each gene codes for 1x protein

Source: https://www.researchgate.net/figure/The-reovirus-replication-cycle-VI-viral-inclusions-ER-endoplasmic-
reticulum_fig1_331945223

- 4: (+)ssRNA Viruses (positive [sense] single-stranded RNA Viruses)
o Eg: Picornavirus, Togavirus
§ Supplies its Own RNA-dependent-RNA-Polymerase for RNA Replication
§ Directly access Host Ribosomes → Viral Poly-Protein Synthesis
• Poly-Proteins are cleaved to form multiple different proteins

Unattributable

- 5: (-)ssRNA Viruses (negative [nonsense] single-stranded RNA Viruses)
o Eg: Orthomyxovirus, Rhabdovirus
§ Can’t directly access Host Ribosomes – Because it is a Nonsense Strand
§ Must first use its Own RNA-dependent-RNA-Polymerase to transcribe a Positive (Sense)
Strand
§ Positive Strand → Accesses Ribosomes → Viral Poly-Protein Synthesis
• Poly-Proteins are cleaved to form multiple different proteins

http://geb.uni-giessen.de/geb/volltexte/2017/13103/pdf/JankauskaiteLina_2017_08_17.pdf

- 6: ssRNA-RT Viruses (single-stranded RNA Reverse Transcriptase Viruses)
o Eg: Retroviruses (HIV)
o Replication Features: (In the Cytoplasm AND the Nucleus)
§ Instead of using the +ssRNA to make proteins, it converts the +ssRNA → dsDNA via Reverse
Transcriptase
§ The resulting DNA is spliced into the Host Genome using Integrase
§ Replication & Protein Synthesis then comes from the viral DNA in the Nucleus

https://clinicalinfo.hiv.gov/en/glossary/binding

- 7: dsDNA-RT Viruses (double-stranded DNA Reverse Transcriptase Viruses)
o Eg: Hepadnavirus (Hep-B Virus)
o Replication Features: (In the Cytoplasm AND the Nucleus)
§ Genome is a ‘covalently closed circle’ (cccDNA) → Nucleus
• →Transcribed to mRNA (Via RNA-Polymerase)
§ mRNA exits Nucleus → Protein Synthesized In Cytoplasm
§ Then, Reverse Transcriptase converts the mRNA Back to DNA → cccDNA

https://sums.ac.ir/page-gehrcen/en/408/article/717-G118/blk-tool_article_sample_gehrcen_block44970

Unattributable

Viral Assembly:
- Assembly = When all of the components of the virus are assembled into a particle
o Occurs when an appropriate concentration Of Virus Proteins & Nucleic Material is reached
o (Note: Some particles self-assemble)

Viral Maturation:
- Maturation = Stage in the Virus Life-Cycle when it becomes infectious
o Involves proteolytic cleavage of capsid or envelope poly-proteins into functional proteins

Targets for Antiviral Therapies:
- 1: Attachment
- 2: Penetration
- 3: Uncoating
- 4: Replication
- 5: Assembly
- 6: Maturation
- 7: Release

Quasispecies:
- A substrain of an organism that develops in an individual by the process of evolutionary selection

MICROBIOLOGY: PARASITES

MICROBIOLOGY: PARASITES

General Features:
- Live at the expense of their host → Acquires Nutrients/Other Benefits without Reciprocal Benefits
- Complex Life-Cycle involving 2 or More Hosts (Definitive Host & Intermediate Host/s)
- Are Successful if:
o Produces minimal disturbance
o Not regarded by host as foreign
- Parasite infections tend to be Long-Term (As opposed to Bacteria/Viruses)
- Many make use of the Host’s growth-factors to promote their own growth
- (Including Protozoa, Metazoa [Helminths/Worms] & Arthropods):

Hosts (Definitive Vs Intermediate):
- Definitive Host:
o - Harbours the Mature, Adult Form of the Parasite
- Intermediate Host:
o - Harbours the Immature, Larval Form of the Parasite

Grouping: Protozoan Vs Metazoan:
- Protozoan Parasites:
o (Single-Celled Parasites)
o 3 Categories of Locomotion:
§ Amoeba – (Move by Crawling) (Eg: Entamoeba Histolytica)

§ Ciliate – (Move by Swimming – via cilia) (Eg: Balantidium Coli)

§ Flagellate – (Move by Swimming – Via Flagella) (Eg: Giardia Lamblia)

§ (Sporozoa) – (No motile structures) (Eg: Plasmodium Malariae; Toxoplasma)

https://www.britannica.com/science/Eimeria

- Metazoan Parasites – (Helminths & Arthropods):
o (Multi-Celled Parasites)
o Helminths:
§ 3 ‘Phyla’:
• Platyhelminthes (Flat worms)
o Trematodes (Flukes)
o Cestodes (Tapeworms)
• Nematoda (Round Worms)
• Acanthocephala (Spiny-headed worms)
o Arthropods: (Animals with segmented bodies, exoskeletons and jointed appendages)

Routes of Entry of Helminths:

Unattributable

Immune Evasion Strategies:
o Antigenic Variation
o Antigenic Drift
o Molecular Mimicry (Expression of Host Proteins)
o Intracellular Localisation
o Self-Isolation in Membrane-bound Vesicle
o Prevent fusion of lysosomes with phagosomes
o Sequestration in privileged sites
o Regulation of host functions
- Helminth Parasites:
o Antigen Shedding
o Protease production → Neutralise some immune components (Eg: Antibodies)
o Superoxide Dismutase → Neutralise Respiratory Burst by Neutrophils
o Regulation of host functions (Immunosuppression/Maladaptive Response)
o Skew the T-Helper Response to Favour Th1-Cells:
§ Favouring Th1→ Reduced class-switching to IgE, the AntiParasitic Ab
o Use Host Cytokines as Parasitic Growth Factors

Immunity Against Parasites:
- Innate Immunity:
o Lysozyme:
§ (in Tears/Saliva/Mucus/Neutrophils)
§ Some parasites are susceptible
o Eosinophils (Eosinophil Granulocytes):
§ Combat multicellular Parasites
§ Degranulate → Release Reactive Oxygen Species → to kill parasites
o Complement Activation:
§ By Alternate Pathway – Complement Activation by Binding to Pathogen Surface
§ By MB-Lectin Pathway – Complement Activation by Binding to Lectin on Pathogen Surface
§ (Note: Classical Pathway is Adaptive – Complement Activation by Ab’s on Pathogen Surface)
o Phagocytes in Spleen:
§ Infected RBCs express specific Parasite Antigens which are opsonised by
antibody/complement → Recognised & Removed by Phagocytes in the Spleen
- Adaptive Immunity:
o Antibodies (B-Cells):
§ Typically for Extracellular Infections (in blood/Tissues)
§ IgE is the Major Isotype (Important in eliminating many helminth infections)
• → (Hence, many infections are associated with Type-1 Hypersensitivity reactions)
o →Oedema, Asthma, Urticaria
§ - Can destroy Tachyzoites (young parasites) in blood
§ - Can neutralise Proteases used by parasites to enter tissues
§ - Can block ‘Anal Pores’ of parasites
§ - Can block enzyme pathways of some helminths (Can arrest egg production)
§ (Note: However, Many parasites are unaffected by antibodies)
o Complement Activation (By Classical Pathway):
§ Complement Activation by Ab’s on Pathogen Surface
§ - Can destroy Tachyzoites (young parasites) in blood
o Cell-Mediated:
§ Typically for Intracellular Infections
§ Th1-Cells Activate Macrophages:
• Macrophages become more Phagocytic and Destroy Intracellular Parasites
• (Note: Typically only Protozoan parasites are small enough to live intracellularly)
§ Th2-Cells Help B-Cells produce Antibodies:
• (Th2 is the predominant response)
§ Tc-Cells Destroy Infected Cells:
• May also directly destroy larvae
o Eosinophils:
§ Note: They are the MAIN Effector Cell against Helminth Infections
§ Activated by:
• Th-Cells (IL-5) & Macrophages (TNF-α, IFN-β, IL-3)
• → Increased Adherence & Degranulation Cytotoxicity

§ Eosinophils have Fc receptors (Allow binding to Parasites covered with IgE-Antibodies)
• Binding of Antigen to Eosinophil-Bound-IgE → Degranulation
• Similar to Mast Cells:

§ Release Granules onto the worm:
• *Major Basic Protein (Damages Cuticle of Helminths)
• Eosinophil-Cationic Protein (A Ribonuclease – Toxic to Helminths)
• Lysophospholipase
• Phospholipase D
§ Respiratory Burst:
• Superoxide
• Chloride Ions
• Hydrogen Peroxide
• Similar to Neutrophils:

Immune Evasion by Parasites:
- Resistance to Immune Effector Mechanisms:
o Eg: Molecular Mimicry:
§ Eg: Expression of Host-Proteins:
• Eg: Some Schistosomes cover themselves with Host Proteins (Eg: Blood-Group
Antigens & MHC products)
o → Avoids Recognition by Effector Immune Mechanisms
o Eg: Protease Production to Neutralise Anti-Parasite Immune Components:
§ Eg: Shistosomula (Helminth) Produces Proteases → Cleave Antibodies
• They also Inhibit Macrophage Function
§ Host Proteases may be Inactivated by Protease Inhibitors

- Immunosuppression or Inappropriate Immune Responses:
o Eg: Helminths – Secrete Soluble Immunosuppressant Factors:
§ →Inhibit Lymphocyte Function
§ →Inhibit Mast-Cell Degranulation

- Sheltering in Immune-Privileged Sites:
o Eg: RBCs:
§ Plasmodium Falciparum (Malaria) – lives inside RBCs which don’t express MHC-I:
• → Can’t be recognised by CD8-T-Cells
• → Are Shielded from Antibodies
§ However, Infected RBCs Can be recognised/destroyed in the spleen:
• To avoid this, Malaria Parasites cause the RBCs to become Sticky →
• RBCs adhere to endothelium in peripheral organs
• (Note: Can lead to peripheral vasculopathies & ischaemic organ failure)

- Exploiting The Immune System to Aid in Life-Cycle:
o Eg: Some Helminths Exploit the Increased Expression of Cell-Adhesion-Molecules in Inflammation:
§ Eg: Helminths which lay eggs need to get the eggs out of the Blood Vessels
• Therefore, by causing Inflammation, Endothelial Cells Increase CAM Expression
• → Eggs use these Adhesion Molecules to adhere to the Endothelium
• → They then secrete Collagenases/Elastases/Proteases → to Exit the Blood Vessel

Parasite Replication Cycles:
o Trophozoite Stage: (“Tropho” = Feeding)
§ Infective, Proliferative Stage – Lives in the definitive host
§ Trophozoites Actively Feed
§ Protozoa can reproduce by Fission, Sexual Reproduction, or be Hermaphroditic
§ Encystation = Conversion of Trophozoite → Cyst
o Cysts Stage:
§ Hardy, thick-walled spore able to survive for lengthy periods outside a host (Organisms that
create oocysts include Cryptosporidium and Toxoplasma)
• Resistant to heat, harmful chemicals
• Can survive without access to nutrients, water, or oxygen
§ Often shed in the faeces (Eg: Giardia)
§ Excystation = Conversion of Cyst → Trophozoite

- Metazoan Parasites: (Platyhelminthes, Nematodes & Acanthocephala)
o Platyhelminthes:
§ Trematodes (Flukes):
• The Eggs of Trematodes (Flukes) pass out in the Faeces, develop into larvae, which
MUST PASS THROUGH THE SNAIL (Intermediate Host) and develop into Cercaria
before the parasite is again infective to humans

Clinical use of chistosoma mansoni antigens as novel immunotherapies for autoimmune disorders; Cleenewerk,
Garssen & Hogenkamp; DOI: https://doi.org/10.3389/fimmu.2020.01821
§ Cestodes (Tapeworms):
• Cysts are shed in Human Faeces → Grass → Eaten by Cow or Pig (Intermediate
Hosts). Humans are infected by eating Contaminated Beef. Adult worm attaches to
SI-Mucosa.

https://medical-dictionary.thefreedictionary.com/tapeworm

o Nematodes (Round worms):
§ Intestinal Nematodes:
• Direct Life-cycle (Horizontal Transmission Without Intermediate Hosts)
• Faecal Oral – Eggs in Faeces → Ingested → Hatch in SI → Burrow into Bloodstream →
Exit blood in lungs → Pass up the Trachea & are Swallowed → Adults mature in Small
Intestine

Public Domain: CDC
§ Filarial Nematodes:
• Microfilariae in the blood are infective to Mosquitoes → Pass on the infection to
other people
• Most Common = Wuchereria Bancrofti → Lymphatic Filariasis & Elephantiasis

Public Domain: CDC

o Acanthocephala:
§ (A Phylum of parasitic worms known as Thorny-headed/Spiny-Headed Worms)
§ Complex Life-Cycles involving a number of hosts:
• Embryo is released in faeces → Ingested by a Crustacean (Eg: A Mollusc) (the
Intermediate Host) → Encystation occurs → Intermediate Host is Ingested by the
Definitive Host → Excystation in the gut → Reproduction

Public Domain: CDC

MICROBIOLOGY: BACTERIA

MICROBIOLOGY: BACTERIA

Structure of the Bacterial Cell:
- Prokaryotic
- Single-Celled Organisms
- DNA Based Genome, but No Distinct Nucleus (Circular Chromosome)
- 3 Layers:
o Plasma Membrane
o A Thick Cell Wall covers the Plasma Membrane (Composition depends on Gram -/+)
§ Gram Positive:
• Thick Peptidoglycan Layer
• & Teichoic Acid
§ Gram Negative:
• Primarily Lipid-Based (Including Lipopolysaccharide – LPS)
• (+Thin Peptidoglycan Layer)
o A Polysaccharide Capsule covers the Cell Wall (Considered a Virulence Factor – Resists Phagocytosis,
Detergents & Dehydration)
- Pili/Fimbriae:
o For Adherence to Cells or Other Bacteria
- Flagellum:
o For Mobility


Taxonomy & Classification:
- Uses a ‘Binomial Nomenclature’ – (Genus + Species):
o Genus = Eg: Staphylococcus
o Species = Eg: Aureus
o (Staphylococcus Aureus)

Classification of Bacteria:
- Staining of Cell Wall Structure:
o Gram Stain:
§ Gram Positive:
• (Stain Blue/Purple)
• Thick Peptidoglycan Layer
o (The Site of Action of β-Lactam Antibiotics)
• & Teichoic Acid
§ Gram Negative:
• (Stain Pink/Red)
• Primarily Lipid-Based (Including Lipopolysaccharide – LPS)
o (Note: LPS = Endotoxin; can → Septic Shock)
• (+ ‘Lipid A’ = Endotoxin; can →Septic Shock)
• (+Thin Peptidoglycan Layer)


o Acid-Fast Stain:
§ (Eg: Mycobacterium Tuberculosis)
§ Doesn’t Stain with Gram
§ Similar Cell-Wall to Gram + Bacteria, but different type of Peptidoglycan
§ Stains with the “Ziehl Neelsen Stain” (‘Acid-Fast Stain’)
• “Acid-Fast” Bacilli stain bright red in contrast to a blue background

CoRus13, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons
- Respiration:
o Aerobic Vs Anaerobic

- Cellular Morphology (Shape):


- Grouping:
o Single
o Pairs (Diplo-)
o Chains (Strepto-)
o Clusters (Staphylo-)

LadyofHats, Public domain, via Wikimedia Commons

Immunity Against Bacteria:
- Innate Immunity:
o **Phagocytosis:
§ By Macrophages/Dendritic Cells/Neutrophils
§ May be Independent, Antibody or Complement Mediated


o *Lysozyme:
§ An Antibacterial enzyme dissolved in bodily secretions (Tears/Saliva/Mucus/Neutrophils)
§ → Splits the Cell Wall Proteoglycans of Bacteria → Lysis
o **Complement Activation – Via Alternative Pathway:
§ →Phagocytosis: C3b opsonisation → Phagocytosis of Bacteria
§ →Lysis: Membrane attack complex formation → Lysis of Bacteria

o **Neutrophils:
§ → Phagocytosis: Neutrophils ingest & kill many Microbes
§ → “Respiratory Burst”: Binding of Fc-portion of Antibodies on opsonised Bacteria stimulate
production of Highly Oxidative Molecules which kills the bacteria

§ → Bactericidal Granules:

o Local Inflammation – (Due to Cytokine Release after Macrophage Phagocytosis):
§ →Local Inflammation
§ →Fever
§ →Acute Phase Proteins
o Acute Phase Proteins:
§ (C-Reactive Protein [CRP], Mannose-Binding Lectin [MBL])
§ Both are:
• Opsonising Agent for microbes → Phagocytosis (Similar action to Antibodies –
except have broad specificity for PAMPs)
• Complement Activators → Activate the Classical (CRP)/Lectin (MBL) Pathways of
the Complement Cascade
- Adaptive Immunity:
o **Antibodies – (Produced by B-Cells):
§ → Exotoxin Neutralisation:
• IgG is Entirely Responsible for this
• IgG essentially competes with the receptor for the toxin → Prevents binding to
cellular target
§ → Endotoxin Opsonisation:
• Fc-Receptor-Mediated Phagocytosis
§ → Bacteriolysis

Neutralisation

Opsonisation

Agglutination

Antibody-dependent cell-mediated cytotoxicity (ADCC)


o CD4-T-Helper Cells:
§ → Activate Macrophages:
• → Destruction of Phagocytosed Bacteria
§ → Activate B-Cells:
• → Secretion of Antibodies


o CD8-T-Cytotoxic Cells → Kill Infected Cells:
§ Infected Cells displaying bacterial peptide on MHC-I are lysed by Perforins released by
Cytotoxic CD8-T-Cells

Bacterial Virulence Factors:
- Molecules Expressed/Secreted by Pathogens that enable them to achieve the following:
o Colonization of a Niche in the host (this includes adhesion to cells)
o Immunoevasion, evasion of the host's immune response
o Immunosuppression, inhibition of the host's immune response
o Entry into & Exit out of cells (if the pathogen is an intracellular one)
o Obtain nutrition from the host
- Eg: Endotoxins – (In the Walls of Gram Negative Bacteria) → Septic Shock:
o (Note: Recognised by Toll-Like Receptors on Macrophages → Cytokines)
o ***Lipopolysaccharide (LPS)
o Surface Array Proteins (Eg: Enzymes)
o Flagellum
o Adhesion Pili
o Capsule Antigens
o Cell Wall Antigens
o Cell Membrane
- Eg: Exotoxins – (Toxic Molecules Released by the Bacteria) → Toxic Shock:
o Eg: Tetani Toxin
o Eg: Staph → Superantigen

- Eg: Ig-Proteases (Eg: Strep Pyogenes) → Break down Antibodies
- Eg: Capsules (Eg: Bacterial cell walls) → Inhibits Phagocytosis

Bacterial Immune Evasion Strategies:
- Antigenic Variation
- Inhibition of Complement Activation
- Resistance to Phagocytosis
- Produce Superoxide Dismutase → Scavenge Free Radicals from respiratory burst of Neutrophils
- Intracellular bacterial evasion:
o Travel b/w cells without being exposed to extracellular fluid
o Escape into vacuole in the cytoplasm
o Prevent fusion of lysosomes with phagosomes
- Depress cellular immunity
- Superantigens → Inappropriate Immune Response

Pathological Consequences - Damage due to:
- Exotoxins:
o = Toxins Secreted from the Bacteria into the system
§ (:. Organisms need not be invasive to produce illness)
o Typically from Gram Positive bacteria
§ Eg: Botulinum Toxin
§ Eg: Tetanus Toxin
o Toxic Shock Syndrome:
§ Some bacteria produce Superantigens → Widespread, Non-Specific activation of Th-Cells →
Massive secretion of Pro-Inflammatory Cytokines → Massive Vasodilation/↑Capillary
Permeability/Hypotension → Toxic Shock Syndrome
• – High Fever
• – Hypotension
• – Potential Multi-Organ Failure → Death
- Endotoxins:
o = Structural (Cell-Wall) Components of the Bacteria that are Antigenic
§ They are Not Secreted and are Not Directly Toxic
§ They are released into the system during Lysis/Death of Gram Negative Bacteria
o Typically from Gram Negative bacteria
§ Eg: Lipopolysaccharide (LPS)
o Septic Shock:
§ Bacteraemia & :. ↑LPS → LPS binds to TLR-4 on Macrophages & Dendritic Cells → Secretion
of Pro-Inflammatory Cytokines & Nitric Oxide → Massive Vasodilation/↑Capillary
Permeability/Hypotension → Septic Shock
• – Fever
• – Tachypnea
• – Tachycardia
• – Hypotension
• – Potential Multi-Organ Failure → Death
- Hypersensitivity Reactions:
o Due to immune response

The Difference between Septic Shock and Toxic Shock:
- Septic Shock:
o From Gram Negative Bacteria
o (Mediated by Liberated Endotoxin from dead organisms – LPS (Lipid A = the toxic part of LPS) →
Directly Activates CD14 & TLR-4 on Macrophages → Cytokine Storm (including IL-1, IL-6, IL-8, TNF-
alpha and PAF) → Shock)
o – Therefore shouldn’t be treated by Bacteriocidals (As they would liberate more Endotoxin)
o Note: Septic Shock can be fatal even after Antibiotic Treatment. Explain why?:
§ 1: If the Antibiotics were Bactericidal, they will liberate more Endotoxin from lysed bacteria
and further exacerbate the septic shock → Death
• :. In Septic Shock, Bacteriostatic Antibiotics are most useful, as they slow bacterial
growth without lysing them
§ 2: Conversely: If the shock is in the irreversible stage, no amount of antibiotics (Even
bacteriostatic) will do any good (As there is irreversible organ failure)

- Toxic Shock: (Eg: From Staph/Strep)
o From Gram Positive Bacteria (Don’t contain Endotoxin – Cell walls are primarily Peptidoglycan)
§ (Mediated by Superantigens secreted from live organisms → Widespread non-specific MHC-
II:TCR interaction → Widespread CD4-T-Cell activation → Stimulates macrophages by γ-IFN
→ Cytokine Storm (including IL-1, IL-6, IL-8, TNF-alpha and PAF) → Shock)
o – Therefore should be treated by bacteriocidals (Don’t need to worry about Endotoxin)

Antibiotic Susceptibility:
- Selective Toxicity:
o Critical to Efficacy & Safety of Anti-Microbials
o Exploits Differences in Cell Biology between Host & Pathogen Cells
o Aim → Kill only the Pathogen Cells

- Antibiotic Action: Key Steps:
o 1: Active drug (Ie: The metabolically active form)
o 2: Present at site of infection
o 3: Bind to bacterial cell surface; X
o 4: Uptake into bacterial cell; X
o 5: Bind to target – molecular interaction with bacterial cell components; X
o 6: Lysis and death or growth inhibition of bacterial cell; X
§ (X = steps where bacterial activity leads to resistance)

- Classification of Antibiotics:
o 1: Bactericidal or bacteriostatic:
§ Bactericidal →kill bacteria (Ie: Makes the organism unviable)
§ Bacteriostatic →inhibit growth → Host defences kill static population
§ Note: Some agents can be both -Eg: chloramphenicol with E-coli and Haemophilus
o 2: Target site:
§ Cell wall synthesis
• Beta lactams
• Glycopeptides
§ Protein synthesis
• Aminoglycosides
• Tetracyclines
• Macrolides
§ Nucleic acid synthesis
• Quinolones
• Folic Acid Pathway:
o Sulphonamides
o Trimethoprim
§ Cell membrane function
• Polymixins
• Colistin
o 3: Chemical structure
§ Beta lactams
§ Glycopeptides
§ Aminoglycosides
§ Tetracyclines
§ Macrolides
§ Quinolones
§ Sulphonamides
§ Trimethoprim

ANTIBACTERIAL DRUG CLASSES:

- 1: Anti Cell-Wall Synthesis Antibiotics – (Bactericidal):
o Target Peptidoglycan Synthesis on Gram-Positive Bacteria

Classical Agents: Common Uses: Mechanism of Action: Side Effects:
β-Lactam Antibiotics:
Penicillins: Gram Positive Bacteria Block “Penicillin-Binding Proteins” GI Upset & Diarrhoea
Penicillins ‘G’ & ‘V’ (Note: Bacteria (Enzymes) →Inhibit Synthesis of the Allergic Rash
Amoxicillin & Ampicillin Producing β-Lactamase Peptidoglycan Layer of the Bacterial Anaphylaxis (Need
Flucloxacillin are resistant) Cell Wall. Adrenaline Handy)
Methicillin
Ticarcillin (Note: Fluclox – for β-
(Suffix = “-Cillin”) Lactamase Resistant)
Cephalosporins: (Note: Cephalosporins (As above)
(Ceftriaxone) – for Non-β-Lactamase + Mild Renal Toxicity
Resistant)
β-Lactamase (In Combination with Inhibits β-Lactamase → Allows β- Nausea/Vom/Diarr
Inhibitors: Penicillins) for Lactams to work on Penicillin- Allergy
Augmentin Penicillin-Resistant Resistant Bacteria.
Gram Positive Bacterial
Infections
Glycopeptide Antibiotics:
Vancomycin Gram Positive Bacteria Prevents incorporation of specific Local Pain
Teicoplanin (As a LAST RESORT for Peptide Subunits into the Phlebitis (Vein Inflam)
Telavancin MRSA) Peptidoglycan Layer of the Bacterial Kidney Damage
(Also if Pt. is allergic to Cell Wall. Hearing Loss
β-Lactams)

- 2: Anti Protein-Synthesis Antibiotics – (Bacteriostatic):
o Exploits differences between Eukaryotic (Human) Ribosomes & Prokaryotic Ribosomes
o Selective Toxicity – Due to specific binding to Prokaryotic Ribosomes
o Note: Aminoglycosides are Solely eliminated by the Kidneys & Are Nephrotoxic (Need to assess
renal function first, then Dose Accordingly)

Aminoglycoside Antibiotics:
Gentamicin Gram Negative Bacteria Bind Specifically to Prokaryotic Ototoxic (Hearing
Streptomycin (Used Synergistically Ribosomal Subunits → Causes Loss & Vertigo)
Tobramycin with β-Lactams to ↑ Misreading of mRNA → Inhibits Nephrotoxic (Kidney
drug entry into Synthesis of Proteins vital to Damage)
Bacteria) Bacteria.
Tetracycline Antibiotics:
Doxycycline Gram Negative Bacteria Bind Specifically to Prokaryotic Nausea/Vom/Diarr.
Tetracycline Syphilis (G-), Chlamydia Ribosomal Subunits → Inhibits Photosensitivity
- -
(Suffix = ‘Cycline’) (G ), Lyme Disease (G ) Binding of tRNA to mRNA → Inhibits Staining of Teeth
(And Malaria - Synthesis of Proteins vital to Renal/Liver Toxicity.
Protozoa) Bacteria.
Macrolides:
Erythromycin, Gram Negative Bacteria Bind Specifically to Prokaryotic Nausea/Vom/Diarr.
Azithromycin Syphilis, Lyme Disease. Ribosomal Subunits →Inhibits Jaundice
release of tRNA → Inhibits Synthesis
of Proteins vital to Bacteria.

- 3: Anti Nucleic-Acid Synthesis Antibiotics – (Bacteriostatic):
o Exploits differences in the Metabolic Pathways of DNA Synthesis – (Humans rely solely on Dietary
Folate, while Bacteria have to make their own):
§ Eg: Competitive Inhibition of Dihydropteroate-Synthase, a key Enzyme involved in Folate
Synthesis in Bacteria
§ Eg: Competitive Inhibition of Dihydrofolate-Reductase, a key Enzyme involved in Folate
Synthesis in Bacteria (Note: Humans share this pathway, but bacteria require it 100x more
than humans)
§ Eg: Inhibition of Bacterial DNA Gyrase/Topoisomerase → Stops DNA
Replication/Transcription

Sulphonamides:
Sulfasalazine Urinary Tract Infections Competitive inhibition of Nausea/Vom/Diarr
(Prefix = “Sulfa”) Dihydropteroate-Synthase, a key Allergy
Enzyme involved in Folate Synthesis. Precipitation in Urine
(Folate is necessary for Nucleic Acid –Kidney Failure
Synthesis → & Hence DNA Synthesis. Leukopenia
Photosensitivity
Trimethoprim:
Trimethoprim Urinary Tract Infections Competitive inhibition of Nausea/Vom/Diarr
Dihydrofolate-Reductase, a key Allergy
Enzyme involved in Folate Synthesis. Precipitation in Urine
(Folate is necessary for Nucleic Acid –Kidney Failure
Synthesis → & Hence DNA Synthesis. Leukopenia
Photosensitivity
(BIRTH DEFECTS)
Quinolones:
Ciprofloxacin Urinary Tract Infections Inhibits bacterial DNA Gyrase or Nausea/Vom/Diarr
Norfloxacin Community Acquired Topoisomerase → Inhibits DNA Allergy
(Suffix = “Floxacin”) Pneumonia Replication & Transcription.
Bacterial Diarrhoea
Gonorrhoea

- 4: Antimycobacterial Drugs:
o 2 Main Types of Mycobacterial Diseases:
§ Tuberculosis
§ Leprosy
o Why are they a Problem?
§ Because Mycobacteria can live inside Macrophages following Phagocytosis
§ Also, Multi-Drug-Resistant strains are on the rise
o Compound Drug Therapy:
§ A frequent strategy to decrease the probability of the emergence of resistant organisms
§ Also requires Long-Term Therapy

Isoniazid:
Isoniazid Combination MOA unknown. Allergic Skin
Treatment of M. (Bacteriostatic & Bactericidal) Eruptions
Tuberculosis Fever
Hepatotoxicity
Haemolysis (in G6PD
Deficiency)
Rifampicin:
Rifampicin Combination Binds to & Inhibits DNA-Dependent Allergic Skin
Treatment of M. Prokaryotic RNA-Polymerase → Eruptions
Tuberculosis Inhibits DNA Transcription & Fever
therefore Inhibits Protein Synthesis. Hepatotoxicity
(Bacteriostatic & Bactericidal)
Ethambutol:
Ethambutol Combination MOA Unknown. Optic Neuritis
Treatment of M. (Bacteriostatic) Visual Disturbances
Tuberculosis Colour Blindness.
Pyrazinamide:
Pyrazinamide Combination Active in Low pH–(In Gout
Treatment of M. Phagolysosomes) GI Upset
Tuberculosis (Bacteriostatic) Hepatotoxicity

- Antibiotic Resistance:
o = “Bacteria Isn’t Inhibited/Killed by an Antibacterial @ Normal Dosage Concentrations”
o Note: Bacterial “Resistance Genes” exist, and Mutation Potential is HIGH!
§ (Due to huge numbers of rapidly proliferating bacteria)
o Antibiotic Usage Preferentially Selects these resistant strains → Transmission of “Resistance Genes”
to offspring
o THEREFORE – “Restraint of antimicrobial use is the best way to ensure their efficacy”

- Categories of Organism Susceptibility:
o Susceptible:
§ Patient is likely to respond to treatment with that Antibiotic @ Normal Doses
§ (Ie: Organism is Killed/Inhibited by the drug @ Normal Doses)
o Resistant:
§ Patient NOT likely to respond to treatment with that Antibiotic @ Normal Doses
§ (Ie: Organism NOT Killed/Inhibited by the drug @ Normal Doses)
o Intermediate:
§ Higher Doses are Needed to ensure treatment success

- Intrinsic Vs Acquired Resistance:
o 1: Intrinsic resistance
§ Normal genetic, structural or physiologic state -lack target site or impermeable to agent
§ Predictable within genus or species
§ Eg: All Gram Neg bacilli are intrinsically resistant to Vancomycin
§ Eg: Bacteria secreting β-Lactamase are resistant to β-Lactams
o 2:Acquired resistance
§ Changes in usual genetic state of bacteria > altered cellular physiology or structural changes
§ Unpredictable > why laboratory methods are necessary to detect resistance
§ Resistance arises from:
• 1) chromosomal mutation
• 2) transmissible plasmids
• 3) Combination of mutation and gene transfer events
§ Multiple mechanisms may exist in 1 organism

This is why you need to test for resistance to ensure efficacy of drugs

- Common Resistant Organisms:
o MRSA:
§ (Methicillin Resistant Staphylococcus Aureus)
§ Due to an alteration in PBP (Penicillin binding protein) in cell wall
§ Also produce β-Lactamase (therefore resistant to all β-lactams, including β-lactamase
Inhibitors)
§ Nosocomial (hospital) strains – Typically Multi-Resistant
§ Community Acquired – Typically not Multi-Resistant
o VRE:
§ (Vancomycin resistant Enterococci)
§ Due to altered Target Site
§ 2 Types:
• Van A – Resistant to both Vancomycin And Teicoplanin
• Van B – Just resistant to Vancomycin
o VISA:
§ (Vancomycin Intermediate/Resistant Staph Aureus)
§ Have Thick Cell walls → Trap Vancomycin
§ Very difficult to detect
o ESBL:
§ (Extended Spectrum Beta Lactamase)
§ Resistance due to β-Lactamase enzymes
• → Hydrolyse β-lactam ring → Inactivate β-Lactam Antibiotics
§ Now many ESBLs exist → influence affinity for β-Lactams
o MDR-GNote:
§ (Multi Drug Resistant Gram Negative bacilli)
§ Resistant to all commonly used antibiotics → limited treatment options

Bacteraemia & Intravascular Infection

A few definitions…
- Bacteraemia: The Presence of viable Bacteria in the Bloodstream
- Septicaemia: (old term) The Spread of Microbes from Wound →Lymphatics→Bloodstream
- Sepsis: Physiological term; A condition where Bacteraemia is Associated with an Inflammatory Response
from the body (→systemic inflammatory response syndrome), characterised by Fever or Hypothermia,
Tachypnoea, Tachycardia and Hypotension

The Human Eco-system:
- Commensal Flora Exist on:
o Skin (Eg: Staphylococcus)
o Pharynx & bronchial tree (Eg: Streptococcus)
o Gut (Eg: E-Coli)
o Vagina (Eg: Lactobacilli)
- Sterile Sites:
o Lungs
o Uterus & fallopian tubes
o Urethra, bladder, Ureters & Kidneys
o Peritoneal Cavity
o Solid organs and tissues
o Blood
o CSF

The Bloodstream Can be a Home for Microbes:
- Favourable Conditions:
o Contains Oxygen, Water & Nutrients
§ (all things required for life – [except For anaerobes])
o Has a neutral pH
o Appropriate temperature for Microbial Growth
§ (Ie: Most cultures are incubated at 37 degrees)
- Unfavourable Conditions: (To balance out those favourable conditions)
o Blood is Constantly Moving
§ →Inhibits Adherence
o Antimicrobial Defence Mechanisms
§ Phagocytes
§ Complement
§ Antibodies
§ Interferon
o Blood recirculates through spleen & liver
§ →Foreign things Get filtered out

Origins of Organisms in Blood Infections:
- Commensal Flora (Ie: Opportunistic Endogenous Organisms)
o Skin
o Nose and pharynx
o Gut
- Sites of infection/Introduction of Pathogens (Ie: Exogenous Organisms)

Things that Can Cause Bacteraemia:
- Chewing food/Brushing Teeth/Dental work (Eg: fillings, extractions):
o Can Introduce mouth flora into blood
- Minor injuries:
o Can Introduce Skin Flora into blood
- G-I Endoscopy, Polypectomy:
o Can introduce Intestinal Flora into blood
- Urinary Catheterisation:
o Can introduce perineal flora into blood
- Abscess Rupture:
o Skin and soft tissues
o Bone
o Visceral abscesses
- Significant infection anywhere:
o Pneumonia
o UTI
o Wound Infection
- Contaminated IV lines or catheters

Conditions Required for Infection:
1. Large Numbers of Organisms
2. Anatomical Defect Facilitating Colonization:
a. Eg: Faulty Heart Valves – Slows down local blood flow, or increases turbulence, giving the organisms
more chance to hang on
b. Eg: Break in Epithelium – No barrier to infection
3. Organisms have protective mechanism/s:
a. Ie: Virulence Factors:
i. Eg: A Capsule [polysaccharide layer outside normal cell wall] → Not Immunogenic & Resists
Phagocytosis
ii. Eg: Secrete Proteinases → Aid in penetrating into tissues
4. Impaired host defence (Ie: Immunocompromise)

At risk patients (May require some form of prophylaxis against infection)
1. Disruption or penetration of anatomical barriers (Ie: Bypassed physical barriers):
a. Wounds
b. IV catheters
c. Contaminated IV drugs
2. Devitalised tissue:
a. Eg: Necrotic tissue has no blood supply (Ie: No way the immune system can get to that area)
3. Defective granulocyte function:
a. Eg: In Chemotherapy/Diabetes
b. (Note: Chemo patients Don’t have many polymorphonucleocytes)
4. Complement defects/deficiency (Immunodeficiencies)
5. Splenic Malfunction/Absence:
a. Ie: Poor filtering of bacteria out of the blood (Especially Encapsulated Bacteria)

Safe Havens For Bacteria:
- Damaged Heart Valves & Endocardium
- Organisms can form Bio-films on foreign material because there is no immune system to prevent their
growth. Eg:
o Catheters
o Prosthetic valves, joints

Diagnosis Of Bacteraemia:
- Blood culture (off antibiotics) (The best)
- Imaging to identify primary & secondary foci of infection
- Histology / Culture of any pathological foci
Common Bacteria to Know:
Gram +ve Bacteraemia:
- Staphylococcus
o -Aureus (Common flora of Skin & Nasopharynx)(Note: Has many Virulence Factors – Eg: a capsule,
toxins, antioxidants)
o -Epidermidis (Common skin flora)
o (Coagulase Positive Vs Coagulase Negative):
§ Coagulase Positive Staphylococcus: (Eg: Aureus)
• Ie: Produce Coagulase → Converts Fibrinogen to Fibrin → Forms a Fibrin Coat around
Bacteria → Resists Phagocytosis → More Virulent
§ Coagulase Negative Staphylococcus: (Eg: Epidermidis)
• Ie: Don’t Produce Coagulase
- Streptococcus
o (α-Haemolytic)(αHaemolysis = Oxidation of Haemoglobin → Greenish colour on Blood-Agar)
§ -Pneumoniae (a Leading cause of Bacterial Pneumonia)(Occasionally causes meningitis)
§ -Viridans (Common flora of Mouth)(Can cause Endocarditis in Bacteraemia)
o (β-Haemolytic)(β-Haemolysis = Complete rupture of RBCs → Wide, clear areas around bacterial
colonies on Blood-Agar)
§ Further Grouped by Serotyping (Based on Cell wall Antigens) – Types: A/B/C/D
§ Group A Streptococcus – (Implicated in Rheumatic Fever and Post-Strep Glomerulonephritis)
o (Non-Haemolytic/γ-Haemolytic)
§ Enterococcus
- Enterococcus (Normal in bowel; doesn’t have many virulence factors, but has high antibiotic resistance)

http://iws2.collin.edu/dcain/CCCCD%20Micro/hemolysis.htm

Gram –ve Bacteraemia:
- Neisseria:
o Meningitides (a common URT/Epithelial flora; cocci)(The only cause of Bacterial Meningitis →
Headache & Neck Stiffness)
o Gonorrhoeae (Responsible for the STI: Gonorrhoea)
- Escherichia Coli (a common Intestinal Flora)(Usually harmless, but can cause Food Poisoning)
- Klebsiella Pneumonia (Gram Negative Rods)(Normal Flora of Skin, Mouth & Intestines)(Can cause
Pneumonia)

NOTABLE INFECTIVE DISEASES

INFECTIVE ENDOCARDITIS
= Infection of the Endothelial Lining of the Heart (including the heart valves)

- Risk Factors:
o Valve Abnormality – (Valve Murmurs, Calcification, Congenital, Artificial)
o Open-Heart Surgery
o Poor Dental Hygiene (Source of Bacteria)
o Bacteraemia
o IV Access – (Haemodialysis, IVDU, Surgery)
o Immunosuppression
- Aetiologies:
o Subacute Bacterial Endocarditis (Most Common - 50-60% of Cases):
§ (Oral) Strep Viridans/(Surgical) Strep Epidermidis (Low Virulence)
§ Epi: Recent Oral Surgery, or Post-Prosthetic Valve Insertion
o Acute Bacterial Endocarditis (Rare – 10-20% of Cases):
§ Staph Aureus (High Virulence - 50% Mortality)
§ Epi: IV Drug Users
- Pathogenesis:
o Bacterial Infection of Valves/Endocardium → Vegetations on Valve Cusps
§ Typically Strep Viridans (Subacute-BE) or Staph Aureus/MRSA (Acute-BE)
§ Affects Aortic & Mitral Valves; (RH-Valves may be affected in IV Drug Users)

- Clinical Signs:
o Symptoms:
§ **Fever + New Murmur** = Endocarditis until proven otherwise
§ +Fatigue, Malaise, Weight Loss
o Physical Signs:
§ Septic Emboli → Infarcts:
• Splinter Haemorrhages (In the nail bed)
• Osler’s Nodes (painful erythematous nodules in pulp of digits)
• Janeway Lesions (Red, nontender lesions on palms/soles)
• Roth Spots (Retinal Haemorrhages - red ring lesions with a yellow centre)
§ Splenomegaly
§ Arrhythmia
o Complications – (Begin ≈2wks after onset):
§ Renal Failure (Renal Emboli/Immune Complex Deposit → Glomerulonephritis, Haematuria)
§ TIA (Cerebral Septic Embolism → Ischaemia → TIA/Stroke)
§ Septicaemia
§ CCF
- Investigations:
o Clinical – (Fever + New Systolic Murmur +/- Septic Emboli)
o 3x Blood Cultures – (@ Different Times & From Different Sites – Eliminate Contamination)
o ECG – (Rule out Ischaemia/MI/Arrhythmias)
o Echo – (Valvular Vegetations & Mitral Regurgitation)
- Management:
o 2-6wks of High Dose IV Vancomycin - (Initially Empirical; Then Culture-Directed Therapy)
o Refer to Cardiac Surgeon – (For ?Valve Replacement Surgery?):
§ If IV-ABs are Unsuccessful
§ Or If Valve is Destroyed (Ie: In Acute-BE) → Heart Failure
- Prognosis:
o 30% Mortality with Rx

LYMPHANGITIS:
- Aetiology:
o Commonly β-Haemolytic-Strep or Staphylococcus Aureus
- Pathogenesis:
o Bacterial Infection Spread to Lymphatics → Acute Inflammation
§ If Severe → Cellulitis/Abscesses
§ If Very Severe → Bacteraemia/Sepsis
- Clinical Features:
o Fever/Chills/Malaise
o Painful Red Subcutaneous Streaks
o Painful Lymphadenitis (Swollen draining lymph nodes)
- Complications:
o Abscesses
o Cellulitis
o Sepsis
- Investigations:
o Blood Culture + Swab any open wounds
o FBC +/- CRP
- Management:
o Immobilisation of Limb
o Antibiotics
o Analgesia

James Heilman, MD, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

MYOCARDITIS – VIRAL & TOXIC:
- What is it?
o “Inflammation of the Heart Muscle”
o + Characterized by Myocyte Necrosis – (Positive Troponin I results seen in 35% of Myocarditis)
- 2 Main Aetiologies:
o VIRAL MYOCARDITIS (Eg: Coxsackievirus, Rhinovirus, Influenza, Parvovirus B19, etc)
§ Either Direct Myocardial Injury OR 2o Autoimmune Response
§ →Heart Thickens & Weakens → Systolic Heart Failure
o TOXIC MYOCARDITIS (Eg: Chemo Drugs, Cocaine, Alcohol, Diuretics, Antibiotics, Venom, CO, etc)
§ Myocardial Damage & Inflammation due to Either:
• Hypersensitivity to Drugs
• Direct Toxic Damage
o (May be Asymptomatic)
o Symptoms:
§ Flu-Like Syx - (Fever, Fatigue, Malaise)
§ LV-Failure – (Dyspnoea/Orthopnoea/PND/Cough)
§ Chest Pain – (Due to Myocarditis +/- Pericarditis)
§ Palpitations (Arrhythmias)
- Complications:
o Cardiomyopathy → Heart Failure
o Arrhythmias → Sudden Death
o Pericarditis → Pericardial Effusion
- Investigations:
o ECG & Continuous Telemetry
o Serial Troponins I/T - (Immediately, then @6hrs, then @24hrs)
o FBC (↑WCC), CRP (↑), ESR (↑)
o CXR (Cardiomegaly)
o Echo (Dilated, Poor Vent-Function)
- Management:
o **Bed Rest
o **CCF Triple Therapy (ACEi/ARB + B-Blocker + Diuretics)
o **Warfarin (Prevent Thromboembolism)
o Supportive Rx (Fluids, Analgesia)
o Treat Underlying Cause if Possible

Mayo Foundation for Medical Education and Research (MFMER); IMG-20456507
PERICARDITIS:
- Aetiology:
o Usually Secondary to:
§ Infection (**Viruses**, Bacteria, Fungi, Parasites)
§ Immuno (Rheumatic Fever, SLE, Post-MI, Drug Hypersensitivity)
§ Other (MI, Post-Cardiac Surgery, Neoplasia, Trauma, Radiation)
- Classification:
o According to Composition of Pericardial Exudate:
§ Serous (Non-Infectious Inflammatory Diseases – SLE, Uraemia, Tumours)
§ Purulent (Infective - by Microbes)
§ Fibrinous/Serofibrinous (Due to Acute MI, Chest Radiation, SLE, Trauma)
§ Caseous (Tuberculosis)
§ Haemorrhagic (Due to Metastasis, Cardiac Surgery)
- Pathogenesis:
o Various Aetiologies → Inflammation of the Pericardium
§ → Thickening of Pericardium→ Pericardial Exudate (Serous Fluid + Pus/Fibrin/Blood)
• →Rubbing of Parietal & Visceral Pericardium → Further Inflammation & Exudate
- Clinical Features & Complications:
o Symptoms:
§ Pleuritic Chest Pain (Better on Sitting Forward; Worse on Inspiration & Lying Down)
§ Fever, Fatigue
§ Dry Cough
§ Syx of CCF (Dyspnoea, Fatigue)
o Signs:
§ Fever, Tachycardia
§ Muffled Heart Sounds
§ Friction Rub
§ ↑JVP
§ Heart Failure Signs if Tamponade
o Complications:
§ Cardiac Tamponade/Pericardial Effusion
§ If >3mths → Chronic → Constrictive Pericarditis (Requires Surgery)
- Diagnosis:
o ECG – (Classical PR-Depression + ST-Elevation + Tachycardia)
o CXR – (Pulmonary Congestion)
o ECHO – (?Pericardial Effusion)
- Management:
o Rx Underlying Cause
o Anti-Inflammatories (NSAIDs / Steroids)
o Analgesia

https://www.nhlbi.nih.gov/health-topics/heart-inflammation
IMPETIGO (SCHOOL SORES)
- What is it?
o Superficial Bacterial Skin Infection
o Most Common in school kids
o Very Contagious – (Spread by Close Contact & Poor Hygiene)
o Usually resolves slowly
- Organism:
o Mostly Staphylococcus Aureus
o Sometimes Streptococcus Pyogenes
§ Can lead to Glomerulonephritis or Rheumatic Fever if it’s Strep
o Staph Aureus (Bullous) - (Pic 1)
o Streptococcus (Non-bullous) – (Pic 2)
- Presentations:
o Occur most commonly on face
o Fragile vesicles rupture & crust
o Can be confused with HSV
o 1: Nonbullous/Crusted Impetigo:
§ (Most common)
§ Yellow crusts and erosions
§ Itchy/Irritating (but not painful)
o 2: Bullous impetigo:
§ Always due to Staph Aureus
§ →Mildly irritating blisters that erode rapidly leaving a brown crust
o 3: Ulcerative lesions:
§ Always due to S-pyogenes
§ Most common in Aboriginal Communities
- Very Infectious
o Epidemic in young children
o Transmitted through skin contact
o Outbreaks associated with poor hygiene / crowded living conditions
- Treatment:
o Cover Affected Areas
o Abstain from School
o Systemic or Topical Antibiotics

1.James Heilman, MD, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons
2.Evanherk, CC BY-SA 3.0 <http://creativecommons.org/licenses/by-sa/3.0/>, via Wikimedia Commons
ERYSIPELAS
- Aetiology:
o Group A Strep (GAS) / Staphylococcus Aureus
o Breaks in skin (Eg: Insect bites/ulcers/cracking skin conditions/eczema)
- Epidemiology:
o Mostly infants & older people
- Pathophysiology:
o Potentially serious bacterial infection of the skin
o → Infection of the upper dermis → extends to superficial cutaneous lymphatics
o A superficial form of Cellulitis
o ‘St Anthony’s fire’ = Intense rash associated with erysipelas
o Rapid onset fevers, chills, rash
o Affected skin has sharp, raised border
o Bright red, firm & swollen
o May blister or become necrotic
o may spread to deeper lymphatics (lymphangitis)
- Management:
o Wound care
o Oral/IV penicillin antibiotic
o Erythromycin/Roxithromycin if Penicillin allergic
o Vancomycin if MRSA

CDC/Dr. Thomas F. Sellers/Emory University, Public domain, via Wikimedia Commons

CELLULITIS
- What is it?
o Bacterial infection of the Dermis and Sub-Cutaneous Tissues
- Organism:
o Adults: 90% due to Staph Aureus/GAS
o Children: H-Influenzae b
o Associated with cat/dog bite: Pasturella multocida
- Presentation:
o Painful, raised and Oedematous Erythema (Most commonly on Lower Leg)
o Possible Blistering
o Lymphadenopathy - & Malaise & Fever
- Distribution:
o Children – Periorbital Area
o Adults – Lower Legs
- There’s typically an underlying cause:
o Lymphedema
o Tinea, Herpes simplex infection, Chronic sinus infection
o Chronic dermatitis
o Poor lower leg circulation
o Wounds
- Treatment:
o Oral/IV penicillin antibiotic
o Erythromycin/Roxithromycin if Penicillin allergic
o Vancomycin if MRSA

Source: https://www.nhs.uk/conditions/cellulitis/

SCABIES
- Organism:
o Sarcoptes scabii (Scabies Mite)
- Epidemiology:
o Human infestations originating from pigs, horses and dogs are mild and self-limiting
o Scabies infestations from other humans never cure without intervention
- Ecology:
o Mites live in stratum corneum (Don’t get any deeper)
o Eat stratum corneal Keratinocytes
o Make “tunnels” by eating
o Mating occurs on the hosts skin
o Fertilized Female Mites Burrow into the Stratum Corneum (1 mm deep)
o Salivary Secretions contain Proteolytic Enzymes →Digest Keratinocytes
- Transmission:
o High prevalence in children (50%) and adults (25%) in tropical remote communities
o Spread by close physical contact
- Presentation:
o Itch (Exacerbated at night and after hot showers)
o Itchy, Excoriated Rash on Trunk, associated with Scaly Burrows on the fingers and wrists
o Often vesicles and pustules on the palms and soles and sometimes on the scalp
- Diagnosis:
o Clinical Diagnosis:
§ Chronic itch with Symmetrical Rash
§ Burrows
o Skin Scraping - Look for Scabies Mites:
§ Intact larvae, nymphs or adults
§ Unhatched or hatched eggs
§ Moulted skins of mites
§ Fragments of moulted skins
§ Mite faeces
- Treatment:
o Topical Permethrin
o Or Oral Ivermectin (But not on PBS – Very Expensive)
o Environmental Measures:
§ Mites can contaminate bedding, chairs, floors, and even walls
• (Usually only a problem with crusted scabies)
§ Wash, sun, vacuum, surface insecticide
o Community Prevention:
§ Treat all close contacts – Especially in Indigenous Communities
§ Simultaneous Effective Treatment
o TREAT AGAIN IN 7 DAYS

Gzzz, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons
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Joel Mills, CC BY-SA 3.0 <http://creativecommons.org/licenses/by-sa/3.0/>, via Wikimedia Commons
LICE (PEDICULOSIS)
- 3 Types:
o 1: Head Lice: Pediculus Humanus Capitis
§ Epidemiology:
• Common in Primary School Children in the Tropics
• Higher prevalence in Aboriginal Children
§ Diagnosis:
• Conditioner + Fine-Tooth Come
• Wipe combings on white tissue paper
o 2: Body Lice: Pediculus Humanus Corporis
§ Live on clothes, and come to the body to feed
o 3: Pubic Lice: Phthirus Pubis
§ Largely sexually transmitted
§ Blood Feeder
§ Can infect any Body Hair (Pubic/Trunk/Legs/Axilla/Beard) but rarely head
- Lifecycle:
o Eggs laid in hair (knits)
o Larvae grow into adults
o Adults – blood sucking (live in hair)
- Transmission:
o head-head contact
- Presentation:
o Scalp and Neck can be Itchy
o Nits are noticeable on the hairs
- Diagnosis:
o Best Method = ‘Conditioner & Comb Technique’:
§ Very Practical for parents
§ Cost Effective
§ High Sensitivity
§ Conditioner ‘Stuns’ the lice by suffocating them → Prevents them from running away
- Management/Treatment:
o Conditioner & Nit Comb
o Physical Removal
o Cut Hair
o Topical Insecticidal Cream
o Good idea to wash pillows and hats though – Hot Wash
o (Treat all body hair – for Pubic lice)
o Reasons for Treatment Failure:
§ Inadequate application of the product
§ Lice are resistant to insecticide
§ Failure to retreat to kill nymphs emerged from eggs
§ Reinfection

1.Public domain: https://commons.wikimedia.org/wiki/File:Pediculus_humanus_var_capitis.jpg
2.https://www.pcds.org.uk/clinical-guidance/pediculosis
HERPES SIMPLEX
- What is it?
o Common Mucosal Viral Infection that presents with localised blistering
o Can reside in a latent state
- 2 Types:
o Type 1: Typically facial/oral infections (Cold sores/fever blisters)
§ Occur mainly in infants & young kids
o Type 2: Mainly Genital
§ Occur after puberty (often transmitted sexually)
- Presentation:
o Stages of Infection:
§ 1: Prodromal Stage Vesicle or "blister" stage
§ 2: Ulcer stage
§ 3: Crust stage

o The virus grows down the nerves and out into the skin → Localised Blistering
o Neuralgia
o Lymphadenopathy
o High Fever
- Recurrences can be triggered by:
o Minor trauma/Other infections/UV radiation/Hormonal factors/Emotional
stress/Operations/procedures on face
- Treatment:
o Mild cases require no treatment
o Sun protection to prevent
o Oral Antiviral Drugs (Stop the virus multiplying)
- Complications:
o Encephalopathy
o Trigeminal Neuralgia (Neurogenic Pain)

Public Domain: CDC

CHICKEN POX (VARICELLA ZOSTER):
- What is it?
o Highly contagious disease
o Typically childhood disease (before 10yrs)
o One infection thought to confer lifelong immunity
- Organism:
o Varicella zoster virus (HHV3) (AKA: Chicken Pox Virus, Varicella, Zoster)
- Transmission:
o Highly Infectious
o From person to person
o Aerosol Droplets
o Direct contact with fluid from open sore
- Pathophysiology:
o Incubation Period ≈ 2wks
o (Chicken Pox) Initial Mucosal Infection → Viremia → Epidermal Lesions
§ May lead to → Latent infection of Dorsal Ganglion Cells of Sensory Nerves
o (Shingles) Reactivation of latent Varicella Zoster Virus in Peripheral Nerves
- Signs/symptoms:
o Itchy rash or red papules
o Begins on the Trunk →Face and Extremities
o May cover entire body
o High fever/headache/cold-like symptoms/vomiting/diarrhoea
- Diagnosis:
o Clinical Diagnosis
o Immunofluorescence
o Test for Elevated VZV-Specific Antibodies
§ (IgM – Primary Infection; IgG – Second Infection)
- Treatment:
o Symptomatic
o Resolves on its own
- Complications:
o Varicella During Pregnancy can → Congenital Varicella Syndrome:
§ Spontaneous Abortion (3-8% in 1st Trimester) or IUGR
§ Skin: Cutaneous Defects, Hypopigmentation
§ Neuro: Intrauterine Encephalitis, Brain Damage, Seizures, Developmental Delay
§ Eye: Chorioretinitis, Cataracts, Anisocoria
§ MSK: Limb Hypoplasia
§ Systemic: cerebral cortical atrophy
§ Renal: Hydronephrosis, Hydroureter
§ GI: GORD
§ CVS: Congenital Heart Defects
o Perinatal Varicella Infection:
§ severe → mortality rate of 30%

1.Camiloaranzales, Public domain, via Wikimedia Commons
2.F malan, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
HERPES ZOSTER (SHINGLES)
- What is it?
o Reactivation of Latent Herpes Varicella Zoster Virus
- Pathophysiology:
o Incubation Period ≈ 2wks
o (Shingles) Reactivation of latent Varicella Zoster Virus in Peripheral Nerves
- Presentation:
o Painful blistering rash along 1/more Dermatomes
o Virus is seeded to nerve cells in spinal cord
o Fever, malaise and headache
o Lymph nodes draining affected area are often enlarged/tender
o Can also result in nerve palsy
- Diagnosis:
o Test for Elevated VZV-Specific Antibodies
o PCR
- Transmission:
o Shingles are infectious
o From person to person
o Direct contact with fluid from open sore
- Treatment:
o Antiviral treatment
o Rest & analgesia
o Oral Antiviral

Fisle, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

MEASLES VIRUS:
• Organism:
– Morbillivirus
• Transmission:
– Respiratory Route (Aerosol)
– Contact with fluids from infected person’s nose/mouth
• Pathogenesis:
– Typically a Respiratory Infection
– →Produces a Viremia → Rash
• Presentation:
– Fever
– URTI - Cough, Rhinorrhoea, Red Eyes
– Maculopapular Erythematous (Morbilliform) Rash
– “Koplik’s Spots” – Seen on the Inside of the Mouth
• Complications Include:
– Croup
– Otitis Media
– Enteritis with diarrhoea
– Febrile convulsions
– Encephalitis (Serious)
– Subacute Sclerosing Panencephalitis (very rare)
§ (Chronic, progressive Encephalitis caused by persistent infection with immune-resistant
Measles Virus)
§ No Cure
§ Fatal
• Diagnosis:
– Clinical Diagnosis (Generalised Maculopapular Rash + Fever)
– Presence of Measles IgM Antibodies
– PCR of Respiratory Specimens
• Treatment:
– No Specific Treatment
– Prevented by MMR Vaccine
• Prevention:
– Attenuated MMR Vaccine (Admin at 12mths & 4yrs)
– Developing Countries: Low Herd Immunity → Higher Prevalence
§ Relatively High Death-Rates in Non-Immune

Photo Credit:Content Providers(s): CDC/Dr. Heinz F. Eichenwald, Public domain, via Wikimedia Commons

CDC, Public domain, via Wikimedia Commons

Public domain: CDC

RUBELLA VIRUS (“GERMAN MEASLES):
• Organism:
o Rubella Virus
• Transmission:
o Respiratory Route
o (Human Reservoir Only)
• Presentation:
o Initial Flu-Like Symptoms
o * Rash on Face → Spreads to Trunk & Limbs
§ Pink-Red, Itchy
o Low-grade Fever, Lymphadenopathy, Joint Pains, Headache, Conjunctivitis
• Prognosis:
o Typically Benign
o Typically Lasts 1-3 Days (Children Recover Quicker)
o Complications may include arthritis, thrombocytopenia purpura, and encephalitis
o *HOWEVER, Maternal Infection During PREGNANCY can be SERIOUS!!
§ If Infected in the 1st 20wks of Pregnancy → Congenital Rubella Syndrome
• →Abortion
• →Cardiac/Cerebral/Ophthalmic/Auditory Defects
§ Specific Foetal Damage Depends on Organ Development @ the Time:
• The 1st Trimester is Worst, as Organ Development occurs during this time
• After 1st Trimester, Organ Growth is the main process
• Diagnosis:
o Presence of Virus-Specific IgM Antibodies
• Treatment:
o No Specific Treatment
o Controlled by vaccination (MMR Vaccine)
o Test pregnant women for immunity early
• Prevention:
o (Note: Rubella Itself is relatively Benign, so why bother Vaccinating?)
o MMR Vaccine:
§ (Live Attenuated)
§ #1 Aim: Prevent Rubella in Pregnant Women → ↓Congenital Rubella Syndrome
§ Aimed at BOTH Males & Females to ↓Male Transmission to Pregnant Females

commons.wikimedia.org, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons

https://www.cdc.gov/rubella/about/photos.html

http://phil.cdc.gov/phil_images/20030724/28/PHIL_4284_lores.jpg

HUMAN PARVOVIRUS B19 (“5TH DISEASE”)
• Organism:
o Parvovirus B19
• Transmission:
o Respiratory Droplet
o Blood-Borne
• Pathophysiology:
o Virus Replicates in Rapidly-Dividing Cells (Eg: Bone Marrow RBC Precursors)
§ → RBC Haemolysis
§ → Severe Anaemia
§ → Can Result in Haemolytic Crisis
o The receptor for the virus is a globoside, which is abundant on tissues of mesodermal origin
o Can cross the placenta into the foetus
§ → Foetal Anaemia
• Presentation:
o Fever/Malaise
o Characteristic Rash
§ Teenagers: ‘Papular Purpuric Gloves & Socks Syndrome’
§ Children: ‘Slapped Cheek Syndrome’
• Note: Foetal Infection →Foetal Damage or Abortion

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2.Sandyjameslord, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons

SCARLET FEVER:
- Organism:
o Certain strains of Strep pyogenes (Which carry a Bacteriophage – A virus infecting the bacteria →
Produce an Eruthrogenic toxin)
- Epidemiology:
o Mostly occurs in kids aged 4-8yrs
- Pathogenesis:
o GAS infection of Tonsils/Pharynx/Skin
o Exotoxin Released by Strep Pyogenes → Local effect on Tonsils/Pharynx/Skin
o →Abnormalities of tongue
§ Initially covered with white exudate
§ Exudate is shed
§ inflammation of underlying tissue
o → Diffuse, Erythematous Exanthem
- Treatment:
o Antibiotics (Usually penicillin for 10days; or single IM dose; or erythromycin if penicillin allergic)
o Antipyretics
o Fluids
o Oral antihistamines to relieve the rash
- Longer-Term Complications:
o Rheumatic fever
o Glomerulonephritis

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2 - www.badobadop.co.uk, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia
Commons

Afag Azizova, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

DERMATOPHYTOSIS - “RINGWORM”/“TINEA”:
• Organism:
o 3 Genera Are Important:
§ Trichophyton
§ Microsporum
• Note: Microsporum Canis – (From Dogs/other animals)
• Note: Fluorescent under Wood’s Lamp
§ Epidermophyton
• Pathogenesis:
o Fungi ONLY Metabolizes Keratin:
§ :. Only infect the Stratum Corneum
§ Note: Can Also Invade Hair Shafts
• Epidemiology:
o Common In Rural Indigenous Populations
• Conditions Named Based On Location of Infection:
o Tinea Corporis (On Body)
o Tinea Capitis (On Head)
o Tinea Crura (Pubic Area)
• Symptoms:
o Well Circumscribed lesions with central clearing
o Focal hair loss due to infection of Hair Follicle
o Focal pityriasis (Skin Flaking)
o Usually not pruritic
o Can infect any keratinised structure
o Nail infections can be severe
o “Tinea Versicolor” (Depigmentation of the Skin)
o “Tinea Imbricata/Concentricum” (As the ringworm grows, it produces concentric silvery rings)
§ Caused by Trichophyton Concentricum
• Diagnosis Of Dermatophytosis:
o Woods lamp – only Microsporum canis fluoresces
o Microscopy of hairs/nail shavings/skin shavings
o Culture for dermatophyte on Sabouraud’s agar
• Treatment:
o Topical Antifungals:
§ Clotrimazole, Miconazole, Econazole, Tolnaftate, Terbinafine
o Oral Antifungals:
§ Griseofulvin for 4 weeks
§ Or Itraconozole / Fluconazole / Terbinafine

Asurnipal, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons

PARASITIC GUT INFECTIONS (Protozoa & Helminths):
• Transmission:
o Faecal-Oral – (Ingestion of Dormant Cysts in Contaminated Food/Water)
• Diagnosis:
o Stool Samples (Looking for cysts) under Direct Microscopy
o Antigen Testing
• Prevention:
o Boiling Water to Eliminate Cysts
o Good Hygiene
o Avoiding Faecal Contact
• Examples:
o GIARDIA:
§ Pathogenesis:
• Not Toxigenic; Rather, it covers the brush border → Malabsorption
§ Diagnosis:
• Cysts in Stools
§ Complications:
• Chronic Infection
• Malabsorption
o → Malnutrition
o → Fatty Stools
§ Treatment:
• Metronidazole

https://www.cdc.gov/dpdx/giardiasis/index.html

o CRYPTOSPORIDIUM:
§ Transmission:
• Ingestion of oocysts (Contaminated Drinking Water/Public Pools)
• Can survive Chlorination
§ Pathogenesis is mostly unknown
• Possibly induces inflammatory response → Disrupts absorptive surface
• Damages Villi → Crypt Cells Replicate faster to replace them → Immature cells in the
villus → Poor absorption
§ Treatment:
• Nitazoxanide (Normally Self-Limiting if Immunocompetent)
§ Long term Effects:
• AIDs patients don’t recover → Chronic Infection
§ Diagnosis:
• Cysts in Stools

https://www.cdc.gov/dpdx/cryptosporidiosis/index.html

o ENTAMOEBA HISTOLYTICA - (The Amoebic Dysentery):
§ Transmission:
• Ingestion of oocysts (Faecal Oral)
§ Pathogenesis:
• Intestinal Invasions → Ulcerations → Dysentery (Bloody Diarrhoea)
§ Diagnosis:
• Cysts in Stools
§ Management:
• Metronidazole

https://www.cdc.gov/dpdx/amebiasis/index.html

POLIOMYELITIS:
- Aetiology:
o Poliovirus Infection
- Epidemiology:
o Eradicated in many countries (A single case would be an epidemic)
- Prevention:
o Vaccination Available
§ Live Attenuated (Oral Polio Vaccine):
• Advantages:
o Easy Administration - Given Orally
• Disadvantage:
o Rarely causes paralysis (1 in 2.5million)
§ Inactivated Polio Vaccine (IPV):
• Advantages:
o Carries NO risk of Vaccine-Associated Polio Paralysis
• Disadvantage:
o Difficult Administration - Has to be injected
- Pathogenesis:
o Transmission:
§ Faecal-Oral
§ or Respiratory
o Initially Enteric Infection → Spreads to Bloodstream → Spinal Cord → Preferentially Infect & Destroy
Motor Neurons
o 90% Asymptomatic
o <10% Minor Viral Illness:
§ Headache
§ Neck/Back pain
§ Abdominal Pain
§ Fever, Lethargy, Vomiting
o 1% CNS Infection → Paralysis
§ Acute Asymmetrical Flaccid Paralysis + Areflexia
§ If ‘Spinal Polio’ → Paralysis of Legs(unilateral)
§ If ‘Bulbar Polio’ → Cranial Nerve Paralysis (Eg: Dysphagia, Dysphasia, Dyspnoea)
§ Or Combination of Both
- Treatment:
o Self-Limiting, but Lasting Disability – Only Supportive Rx (Eg: Ventilation, Physiotherapy)
o But Vaccine Preventable

MENINGITIS:
- Aetiology:
o Bacterial/Septic Meningitis – Neisseria meningitides, Haemophilus influenza, Group B Streptococci
§ Adults = Neisseria meningitides (Note: Vaccine preventable – Meningococcal A & C)
§ Children = Haemophilus influenza (Vaccine Preventable – HIB Vaccine)
§ Neonates = Group B Streptococci (or E-coli)
o Viral/Aseptic Meningitis – HSV, Enteroviruses (Echo/Coxsackie), Influenza, Mumps, HIV
o Chronic Meningitis – Miliary Tuberculosis
o Fungal Meningitis - Typically in immunosuppressed patients
- Pathogenesis:
o Meningeal Infection → Inflammation & Oedema → ↑ICP → Vomiting, Drowsiness
o Note: Meningococcal Sepsis can → Thrombocytopenia → Maculopapular Rash →DIC
- Morphology:
o Bacterial → Exudate within Meninges (Pus beneath the meninges)
o Viral → No pus
o Engorged Meningeal Vessels
o ***Meningism:
§ *1: Neck Stiffness (Due to Inflammation of the Meninges)
• :. Brudzinski’s Sign Positive (Flex the Neck → Pt bends knee)
• :. Kernig’s Sign Positive (Flex the hip and attempt knee extension → Pain
§ *2: Photophobia
§ *3: Headache
o <1% Papilloedema = Swelling of the Optic Disc secondary to the ↑Intracranial Pressure
o + Constitutional Syx:
§ Fever/Malaise
§ Nausea/Vomiting
§ May eventually have loss of consciousness (Rare)
§ Irritability
§ Poor Feeding
o Features Suggestive of Aetiology
§ Non-Blanching Maculopapular Rash → Suggests Meningococcus
§ CSF Rhinorrhoea/Otorrhoea - basal skull fracture → Suggests Pneumococcus, HiB, Strep
- Diagnosis:
o **Clinical Suspicion: (Meningism +/- Rash +/- Fever/Malaise/Vomiting +/- Headache/ALOC
§ +/- (Brudzinski’s Sign +, Kernig’s Sign +)
o Blood Cultures BEFORE IV Antibiotics!!
o L3-L5 Lumbar Puncture → CSF Examination:
§ LP can → Coning if ↑ICP :. DO NOT do LP if:
• 1: Papilloedema
• 2: Cushing’s Response (Triad – ↑BP, ↓HR, Irregular Breathing)
• 3: Unresponsive Pupils
§ Can → “Cerebral Herniation” (Aka: Cistern Obliteration) → Often Fatal
o CSF Samples (Take 3):
§ Sample 1 → Serology (or PCR)
§ Sample 2 → Biochemistry (Glucose, Protein)
§ Sample 3 → Bacteriology – Most Precious (Gram Stain + Culture)
o CSF Interpretation:
Normal Bacterial Meningitis Viral/Aseptic Meningitis
(Usually Herpes Virus)
CSF Pressure Normal Normal-Raised Normal-Raised
White Cell Count Normal Raised (Polymorphs) Raised (Lymphocytes)
Glucose Same as Serum Lower than Serum (Hungry Bacteria) Normal
Protein Normal Raised (produced by the organisms) Raised (produced by the
organisms)
Gram Stain None Presence of Bacteria Nothing (“Aseptic Meningitis”)
- Treatment:
o (Bacterial Meningitis = Emergency – Can be Fatal)
o (Viral Meningitis = Usually Self-Limiting & Less Fulminant Clinically)
o ***Treat on Suspicion!! – (Don’t wait for lab results!)
o 1: Blood Cultures BEFORE IV Antibiotics!!
o 2: Early Antibiotic Therapy is Essential for Good Outcome!!!
§ IV Benzylpenicillin G, or IV Cephtriaxone (why? – Because they can enter the BBB)
o 3: Corticosteroids (Dexamethasone) WITH the Antibiotics →↓CNS Inflammation:
§ →Improves Neurological Outcome of bacterial meningitis
o 4: Fundoscopy, Then Lumbar Puncture – (Check for Papilloedema before doing LP)
§ CSF – MCS
o (+ Prophylactic Measures for Close Contacts):
§ Meningitis Prophylaxis: Rifampicin, Ceftriaxone or Ciprofloxacin:
§ Offered to Household, child care and CLOSE CONTACTS
- Prognosis:
o Good prognosis with Aggressive Treatment
§ :. Treatment on Suspicion: Empirical Antibiotics (or Antivirals)
- Complications:
o Acute:
§ Encephalitis
§ Cerebral infarction
§ Oedema
§ Herniation
§ Waterhouse-Frederichson Syndrome (Acute Adrenal Infarction)
• (→Petechial Haemorrhages, DIC, Septic Shock)
o Late:
§ Abscess
§ Subdural Empyema
§ Epilepsy
§ Leptomeningeal Fibrosis & Consequent Hydrocephalus

https://medlineplus.gov/ency/imagepages/19069.htm

https://www.abc.net.au/news/2021-07-21/sa-meningococcal-case/100311578
ENCEPHALITIS:
- Aetiology:
o Almost Always Viral – (**Herpes Simplex Virus, VZV, CMV, Poliovirus, Rabies [Rhabdovirus], JEV)
o Parasites such as Toxoplasma gondii and Plasmodium falciparum
o Fungi such as Cryptococcus neoformans
o Bacteria such as Treponema pallidum
- Pathogenesis:
o Viremia → Crosses BBB → CNS Infection →→ Cerebral Oedema → ↑ICP → Neurological Signs
o Infective Syx – Fever, Nausea, Vomiting
o + Cerebral Syx – Encephalopathy – (Altered Mental State/Abnormal Behaviour/ALOC/Drowsiness)
§ +/- Seizures
- Treatment:
o Treat on Suspicion – (Acyclovir + Dexamethasone)
- Prognosis:
o Poor - Once symptomatic, rapid inflammation & necrosis → Brain-Death or Neurological Deficit
o 70% Mortality Untreated
- Investigations:
o FBC – (Lymphocytosis)
o LP – (↑Lymphocytes, Normal Glucose, ↑Protein, Negative Cultures)

Normal Bacterial Viral Meningitis Encephalitis
Meningitis (Usually Herpes (typically viral)
Virus)
CSF Pressure Normal Normal-Raised Normal-Raised Markedly Raised
White Cell Count Normal Raised Raised Raised
(Polymorphs) (Lymphocytes) (Lymphocytes)
Glucose Same as Serum Lower than Normal Normal
Serum (Hungry
Bacteria)
Protein Normal Raised (produced Raised (produced Raised
by the organisms) by the organisms)
Gram Stain None Presence of Nothing (“Aseptic Nothing
Bacteria Meningitis”)

MRI shows high signal in the temporal lobes and right inferior frontal gyrus in someone with HSV encephalitis.

dr Laughlin Dawes, CC BY 3.0 <https://creativecommons.org/licenses/by/3.0>, via Wikimedia Commons
COMMON COLD (ACUTE RHINITIS)
• Aetiology:
o Rhinoviruses, Adenoviruses, Paramyxoviruses, Influenza viruses, Myxoviruses,
• Pathogenesis:
o Transmission – (Droplet Transmission/Contact Secretions)
o Viral Infection of URT Mucosa → URT Inflammation → Mucous Hypersecretion
o (Note: No Cross-Protection between Serotypes → Possibility of Repeated Infections)
• Clinical Features
o Short Incubation Period (2-3 days)
o 1wk Of Symptoms:
§ Local - Nasal Congestion, Sneezing, Sore Throat, Hoarseness, Cough, Conjunctivitis
§ General - Malaise, Headache, Myalgias, Mild Fever
o Signs
§ Rhinorrhoea
§ Inflamed Nasal/Oropharyngeal Mucosa
§ Lymphadenopathy
§ Note: Normal Chest Exam
o Complications
§ Secondary Bacterial Infection: (Otitis Media, Sinusitis, Tonsillitis, Bronchitis, Pneumonia)
§ Asthma/COPD Exacerbation
§ Benign Inflammatory Nasal Polyps
• Diagnosis:
o Differentials:
§ Allergic Rhinitis, Pharyngitis, Influenza, Laryngitis, Croup, Sinusitis, Bacterial Infections
o Clinical Diagnosis – (Symptoms + Nasal Exam + Inflamed Mucosa + Watery Discharge)
o Laboratory Diagnosis – ONLY if Other Conditions are Suspected
• Management:
o Patient Education
§ No Antibiotics Indicated Because Of Viral Etiology
§ Consider 2o Bacterial Infection if NO Resolution after 3-10 Days
o *Symptomatic Relief:
§ Paracetamol
§ Decongestants (Phenylephrine/Pseudoephedrine), Antihistamines
§ + Rest, Hydration, Gargling Warm Salt Water, Steam
§ +(↑Dependence On Bronchodilators/Inhaled Steroids For Asthmatics & COPD)

https://journals.asm.org/doi/10.1128/CMR.12.1.9
PHARYNGITIS (SORE THROAT)
• Definition
• = Inflammation of the Oropharynx (Without inflammation of the tonsils)
• Aetiologies:
• Viral (40-60%) – Most Common:
§ Adenovirus, Coxsackie, HSV, EBV, Influenza Virus (Orthomyxovirus),
• Bacterial
§ “Strep Pyogenes” (GABH-Streptococcus) – (*Rh-Heart Disease, PSGN & Scarlet Fever)
§ Neisseria gonorrhoea, Chlamydia pneumoniae, Mycoplasma pneumoniae, Corynebacterium
diphtheria
• Morphology:
• Red, Inflamed Oropharynx
• May have white lesions
• May have pus

Viral: https://commons.wikimedia.org/wiki/File:Pharyngitis.jpg
Strep: https://commons.wikimedia.org/wiki/File:Pos_strep.JPG
• Typically a self-limited infection with no significant sequelae
• Bacterial - Group A Beta-Hemolytic Streptococcus
§ Absence Of Cough, Pharyngitis, + Flu-Like Illness
§ Signs: Fever + Tonsil Exudate + Lymphadenopathy + <15yo + NO Cough
§ Complications!! - Rheumatic Fever, Glomerulonephritis, Meningitis
• Viral - Adenovirus
§ Cough – (Due to Rhinorrhoea), Pharyngitis, + Flu-Like Illness
• Viral - Ebv (Infectious Mononucleosis)
§ Pharyngitis, Fever, Lymphadenopathy, Fatigue, Rash
• Investigations
• Suspected GABH-Strep:
§ Throat Culture = Definitive (But TOO SLOW in the real world!!)
§ RDT For Streptococcal Antigen
§ ASOT (Anti-Streptolysin-O-Titres) – (But only shows recent infection)
• Suspected EBV (Infectious Mononucleosis):
§ Peripheral Blood Smear – (Reactive Lymphocytes)
§ “Monospot” Test (IE: The Latex Agglutination Assay, Or "Monospot")
§ EBV Serology
• Management
o If ?GABH-Strep:
§ **Throat Swab if: Fever + Tonsil Exudate + Lymphadenopathy + <15yo
§ Antibiotics!!: Penicillin-V/G or Erythromycin if Penicillin Allergic
o If ?Viral Pharyngitis:
§ Antibiotics NOT indicated
§ Paracetamol/NSAIDs
§ Decongestants (Phenylephrine)
o If ? Infectious Mononucleosis (EBV):
§ Antibiotics NOT indicated; Note: Penicillin will → Rash (Pathognomonic)
§ Self-Limiting Course; Rest During Acute Phase Is Beneficial
§ Supportive Treatment: NSAIDS for fever, sore throat, malaise
Other Notable Pharyngitis’s:
- (EPSTEIN BARR VIRUS) – INFECTIOUS MONONUCLEOSIS (GLANDULAR FEVER):
o Aetiology:
§ Epstein Barr Virus
o Pathogenesis:
§ Transmitted through Saliva (Ie: Kissing Disease)
§ Incubation period <8wks
§ Preferentially Infects B-Cells → Reactive B-Lymphocytes → “Mononucleosis”
o Morphology:
§ Tender Cervical Lymphadenopathy
§ Blood Smear – Lymphocytosis with Atypical Lymphocytes

Creative commons: https://www.flickr.com/photos/euthman/145052721

§ Signs/Symptoms:
• Fever +
• Glandular Fever Triad:
o Fatigue/Malaise (Anorexia/Lethargy)
o Pharyngitis (Sore Throat)
o Lymphadenopathy (Especially Cervical)
• Others – (Splenomegaly, Hepatitis, Haemolysis, Jaundice)

James Heilman, MD, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

o Diagnosis:
§ Typically Clinical
§ Peripheral Blood Smear – (Reactive Lymphocytes)
§ “Monospot” Test (IE: The Latex Agglutination Assay, Or "Monospot")
§ EBV Serology
§ + LFTs
o Treatment:
§ Antibiotics NOT indicated; Note: Penicillin will → Rash (Pathognomonic)
§ Self-Limiting Course; Rest During Acute Phase Is Beneficial
§ Supportive Treatment: NSAIDS for fever, sore throat, malaise
o Complications:
§ EBV is an Oncogenic Herpesvirus → Tumours:
• →Burkett’s Lymphoma
• →Hodgkin’s Lymphoma
• →Nasopharyngeal Carcinoma

Creative Commons: https://media.springernature.com/lw685/springer-
static/image/art%3A10.1038%2Fnrc.2016.92/MediaObjects/41568_2016_Article_BFnrc201692_Fig3_HTML.jpg

- DIPTHERIA:
o Aetiology:
§ Gram Positive Bacterium – Corynebacterium Diptheriae
o Pathogenesis:
§ Transmission – Aerosol, Physical Contact
o Morphology:
§ Adherent Whitish Pseudomembrane Over Pharynx & Tonsils (May → Obstruction)
§ High Fever, Sore Throat, Fatigue, Nausea & Vomiting
§ Pseudomembrane on Tonsils & Pharynx - May have Airway Obstruction & Dysphagia
o Complications:
§ Systemic Exotoxin →
• Myocarditis (Potentially fatal toxigenic Cardiomyopathy → Heart Failure)
• Peripheral Neuritis
• Chronic Non-Healing Ulcers
o Diagnosis:
§ Swab M/C/S
§ + Toxin Detection
o Treatment:
§ Penicillin or Erythromycin (if Penicillin Allergic)

User:Dileepunnikri, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

- SCARLET FEVER (“STRAWBERRY TONGUE”):
o Aetiology:
§ Certain strains of GABH-Strep “Pyogenes” (Which are infected with a “Bacteriophage”
[Virus] → Produce an Eruthrogenic toxin)
o Pathogenesis:
§ GABH-Strep Infection → Exotoxin → Local effect on Tonsils/Pharynx/Skin
• →Tongue
o Initially covered with white exudate
o Exudate is shed
o inflammation of underlying tissue
• → Skin
o Diffuse, Erythematous Rash
o Complications:
§ Rheumatic Heart Disease
§ PSGN
o Diagnosis:
§ **Throat Swab if: Fever + Tonsil Exudate + Lymphadenopathy + <15yo
o Treatment:
§ Antibiotics!!: Penicillin-V/G or Erythromycin if Penicillin Allergic

1 - Estreya at English Wikipedia., CC BY 2.5 <https://creativecommons.org/licenses/by/2.5>, via Wikimedia Commons
2 - www.badobadop.co.uk, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia
Commons

Afag Azizova, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

ACUTE LARYNGOTRACHEOBRONCHITIS (CROUP)
• What is it?
o Inflammation Of Tissues In Subglottic Space ± Tracheobronchial Tree
o + Thick, Viscous, Mucopurulent Exudates Which Compromises Upper Airway →Barking Cough
• Etiology – Viral:
o *RSV or Parainfluenzae (Most Common), II, III, Influenza A And B
• Pathogenesis:
o URTI
o →Inflammation Of Tissues In Subglottic Space
o →Thick, Viscous, Mucopurulent Exudates Which Compromises Upper Airway →Barking Cough
• Morphology:
o Inflamed Upper Airways + Larynx
o Typically Children <5yrs
o Signs of Croup - the 3 S's
§ 1: Stridor
§ 2: Subglottic swelling
§ 3: Seal bark cough
o +/- Cyanosis & Respiratory Distress
• Treatment
o (Note: Viral :. NO Antibiotics)
o Oral/IM Corticosteroids (Dexamethasone / Prednisone)
o Nebulised Epinephrine
o Humidified O2
o +/- Intubation If Severe

https://www.aboutkidshealth.ca/croup

ACUTE EPIGLOTTITIS
• Etiology
o HiB – (Haemophilus Influenzae type B) (Uncommon due to HiB vaccine)
§ (Gram neg coccobacillus)
o Typically Children 1-4yo
o High Fever & Unwell
o Sore Throat, Dysphagia, Anorexia
o Obstructive Symptoms – MEDICAL EMERGENCY → INTUBATE:
§ Difficulty Swallowing, DROOLING, cyanotic/pale, inspiratory stridor, slow breathing,
• Investigations:
o Preparations For Intubation Or Tracheotomy Must Be Made Prior To Any Manipulation
o Lateral Neck XR - Cherry-Shaped Epiglottic Swelling ("Thumb Sign") - Only If Stable
o WBC (Elevated)
o Blood And Pharyngeal Cultures After Intubation
• Treatment
o *Admit to ICU
o Urgent Intubation → Secure Airway
§ + Humidified O2
o Antibiotics – (Ceftriaxone + Clindamycin)
o Extubate When Afebrile
o Watch For Meningitis

https://commons.wikimedia.org/wiki/File:Epiglottitis_endoscopy.jpg

PERTUSSIS - WHOOPING COUGH:
• Aetiology:
o Bordetella pertussis – (Only a human pathogen)
• Pathogenesis:
o Infection of Trachea & Bronchi → Toxins → Widespread Trachea/Bronchi Inflammation
o Pertussis toxin → increased secretions → Cough
o Dermonecrotic toxin → vasoconstriction, Ischaemia
o Tracheal cytotoxin → inhibition of cilia movement
• Clinical Features:
o Severe childhood disease
§ → Dyspnoea
§ → Chronic, Severe Coughing Fits
o Highly Contagious (infants <12mths)
• Investigations:
o Diagnosed on Clinical Suspicion
o (Culture takes <2wks – TOO Long!)
• Management:
o Empirical Antibiotics – (Azithromycin / Clarithromycin / Erythromycin)
o + Booster Vaccination (Unvaccinated / Adolescents / Adults)
o + Vaccinate close contacts (DTP Vaccine)
o +/- Post-Exposure Prophylaxis in Close Contacts (Azithromycin)

https://www.canada.ca/en/public-health/services/reports-publications/canada-communicable-disease-report-
ccdr/monthly-issue/2018-44/issue-9-september-6-2018/article-1a-pertussis-whooping-cough-still-danger-infants-
infographic.html

Q-FEVER
- Aetiology:
o Coxiella Burnetii - (found in cattle, sheep, goats and other domestic mammals, (cats and dogs))
- Transmission:
o Inhalation of Endospores / Contact with Unpasteurised Milk, Urine, Faeces of infected animals
- Pathogenesis:
o 2-3wk Incubation
o Two-Stage Disease:
§ Acute Stage (Headaches, chills, and respiratory symptoms)
§ Chronic Stage (Asymptomatic, Insidious)
o Acute Symptoms:
§ Flu-Like Symptoms: Abrupt Onset Fever, Chills, Sweats & Malaise
§ Respiratory - Dry Cough, Pleuritic Pain
§ GI Symptoms - Nausea, Vomiting And Diarrhoea
§ Neuro: +/- Severe Headache & Confusion
§ MSK: +/- Myalgia & Arthralgia
- Diagnosis:
o Serology
o PCR
o TOEcho – (If Suspected Endocarditis)
o LFT – (↑ALT & AST)
- Treatment:
o Antibiotics – Doxycycline
- Complications:
o Progression to Atypical Pneumonia → life threatening ARDS
o Rarely Granulomatous Hepatitis which can → hepatomegaly and RUQ pain
o Chronic form of Q fever → Endocarditis
- Prevention:
o Q-Vax (Whole-cell, killed vaccine via intradermal injection)
o (Note: Skin and blood tests should be done first to identify pre-existing immunity; vaccinating
subjects who already have an immunity can result in a severe local reaction)

https://tophealthdoctors.com.au/q-fever-vaccine/
LEPTOSPIROSIS (“Weil's syndrome”, “Cane field Fever”, “7-Day Fever”, “Rat Catcher’s Fever”):
- Aetiology:
o Spirochete Bacteria – Leptospira spp
- Pathogenesis:
o Zoonotic Disease – (Mammals, Rats, Birds, Reptiles) – Transmission through water, food, soil
containing urine of infected animals
§ NO person to person transmission
- Morphology:
o Micro:
§ Spirochete Bacteria
o Symptoms – Note: Biphasic Presentation:
§ 1st Phase (First 7-10 Days):
• Flu like symptoms – Fevers, Chills, Myalgias, Headache & Leptospiral rash. Note:
Resolves after 1 wk
§ *Brief Asymptomatic Period...then
§ 2nd Phase (After 10 Days):
• Meningitis (*Photophobia), Liver Damage (*jaundice), Renal Failure, Red Eyes
(Uveitis)
o Signs:
§ Fever (PUO)
§ Palmar Erythema
§ Leptospiral rash
§ Jaundice
§ Hepatomegaly/Splenomegaly
§ Costovertebral Angle Tenderness (Nephritis)
o Complications:
§ Myocarditis, Pericarditis
§ Meningitis
§ Liver Failure
§ Renal Failure
§ Respiratory Distress
- Diagnosis:
o Blood Cultures – if in 1st phase
o **Urine Cultures or Serology – if in 2nd phase
o (DDX’s: Dengue, Hepatitis, Meningitis, Malaria, Typhoid)
- Treatment:
o Penicillin/Cephalosporins

New Hypothesis for Cause of Epidemic among Native Americans, New England, 1616–1619 - Available from:
https://www.researchgate.net/figure/Leptospiral-life-cycle_fig3_41188404

Epidemiology: From Recognition to Results - Available from: https://www.researchgate.net/figure/Leptospirosis-
reservoirs-and-transmission-to-humans-Source-Ko-et-al-2009-Reproduced_fig3_323678367

MELIOIDOSIS
- Aetiology:
o Burkholderia Pseudomallei (Intracellular Gram Negative Bacteria)
o Lives in soil & fresh surface water (Seasonal in wet seasons)
- Pathogenesis:
o Transmission – Percutaneous Inoculation from Wet Soils/Surface Water. Or inhalation
§ Risk factors – Immunosuppression, chronic lung disease
o Immune Mechanisms - Pseudomallei lives Intracellularly:
§ Cell-Mediated Immunity = Most Important
§ Humoral Immunity is Ineffective
- Morphology:
o Macro:
§ Cavitatory Lesions in Upper Lung Lobes
§ Skin Abscesses
o Micro:
§ Fluorescence stain – Rod-shaped, gram negative, bacilli
o Typical Presentation - Pneumonia:
§ Pneumonia + (Cavitatory Lesions in the upper lung lobes (SIMILAR TO TB))
• :. Cough, Sputum, Respiratory Distress
§ + PUO (Fever), Chills, Rigors
§ + Skin Ulcers/Abscesses
o (May → Sepsis → Death)
- Diagnosis:
o Cultures
- Treatment:
o Note: Organism is resistant to Broad Spectrum Antibiotics
o Long-Course Antibiotic Therapy

Source: New England Journal of Medicine
PNEUMONIAS (“Infections of the Lung”):
- Aetiology:
o Community Acquired:
§ Usually Gram-Positive – (Strep pneumonia [90%])
§ Occasionally Gram-Negative – (H-Influenzae)
o Hospital Acquired (Nosocomial - >48hrs POST Admission):
§ Usually Gram-Negative – (Pseudomonas aeruginosa, E-coli, Klebsiella)
o Atypical/Interstitial Pneumonia (“Walking Pneumonia”):
§ Intracellular Bacteria – (Mycoplasma, Chlamydia, Legionella, Coxiella Burnetii)
o In Immunocompromised:
§ Cytomegalovirus
§ Pneumocystis jirovecii
§ Fungal (Candida/Aspergillus)
o General Pneumonia Triad (WHO):
§ Fever
§ Tachycardia
§ Tachypnoea (+/- Breathlessness)

- Types of Pneumonias - Based on Morphology:
o LOBAR-PNEUMONIA (Well Defined; One Lobe):
§ Aetiology:
• Typically Strep Pneumoniae (Gram Positive Diplococci)
• (Or Klebsiella in Aged)
§ Pathogenesis:
• Whole Lobe Involvement
• Exudate Within Alveolar Spaces → Alveolar Consolidation
§ Morphology:
• Follows Anatomical Boundaries (Physically & on CXR)
• Entire Lobe Consolidation/Opacity on CXR
§ Clinical Features:
• Symptoms:
o Abrupt onset High Fever + Chills
o Productive Cough (Occasionally Rusty Sputum &/or Haemoptysis)
o Pleuritic Chest pain + Pleural Rub
• Signs:
o Usually Unilateral
o Exudation – Entire Lobe Consolidation
o Cardinal Pneumonia Signs –(Fever, Tachycardia, Tachypnoea)

Heart, Lung and Blood Institute - http://www.nhlbi.nih.gov/health/health-topics/topics/pnu/causes.html
o BRONCHO-PNEUMONIA (Patchy; Multiple Lobes):
§ Aetiology:
• Secondary to Debilitating Diseases, Extremes of Age, or Post-Surgery:
o Gram Pos - Strep Pneumoniae, Staph Aureus
o Or Gram Neg – H-Influenzae
§ Pathogenesis:
• Patchy Areas of Acute Suppurative Inflammation → Patchy Consolidation
• Basal Lower Lobes Common (Due to gravity – bacteria settle in the lower lungs)
§ Morphology:
• Doesn’t follow anatomical boundaries – Often Multi-Lobar & Bilateral
• Usually Bilateral Patchy Consolidation →Scattered Opacities on CXR
• Symptoms:
o Abrupt onset High Fever + Chills
o Productive Cough (Occasionally Rusty Sputum &/or Haemoptysis)
o Pleuritic Chest pain + Pleural Rub
• Signs:
o Usually Bilateral
o Patchy Consolidation – Usually Bilateral
o Cardinal Pneumonia Signs –(Fever, Tachycardia, Tachypnoea)

1.Franquet T., Chung J.H., CC BY 4.0 <https://creativecommons.org/licenses/by/4.0>, via Wikimedia Commons
2.Suraj at Malayalam Wikipedia, Public domain, via Wikimedia Commons

o ATYPICAL, INTERSTITIAL PNEUMONIA (“Walking Pneumonia”):
§ Aetiology:
• Typically Intracellular Bacteria:
o Mycoplasma, Chlamydia pneumonia, Legionella, Q-Fever (Coxiella burnetii)
• Or Viral:
o Influenza A/B, RSV – Respiratory Syncytial Virus, Corona Virus (SARS)
§ Pathogenesis:
• Interstitial Inflammation (NOT within the Alveolar Spaces)
• Note: 2o Bacterial Pneumonia (Typically Strep/Staph) may follow
§ Morphology:
• Inflammation localised to Alveolar Wall/Septa (Interstitium); NO Alveolar Exudate
• Typically Bilateral
• Symptoms:
o Initial URTI → SLOW Onset (Days-Weeks)
o Symptoms more General & ‘Flu-like’
o Few Localizing Symptoms:
§ Often NO Cough
§ Wheezing (Not seen in other pneumonias)
• Signs:
o No Physical Signs of Consolidation
o Unresponsive to Common Antibiotics

https://www1.racgp.org.au/ajgp/2018/march/an-atypical-case-of-typical-pneumonia

Yale Rosen from USA, CC BY-SA 2.0 <https://creativecommons.org/licenses/by-sa/2.0>, via Wikimedia Commons

- Investigations For Pneumonia:
o CXR – (Consolidation Lobar/Broncho/Interstitial)
o Sputum MCS – (Sputum / NPA – Nasopharyngeal Aspirate / BAL – Bronchio-Alveolar Lavage)
o Blood Culture if ?Septic
o Serological Testing – (If ?Atypical Pneumonias)
- Management:
o ?Admit to ICU? – CURB-65 – (Score >3 → ICU):
§ Confusion
§ Uraemia
§ Resp Rate >30
§ BP <90/60
§ >65yo
o Antibiotics:
§ Empirical:
• ?G-Pos: Amoxicillin / Benz-Penicillin-V / Doxycycline / Clarithromycin
• ?G-Neg: Gentamicin / Ceftriaxone
• Severe: + Meropenem / Imipenem
§ But Ultimately Dictated by MCS
o Fluids
o O2 if Sats <92%
o +/- Ventilation
- Possible Complications of Pneumonia:
o ARDS – Acute Respiratory Distress Syndrome:
§ Severely Impaired Gas Exchange → Hypoxia & Confusion
§ Rx: Mechanical Ventilation and ICU
o Lung Abscesses
o Pleuritis/Pleural Effusion/Empyema
§ Inflammation of the pleura (Strep Pneumoniae)
§ Blood Rich Exudate/Pus in Pleural Space
§ Rx: Drainage + MCS → IV Antibiotics
o Septicaemia, Meningitis
o Fibrosis, Scarring, Adhesions
o Rarely Adenocarcinoma

BRONCHIOLITIS:
• Aetiology:
o Respiratory Syncytial Virus (RSV) (>50%)
o parainfluenza, influenza, rhinovirus, adenovirus, rarely M-pneumoniae
• Clinical Presentation
o Common, affects 50% of children in first 2 years of life
o Initial URTI with cough and fever → Respiratory Distress
§ Wheezing, Tachypnea, Tachycardia
§ Intercostal Recessions, Tracheal Tug, Supraclavicular Recessions, Rib Flaring
o + Feeding difficulties, irritability
• Investigations
o CXR (Air trapping, peribronchial thickening, atelectasis, increased linear markings)
o NPA for PCR
o FBC (Lymphocytosis)
• Treatment
o Fluid Rehydration
o Paracetamol (fever)
o Humidified O2
o Bronchodilator (Ventolin [Salbutamol])
o If Severe → Intubation and Ventilation
o Indications For Hospitalization
§ Hypoxia: SpO2 <92%
§ Resting Tachypnea >160/minute
§ Respiratory Distress even after Salbutamol
§ <6 months old
§ Feeding Problems

https://www.healthing.ca/other/respiratory-syncytial-virus-rsv/

https://www.ncbi.nlm.nih.gov/books/NBK442240/figure/ch5.f3/

https://m.theindependentbd.com//magazine/details/159068/Bronchiolitis:-Not-to-be-treated-lightly

SEASONAL FLU (INFLUENZA A & B):
• Aetiology:
• Influenza Virus A & B
• Pathogenesis:
• Transmission: airborne spread; droplet
• Incubation Period: 1-4 days
• Contagious for: 1day Before Syx Onset, and the next 7days
• Viral-Induced Epithelial Dysfunction & Destruction
• Symptoms: Chills, Fatigue, Cough, Myalgias, Arthralgias, Headache
• Signs: High Fever (<42C); But Chest Clear (Unless 2o Bacterial Pneumonia)
• Complications: 2o Bacterial Pneumonia, Otitis Media, Sinusitis
• Diagnosis:
• Clinical Diagnosis (Signs & Symptoms)
• +/- Nasopharyngeal Swabs
• +/- Serology
• Note: CXR is usually Normal
• Treatment and Prevention
• Primarily Supportive Treatment:
§ Bed Rest, Fluid, Paracetamol/Analgesics, Antitussives, Decongestants
• +/- Antivirals (Effective within 48 hours of onset):
§ Oseltamivir (Tamiflu TM) / Zanamivir (Relenza TM) → Reduce <24hrs of Symptoms
• Vaccine:
§ FluVax is recommended Annually for Everyone
§ (Note: Vaccine is reformulated each year to include current serotypes)

Source: WHO
BIRD FLU (H5N1):
• Aetiology:
• Influenza H5N1
• Pathogenesis:
• Transmission – Aerosol/Direct Contact
• Incubation Period Generally 2-8 Days
• Infection with Influenza H5N1 → Viral Replication → Virus-induced Epithelial Dysfunction
• Mortality Rate ≈63%
• Symptoms: High Fever (>38"C), Headache, Myalgias, Cough (± Sputum ), Dyspnoea + Others
• Pneumonia: Consolidation, Tachypnoea, Tachycardia
• Often Progresses To ARDS → Multi-Organ Failure → Death
• Investigations:
• NPA → PCR
• CXR - (Infiltrates +/- Pleural Effusions)
• Treatment
• ICU - (Ventilation, Fluids)
• Antivirals – (Oseltamivir (Tamiflu TM) / Zanamivir (Relenza TM))
• Prevention
• No Vaccine
• Hygiene Precautions
• Post-?Exposure-Prophylaxis – (Oseltamivir / Zanamivir)
• Notify Public Health
• Contact Tracing and Quarantine

Source: CDC

SWINE FLU (H1N1):
• Epidemiology
• HUMAN to HUMAN - NOT by pigs; documented mass pig slaughtering was unnecessary
• Incubation Period 24--48 Hours
• Aetiology:
• H1N1 – (A Novel strain - genes from 5 different flu viruses)
• Pathogenesis:
• Droplet Transmission – Human to Human
• Respiratory Tract Infection
• Low Mortality Rate - 2 deaths in first 600 cases in the US
• Infects The Young (<5yrs) And Old (>65yrs)
• Transmission: Aerosol/Contact (Human:Human)
• Symptoms: Fever, Cough, Sore throat, N/V/Dia (25%), Myalgia/Arthralgia, Headache

• Diagnosis:
• Clinical Suspicion
• PCR – (Nasal/Nasopharyngeal/Oropharyngeal)
• Notify Public Health
• Contact Tracing and Quarantine
• Treatment
• Antivirals – (Oseltamivir (Tamiflu TM) / Zanamivir (Relenza TM))
• +Supportive

https://www.cdc.gov/flu/swineflu/keyfacts_pigs.htm
SARS & COVID – SEVERE ACUTE RESPIRATORY SYNDROME:
• Definition
o Rapidly progressing viral pneumonia caused by the SARS-associated coronavirus (SARS-CoV)
• Aetiology:
o SARS-Associated Coronavirus
o Incubation: 2-7 days
• Pathophysiology
o Droplet Transmission – Human to Human
o Respiratory Tract Infection with SARS-Associated Coronavirus
o → Atypical Pneumonia +/- Respiratory Distress Syndrome
o Difficult To Differentiate SARS from other Community-Acquired Pneumonias Because:
§ Initial Symptoms Are Not Specific:
• Fever, Chills, Malaise,
• Headache, Myalgia,
• Cough, Sore Throat, Productive Cough
§ However, 2/3 Of Patients Deteriorate with:
• Persistent Fever,
• ↑SOB & Desaturation
§ 20% Require ICU Admission and Mechanical Ventilation
• Complications
o Respiratory failure
o Liver failure
o Heart failure
• Diagnosis:
o Clinical Suspicion – Symptoms, Hx of Travel, Hx of Contact
• Investigations:
o CXR – Features of Atypical Pneumonia
o Lab – Neutrophilia, Lymphopenia, ↑CRP, & ↑LDH
o RT-PCR – from Blood/Sputum/NPA/Swabs
o Serology – (antibody detection via ELISA)
• Treatment
o Notify public health
o Quarantine (negative-pressure room, N95 Mask, gown, gloves, eye protection)
o Antivirals – (Ribavirin)
o Steroids - (To prevent immune mediated lung damage)

https://www.cdc.gov/ncidod/eid/vol9no6/03-0264.htm
GENITAL HERPES SIMPLEX:
- Aetiology:
o HSV2 in Genital Herpes (12.5% Prevalence!!)
o (HSV1 in Cold sores; but can still cause genital infections) (70% Prevalence!!)
- Pathogenesis:
o Contact Transmission
o 1:Lives in Neurons → Latent...2:Reactivation → Travels down Axon into Skin → Lesions
- Morphology:
o Papular/Vesicular lesions on external Genitalia
- DDXs of Genital Ulcers:
o Infection: Herpes/Syphilitic Chancre/Donovanosis/Lymphogranuloma Venereum
o Trauma: Mechanical/Chemical
o Allergic: Contact Wet Dermatitis
o 2F:1M
o Symptoms:
§ Course:
• <3wks Incubation
• Prodrome – Paraesthesia, Itching, Redness
• Symptoms last for <2wks if untreated
o Clusters of PAINFUL, ITCHY, Papules/Vesicles on External Genitalia
o Vesicles may Rupture → Painful Ulcerations
• Recrudescences:
o Typically milder than 1st presentation
o 1-2 day prodrome (Paraesthesia)
§ +/- Proctitis/Cervicitis
§ (Note: ANY genital ulcer, scabbed, red-edged, multiple, and painful = Think Herpes!)
- Diagnosis:
o Swab Vesicle → HSV 1&2 PCR
o Tzanck Smear (Typical intranuclear inclusion bodies & multi-nucleated giant cells)
o HSV Serology (limited use)
- Treatment (NO CURE; Symptomatic & Suppressive Therapy ONLY):
o Valaciclovir/Famciclovir/Aciclovir – (Nucleoside Analogue Anti-Virals) (BD 10 days)
§ Note: “Suppressive Therapy” → 50% Reduction in Transmission
o Analgesia – Lignocaine Gel
o Counselling & Sex-Education
§ 90% of HSV2 will have recurrences >5x/year
§ (Note: HSV1 have annual recurrences)
o Advise Abstinence in the Prodrome or when Lesions are Present
§ BUT Note: Asymptomatic Viral Shedding Still Occurs!!!!

Creative Commons: https://en.wikipedia.org/wiki/File:SOA-Herpes-genitalis-female.jpg
HUMAN PAPILLOMA VIRUS:
- Aetiology:
o *HPV Types 6 & 11 → Genital Warts (Preventable by Gardasil)
o HPV Types 16, 18 & 45→ Cervical Cancer (Somewhat preventable by Gardasil)
- Transmission:
o (Direct Contact/Sexual Transmission – Highly Contagious)
- Pathogenesis:
o Contact & Fomite Transmission
o 3mth Incubation Period
o HPV Infection → Cell-Cycle Dysregulation → Benign Overgrowth
- Morphology:
o Macro:
§ Genital/Cervical Warts (6/11) - Warty Papillomas – External Genitalia/Oral/Anal

https://www.ncbi.nlm.nih.gov/books/NBK441884/figure/article-22202.image.f2/

§ Cervical Ca (16/18/45) – Abnormal looking cervix (Loss of normal smoothness, obvious
dysplasia)

https://oacapps.med.jhmi.edu/OBGYN-101/Text/Pap/Moderate%20Dysplasia.htm

o Micro:
§ Genital/Cervical Warts (6/11) – “Koilocytosis” = Cells with “halo” cytoplasm
§ Cervical Ca (16/18/45) – Squamous Cell Carcinomas, or Adenocarcinomas
o Symptoms:
§ Infection is long-term, latent, and usually asymptomatic
§ Genital Warts (6/11) → Painless, papillary outgrowth on external genitalia
§ Cervical Ca (16/18/45) → Abnormal Vaginal Bleeding, Dyspareunia, Weight-Loss, Fatigue,
Pelvic Pain (May be Asymptomatic)
- Diagnosis:
o Pap smear &/or Cervical Biopsy
o DNA detection
o Tam Pap (Self-sampling HPV DNA test)
- Complications:
o Cervical Cancer - Metastasis
- Treatment:
o Genital Warts (6/11) – Podophylin Cream, Aldara (Imiquimod) Cream, Excision or Cryotherapy –
BUT Will Recur
§ + Counselling
§ +/- Refer to Gynae if – Extensive, Chronic/Recurrent, Cervical or Rectal
o Cervical Ca (16/18/45) – Surgical Excision +/- Chemotherapy +/- Radiotherapy
- Prognosis:
o Genital Warts (6/11) – Benign
§ 70% clear by 12mths (Note: Warts may disappear, but virus may persist)
o Cervical Ca (16/18/45) - Malignant

SYPHILIS:
- Aetiology:
o Treponema Pallidum (Spirochete)
- Transmission:
o Contact, Sexual, & Blood (IVDU) Transmission
o !!Vertical – 100% Transmission if mother is untreated!!
- Pathogenesis:
o Four Stages – Primary, Secondary, Latent, Tertiary (CVS/Neurosyphilis)
o Primary Syphilis:
§ 10d-10wks Post-Infection →Painless Chancre (ulcer) + Lymphadenopathy

https://jetem.org/syphillis_chancre/

o Secondary Syphilis – (Note: Most contagious during secondary syphilis):
§ 4-8wks Post-Chancre → Characteristic Rash (Palms, Feet), Lymphadenopathy,
Hepatosplenomegaly, Flu-like Illness & “Condylomata Lata” (Wart-like Growths)

https://www.nejm.org/doi/full/10.1056/NEJMicm1502476
o Latent Syphilis:
§ Mths-Lifetime Post-Secondary-Stage → Asymptomatic but positive serology
§ ¼ of cases → Tertiary Syphilis (Most remain latent for life)
o Tertiary Syphilis:
§ >1yr Post-Infection → Formation of ‘Gummas’ (Highly-Destructive → bones, skin, nervous
tissue, heart & arteries) → Serious complications are Cardiovascular (Aneurysms) &
Neurosyphilis (Dementia/Psychosis/Paresis/etc)

https://pharmaceutical-journal.com/article/ld/syphilis-diagnosis-and-management-options

- Syphilis in Pregnancy:
o Note: Transmission to the Foetus Typically occurs in the 3rd Trimester of Pregnancy
§ Trans-Placental Transmission
• Can → Miscarriage/Premature labour
o → Early Congenital Syphilis:
• Snuffles – Profuse Runny Nose
• Cutaneous Lesions (Often on Palms and Soles)

CDC/ Dr. Norman Cole, Public domain, via Wikimedia Commons

o →Late Congenital Syphilis:
• Frontal bossing
• Short maxilla
• High palatal arch
• Deafness

CDC/Susan Lindsley, Public domain, via Wikimedia Commons
- Diagnosis:
o Organism can’t be cultured
o Dark-Field Microscopy
§ (Too small for Gram stain)
§ 1: Dark field Microscopy
§ 2: Fluorescence (Ag labelling)
o Serology (May remain +ve for years after recovery)
§ 1: TPHA: T-pallidum haemagglutination assay
§ 2: FTA-AB: Fluorescent Treponemal Antibody Absorption
§ 3: VDRL: Venereal Disease Research lab tests
§ 4: RPR – Diagnostic Standard: Rapid Plasma Reagen
• Tests for Non-Specific Antibodies in the blood
• Good Sensitivity, Poor Specificity
• Interpretation:
o A 2 Titre rise Indicates infection
o A 2 Titre fall indicates effective treatment
- Complications:
o Neurosyphilis → Meningitis, paresis, personality change, ataxia, dementia
o Cardiovascular Syphilis → Typically Syphilitic Aortitis → Aneurysm
o Congenital Syphilis – 25% Miscarriage; 25% Neonatal Death; The rest are DEFORMED!!
§ → Early Congenital Syphilis:
• Snuffles – Profuse Runny Nose
• Cutaneous Lesions (Often on Palms and Soles)
§ →Late Congenital Syphilis:
• Frontal bossing
• Short maxilla
• High palatal arch
• Deafness
- Treatment:
o Azithromycin/Doxycycline
o Or Single Dose IM Penicillin-G
o Treatment of Early Syphilis:
§ Benzathine Penicillin
§ If Truly Allergic to Penicillin –(Azithromycin)
o Treatment of Late/Latent/Unknown Duration of Syphilis:
§ Benzathine Penicillin (Intramuscular Injection)
§ (Painful)
o (Treatment Failure):
§ Treatment Failure = Failure to achieve a 4x Fold drop by 6 months
§ Failure is more common in late syphilis & most common with neurosyphilis
o (Why treat syphilis?):
§ To prevent transmission to others
• Sexual
• Neonatal
§ To Prevent long term complications
• Ie: Tertiary syphilis
• (30% chance of tertiary syphilis if untreated)
§ To reduce chance of transmission of HIV
• HIV transmission increases greatly with concomitant transmission

CHLAMYDIA:
- Aetiology:
o Chlamydia Trachomatis
- Pathogenesis:
o Vaginal, Anal, Oral & Vertical Transmission
o Obligate Intracellular Replication – (Ie: Replicate like Viruses → Shed by Infected cell lysis)
- Morphology:
o Micro: Obligate Intracellular Bacteria → Chlamydial Intracellular Reticulate Bodies
o Symptoms:
§ Males – The COMMONEST cause of Urethritis
• (May also → Epididymitis, Orchitis, Prostatitis & Proctitis)
• (Note: A Non-Gonococcal Urethritis: Ie: Clear, Watery Discharge)
§ Females – Asymptomatic, or Urethritis
• (May → Cervicitis, Salpingitis/PID)
§ Neonates:
• Neonatal conjunctivitis (similar to Gonorrhoea)
• Chlamydial pneumonia

Unattributable
- Diagnosis:
o Sample for PCR:
§ 1st Catch Urine (Unisex)...or
§ Women – Endocervical/High-Vaginal Swab
§ Men – Swab of Urethral Discharge
§ +/- Throat Swabs:
o → Antigen Detection Tests – PCR
o → Gram stain & Immunofluorescence - Intracytoplasmic inclusion bodies – Replicate intracellularly
o (Note: All Females <25 are screened for Chlamydia) – (Via Non-Invasive PCR)
- Complications:
o Trachoma – (Chlamydial Conjunctivitis)
o Lymphogranuloma Venereum - (Lymphatic Chlamydial infection) → Groin Abscesses/Buboes → May
become ulcerative
o PID – can → Infertility, ↑Risk of Ectopic Pregnancy, Chronic Pelvic Pain
o Reiter’s Syndrome Triad - Reactive Poly-Arthritis + Conjunctivitis + Urethritis

https://www.cehjournal.org/article/who-simplified-trachoma-grading-system/
- Treatment:
o 1 Dose Azithromycin 1g
o or Doxycycline 10days 100mg BD
o Note: Resistant strains may exist in certain communities and susceptibility-directed therapy is
recommended.
GONORRHOEA:
- Aetiology:
o Neisseria Gonorrhoeae (Gram Negative)
- Transmission:
o Horizontal via Direct Sexual Contact:
o Vertical – (During childbirth; not trans-placental [like syphilis & hep B])
- Pathogenesis:
o Virulent, Fastidious (Delicate), aerobic, gram negative diplococcic
§ Pili – anchors to urethral epithelium → Resists Flushing → Infiltrates Epithelium
§ Gonococcal Toxin – Endotoxin
§ Protease – Destroys secretory IgA
- Morphology:
o Macro - Inflamed Urethra + Thick, Milky-white Discharge
o Micro - Intracellular Diplococci on Gram Stain (Typically inside neutrophils)
o Symptom Onset within <1wk of Infection
o Men → Acute Gonococcal Urethritis + Dysuria + Discharge (Thick & milky)
o Women → Acute Gonococcal Cervicitis + Vaginal Discharge (May also be Asymptomatic in Women)
+ (Note: Can → PID in females)
- Diagnosis:
o Clinical:
§ Note: Differentiating Gonococcal Urethritis Vs Non-Gonococcal Urethritis:
• Gono – Thick, milky, Penile discharge. Gram Negative Diplococci on gram stain of
discharge
• Non – Thin, watery discharge. No organisms on Gram Stain (Typically Chlamydia)
o Sample for PCR:
§ 1st Catch Urine (Unisex)...or
§ Women – Endocervical Swab
§ Men – Swab of Urethral Discharge
o Men + Women – Throat Swabs
- Complications:
o PID (Females)– can → Infertility
o Urethral Stricture → Urinary Obstruction → Hydronephrosis
o Epididymitis, Prostatitis
o Endocarditis
o Gonococcal Arthritis
o Ocular Infections, Neonatal Conjunctivitis
- Treatment:
o Stat Dose IM Ceftriaxone + Stat Dose PO Azithromycin
o (Or BD Doxycycline for 1wk)

Unattributable
DONOVANOSIS:
- Aetiology:
o Klebsiella Granulomatis (Gram Neg)
o (Formerly: Calymmatobacterium granulomatis)
- Pathogenesis:
o Direct Contact Transmission with OPEN sores
- Morphology:
o Macro:
§ Painless, Oozing, Red Ulcers with Characteristic Rolled Edges of Granulation Tissue
o Micro:
§ Donovan Bodies = Intracellular Rod-Shaped, Oval Organisms seen inside Phagocytes
o Symptoms:
§ → Chronic, painless, offensive, oozing genital ulcers (As opposed to Syphilis = dry) + genital
disfigurement (Lesions occur on Penis, Labia, or Perineum)
§ Note: NO Lymphadenopathy (As opposed to Syphilis = Lymphadenopathy Present)
- Diagnosis:
o Thorough history and examination
o Scrape → Microscopy (Donovan Bodies)
o Swab → PCR
o + Rule out Syphilis (RPR, VDRL, TPHA)
- Complications:
o Genital Disfigurement
- Treatment:
o Doxycycline/Azithromycin/Erythromycin

Creative Commons: https://commons.wikimedia.org/wiki/File:SOA-Donovanosis-female.jpg
HEPATITIS C:
- Aetiology:
o Hepatitis C Virus
- Transmission:
o Blood (Eg: IVDU/needle sharing): As little as 0.0001 mL of blood can transmit the infection
o Body fluids (Eg: Sexual): (Including Cervical Secretions and Semen)
o Vertical (Uncommon)
- Note: Epidemic Potential:
o No Vaccines
- Pathogenesis:
o Viral Infection (Horizontal/Vertical) →Virus Replicates in the Liver
§ Note: Virus is NOT directly Cytopathic; Damage is due to CD8-T-Cell Attack
o → Cellular (CD8) Immune Attack on Infected Hepatocytes
o → Chronic, Low-Grade Inflammation → Eventually leads to Fibrosis → Cirrhosis
- Morphology – Mostly Chronic:
o Chronic ‘Peri-Portal’ Inflammatory Infiltrates
o Necrosis, Apoptosis & Fibrosis → Cirrhosis
o (Hep C – Mild Fatty Change [Microvesicular Steatosis])
o 10% →Acute with Recovery – (Mild Viral Illness + Jaundice)
§ May have Non-Specific Viral Symptoms (Nausea/Anorexia/Fatigue)
§ May have Jaundice
o 90% →Chronic with Extrahepatic & Intrahepatic Manifestations:
§ Asymptomatic for years (Usually Incidental Diagnosis)
§ May have Sporadic Mild Viral Illnesses + Jaundice
§ +/- Arthritis
§ +/- Glomerulonephritis
o END STAGE (CIRRHOSIS):
§ 20-30% → Cirrhosis (within 10-30yrs)
§ 5% → Hepatocellular Carcinoma – (Hep C Directly inactivates P53)

- Investigations:
o Usually discovered on Routine LFTs – (Mildly ↑ ALT/AST)
o Hep C Serology – ((+) Anti-HCV)
o Hep C PCR – ((+) HCV-RNA)
- Treatment:
o Post-Exposure/Acute (Eg: Needlestick):
§ IFN
§ Ribavirin
o Previously incurable
o Now up to 95% ‘curable’ with ‘Direct-Acting Antivirals’ (DAA’s):
§ Epclusa® (sofosbuvir + velpatasvir)
§ Maviret® (glecaprevir/pibrentasvir)
§ Harvoni® (sofosbuvir + ledipasvir)
HUMAN IMMUNODEFICIENCY VIRUS:
- Aetiology:
o HIV
- Transmission:
o Blood (IVDU, Transfusion)
o Body Fluids (Sexual – Particularly Anal Sex)
o Vertical (Cross-Placental & Breastmilk)
- Pathogenesis:
o Lymphotrophic – Preferentially infects CD4-T-Cells → Integrates into Genome → Uses host DNA-
Replication for Reproduction
o CD4-T-Cell Lysis → CD4-T-Cell Depletion (Including Memory T-Cells) →Immunosuppression By:
§ ↓IFNy Production
§ ↓Antibody Production
§ ↓Antibody Isotype Switching
§ ↓Macrophage Activation
§ ↓CD8-T-Cell Activation
o Symptoms:
§ 1-2 months:
• Acute infection (Flu-like symptoms + Maculopapular Rash (ITP))
• Following the acute infection, Antibody titres rise (Detectable after 2.5mths)
§ 2-4 Years:
• Asymptomatic Chronic Infection – (Equilibrium between T-Cells & Viral Mutation
Rate)
§ 8 years:
• Symptomatic Chronic Infection – (Disequilibrium – HIV Quasispecies outnumber T-
Cell Diversity → Body starts to lose the battle)
§ 10-12 years: (If no intervention)
• AIDS - Advanced infection – (T-Cell Depletion)
- Diagnosis:
o Serology (Ab Detection)
o Viral PCR (Ag Detection)
- Complications:
o ↑Infections
o ↑Cancer (Especially Kaposi’s Sarcoma),
- Treatment:
o Fusion Inhibitors – (Eg: CCR5 Inhibitors) - Prevent binding of HIV to Cell
o Reverse Transcriptase Inhibitors (RTI’s) – (Blocks addition of nucleotides to DNA)

https://www.wikidoc.org/index.php/HIV_AIDS_natural_history,_complications,_and_prognosis
TRACHOMA:
- What is it?
o The leading cause of the world’s infectious blindness
o Untreated, repeated trachoma can result in “Entropion”, where the eyelids turn inward → eyelashes
scratch the cornea
- What causes it?
o Causative Organism = Chlamydia Trachomatis
§ Often acquired in the birth canal → Neonatal infections
o Chlamydia Trachomatis is also associated with:
§ Chlamydia STI’s
§ Lymphogranuloma Venereum
§ Neonatal Infections (Eyes & pneumonia)
- How is it Spread?:
o Close Contact, especially with poor facial hygiene
o Contact with Affected Individuals:
§ Eye Secretions
§ Nasal Secretions
§ Throat Secretions
o Or contact with objects (shared Clothes/Towels/Flies) that have had similar contact with these
secretions
- Main Risk Groups & Factors:
o Children
o Mothers
o Carers of children
o Other people in close contact with infected children
o Poor Personal Hygiene
o Overcrowding
- Disease Process (Up to 30 years):
o Acquisition of C-Trachomatis
o Chronic asymptomatic infection
o Chronic inflammation of the conjunctiva
§ → Limbal follicles
§ → Pannus
§ → Herbert’s Pits
o Inflammation of Conjunctiva
§ → Scarring of the conjunctiva underneath the eyelid
§ → Contraction of eyelid scarring (Entropion)
§ → Eyelashes pulled inwards by contracting eyelid
o Eyelashes touch the eye (Trichiasis)
o Corneal Scarring
o Loss of vision
- Pathophysiology:
o Infection with C-Trachomatis → Chronic Inflammation of the Upper tarsal conjunctiva → Scarring of
the Conjunctiva → Retraction of scarring → Pulls eyelid inwards → Eyelashes abrade the cornea →
scarring of the cornea → Opacity & Blindness
- Signs and Symptoms of Trachoma:
o Conjunctivitis:
§ Inflammation of the Conjunctiva
§ The result of “Active Trachoma”

o Trachomatous Inflammation, Follicular (TF):
§ Conjunctival Follicles = situated on the Undersurface of the Upper Eye-Lid
• 5 or more is Diagnostic of Trachomatous Inflammation
§ Limbal Follicles = Follicles can also appear at the Limbus (Junction between Cornea and
Sclera)
• A sign of chronic inflammation of the Corneal Conjunctiva
§ Follicles are White Dots = Essentially Lymphoid germinal centres

https://wikem.org/wiki/Trachoma

o Trachomatous Inflammation, Intense (TI):
§ ‘Papillary’ (tiny projection-like) Hypertrophy (Red Dots) & Inflammatory Thickening of the
upper Conjunctiva
§ Red Dots = ‘Papillae’
§ Rough surface
§ Obscured blood vessels


o Trachomatous Scarring (TS):
§ (AKA: “Cicatricial” (Scarred) Trachoma)
§ Scarring of upper-eyelid Conjunctiva


o Entropion:
§ Contraction of scarring on the underside of the lid → Pulls the eyelid inwards
§ Edge of the eyelid has a ‘rolled’ appearance

Unattributable

o (Trachomatous) Trichiasis (TT):
§ Eyelashes touching the eye

o Corneal Opacity (CO):
§ Causes blindness

https://www.cehjournal.org/article/who-simplified-trachoma-grading-system/

- Treatment: “SAFE” Trachoma Management Strategy:
o Surgery
o Antibiotics (1-2 doses of Azithromycin)
o Face-Washing (Hygiene)
o Environmental control

- Trachoma Screening:
o Test person’s visual acuity using a Snellen’s chart
o General examination of the external eye
o Look for trachoma in both eyes using the WHO Screening Criteria (See Below)

PULMONARY TUBERCULOSIS:
- Aetiology:
o Infection with Mycobacterium Tuberculosis (An Acid-Fast Bacilli) (Droplet Transmission)
- Pathogenesis:
o Pulmonary Tuberculosis:
§ M-Tuberculosis Inhaled → Reaches Alveoli
§ → Invade & Replicate within Alveolar Macrophages
§ (3wks Later) T-Cell Sensitization → Chronic Hypersensitivity reaction to TB Antigens
• Th-Cells Secrete IFNy → Activate Macrophages → Caseating Granulomatous
Inflammation

https://slideplayer.com/amp/3863668/

o Miliary Tuberculosis:
§ M-tuberculosis overrun draining Lymph Nodes and enter the Circulation
§ Organisms are ‘seeded’ back into the lung → Forming Many lesions
§ Miliary lesions Coalesce & Erode the lung parenchyma → Pleural Effusion/Haemoptysis/
Empyema
- Morphology:
o Typically Affects Upper Lung Lobes First
o Caseating Granulomas (Pulmonary or Miliary/Systemic)
§ Nodular, Cavitating, Fibrosing
§ T/B-Lymphocytes, Macrophages, Langerhan’s Giant Cells & Fibroblasts
§ Caseating Necrosis (looks like soft, white cheese)
§ Rim = Fibroblastic + Lymphocytes
§ Centre = Multinucleated Langerhan’s Giant Cells
o Ghon Focus:
§ 1-1.5cm area of Gray-white inflammation with consolidation
§ Central Caseous Necrosis
o Ghon Complex:
§ Ghon Focus + Nodal Involvement

https://pubs.rsna.org/doi/full/10.1148/rg.2017160032

o May be Asymptomatic/Latent
o Classic Symptoms:
§ Chronic Cough
§ Fever, Night Sweats
§ Weight Loss
§ Pleuritic Chest Pain
§ Cavitation & Erosion can → Pleural Effusion &/or Haemoptysis
§ Extrapulmonary Symptoms – Depend on the Organ Affected
o Miliary Tuberculosis:
§ M-tuberculosis overrun draining Lymph Nodes and enter the Circulation
§ Organisms are ‘seeded’ back into the lung → Forming Many lesions
§ Miliary lesions Coalesce & Erode the lung parenchyma
o Diagnosis:
§ Mantoux Test (Tuberculin Test):
• Intradermal Hypersensitivity test to injected PPD (Purified Protein Derivative)
• Only works after 2-4wks post infection; but once infected, will be positive for life
• Signifies T-Cell Sensitivity to Mycobacterial Antigens

CDC: https://phil.cdc.gov/details.aspx?pid=6806
§ CXR:
• Upper Lobe Consolidation
• “Ghon Focus” - ≈1.5cm area of gray-white inflammation with Caseous Necrosis
§ Serology:
• PCR Amplification (Much more sensitive)
§ Microscopy:
• Acid-Fast Sputum Smears
• Culture & Sensitivity

https://www.tbonline.info/posts/2016/3/31/pulmonary-tb/

o Treatment:
§ Combined Antibiotics
• Pyrazinamide
• Ethambutol
• Isoniazid
• Rifampicin

INTESTINAL TUBERCULOSIS:
- Aetiology:
o Reactivation of Primary Mycobacterium tuberculosis (Typically from Pulmonary TB)
o Typically in Immunocompromised (HIV/Drugs)
- Pathogenesis:
o Spread/Reactivation of Tuberculosis:
§ (i) hematogenous spread from the primary lung focus
§ (ii) ingestion of bacilli in sputum from active pulmonary focus;
§ (iii) direct spread from adjacent organs;
§ (iv) through lymph channels from infected nodes
- Morphology:
o Mesenteric Thickening
o Lymphadenopathy
o Ulceration of Transverse Colon
o Multiple Granulomas in Lymph Nodes or Below Ulcers
o Fibrosis, Thickening and Stricturing of the bowel wall
o Symptoms/Signs:
§ **Fever + Night Sweats
§ **Weight Loss
§ *Ileocecal Area is most commonly affected → RIF Abdominal Pain, Palpable Masses
§ Generalised Peritonitis
§ Anaemia
§ Obstruction
o Diagnosis:
§ Histology & Culture
§ CXR (50% have evidence of Pulmonary TB)
o Treatment:
§ Combination Antibiotics:
• Rifampicin
• Isoniazid
• Pyrazinamide
• Ethambutol

Yale Rosen from USA, CC BY-SA 2.0 <https://creativecommons.org/licenses/by-sa/2.0>, via Wikimedia Commons

LEPROSY
• Organism:
o Mycobacterium leprae
• Pathogenesis:
o Chronic disease of skin and nerves
• Presentation:
o Some skin lesions of leprosy can look like dermatophytosis
o Decreased sensation and no sweating
o Lesions can be:
§ Depigmented or Reddish/Copper-coloured
§ flat or raised
§ do not itch/hurt
§ Can appear anywhere
o Becomes severely disfiguring if untreated
• Differential Diagnoses:
o Birthmark
o Vitiligo
o Contact Dermatitis
o Lichenoid Dermatitis
o Tinea Versicolor
• Diagnosis Of Leprosy:
o Clinical
§ Skin lesions
§ Thickening of cutaneous nerves
§ Loss of sensation
o Split Skin Smears
§ Acid fast bacilli (AFB)
o Biopsy

Centers for Disease Control (USA), CC0, via Wikimedia Commons

CC BY 4.0 <https://creativecommons.org/licenses/by/4.0>, via Wikimedia Commons
WHIPPLES DISEASE
- Aetiology:
o Chronic Infection with Bacterium: Tropheryma Whipplei
- Pathogenesis:
o Tropheryma Whipplei is a Relative of Mycobacteria → :. Intracellular (in Macrophages)
o Systemic Infection → Systemic Disease
- Morphology:
o Endoscopy – Pale, Shaggy Duodenal Mucosa + Eroded, Red Friable Patches
o **Biopsy – Characteristic 3-Layered Cell Wall of T-whipplei Within Foamy Macrophages
- Symptoms/Signs:
o Initially – Arthritis & Arthralgia (but in Middle Aged)
o Progression to – Weight Loss, Diarrhoea, Abdo Pain, Fever
o Involvement of – Lymph nodes, Heart, Lung, Joints & Brain (Neuro Symptoms)
- Investigations:
o Blood Tests – Features of Chronic Inflammation & Malabsorption
o Endoscopy – Pale, Shaggy Duodenal Mucosa + Eroded, Red Friable Patches
o **Biopsy – Characteristic 3-Layered Cell Wall of T-whipplei Within Macrophages
o Immunohistochemistry – T-whipplei Antibodies
o PCR
- Treatment:
o Long-Course Antibiotics that Cross the BBB – Eg: Trimethoprim or Co-Trimoxazole
- Prognosis:
o Fatal if untreated

Electron Micrograph showing the Tri-Laminar Cell Wall of Trophyrema whipplei

The characteristic feature of Whipple's disease; foamy macrophages are present in the lamina propria:

Nephron, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
METAZOAN PARASITES:
- Soil Transmitted Helminths:
o Live in GIT
o Pass Progeny in the Faeces (Usually Eggs, Sometimes larvae)
o Use soil for Development from Early Stage (Egg/Larvae) → Infective Stage → Host
o Common in tropical Climates – Warmth & Humidity Critical
o ROUNDWORM (“ASCARIS LUMBRICOIDES”):
§ Larvae grow in the Lungs
§ Adults Live in Small Intestine
• Feeds on Intestinal Contents
• Strong Swimmer (has no ‘attachment organ’)

https://www.cdc.gov/dpdx/ascariasis/index.html
o WHIPWORM:
§ Lives in Large Intestine
§ Whip-like Tail Anchors to Large Intestine Wall

https://upload.wikimedia.org/wikipedia/commons/9/92/Trichuriasis_lifecycle.jpg

o HOOKWORM:
§ Live in Small Intestine
§ Uses Mouth to Attach to Intestine Wall → Feed on Blood
§ Eggs → Soil → Hatches in Soil → Larvae Chase Heat → Burrow Through Skin → Circulation →
Lungs → Trachea → Down Oesophagus → Stomach → Small Intestine

https://www.cdc.gov/parasites/hookworm/biology.html

o STRONGYLOIDES:
§ Lives in Small Intestine
§ Eggs → Soil → Hatches in Soil → Larvae Chase Heat → Burrow Through Skin → Circulation →
Lungs → Trachea → Down Oesophagus → Stomach → Small Intestine

https://www.cdc.gov/parasites/strongyloides/biology.html
- LYMPHATIC FILARIASIS:
o Vector:
§ Mosquitos
o Pathogen:
§ Filarial Worms (Parasite)
§ Live in Lymphatics + Nodes
o Life Cycle:
§ Adults in Lymphatics → Release Baby Worms (Microfilaria)
§ Microfilaria → Sucked up By Mosquito → Develops inside mosquito
§ New Host Next Bite
o Results in Morbidity, not Mortality
§ Elephantiasis – Massive Oedema
• Extensive Lymphatic Damage
• Suppresses Immune System → Recurrent Infections
• Fevers
• Genital Disease
• Social Isolation/Stigmatisation/Depression
o 4 Aspects of Management:
§ 1: Preventative Chemotherapy (Prevention)
• 1x Dose every year for 5 years = good protection
§ 2: Hygiene
• Care of Entry Lesions (wounds)
• Wash affected limb with Soap + Water
• Prevents Secondary Infections
§ 3: Elevation:
• To Maximise Lymphatic Drainage
§ 4: Exercise:
• To Maximise Lymphatic Drainage
o Acute Attack of Filariasis:
§ Caused by secondary bacterial infection
• Increased swelling
• Fever
• Sore Glands
• Headache
• Nausea
§ Treatment:
• 1: Cool leg with cold, clean water
• 2: Take medicines for Fever + Drink More Water
• 3: Keep Washing as per Usual
• 4: Rest

https://mectizan.org/diseases/lf-2/

https://www.cdc.gov/parasites/lymphaticfilariasis/biology.html

MALARIA:
- Pathogen = Plasmodium
o Eukaryotic Protozoan Parasite
o Widespread in Tropical & Subtropical regions
o 5 Species:
§ Plasmodium Falciparum (Most Serious) (Not Persistent in Liver)(80% of Cases)
§ Plasmodium Vivax (Less Serious) (Persistent in Liver)
§ Plasmodium Ovale (Less Serious) (Persistent in Liver)
§ Plasmodium Malariae (Less Serious) (Not Persistent in Liver)
§ (Plasmodium Knowiesi – Mostly A Zoonosis)
- Vector:
o Anopheles Mosquito:
§ (A Night Biter)
§ Breeds in shaded, heavily vegetated permanent water
- Two Patterns of Transmission:
o 1: Stable Transmission:
§ Constant Endemic Rates
o 2: Unstable Transmission:
§ – Periodic Epidemic Outbreaks
- Lifecycle:
o By the bite of a female Anopheles Mosquito
o 1: Bites an Infected Person (Blood contains malaria Gametocytes)
o 2: Gametocytes develop in the Anopheles Mosquito → Oocysts in the Gut Wall
o 3: Oocysts rupture → Sporozoites Released → Migrate to Mosquito’s Salivary Glands
o 4: Sporozoites are injected in the Anopheles Mosquito’s Saliva → Into the Human Host
o 5: Sporozoites in Bloodstream → Infect Liver & Multiply → Thousands of Merozoites
o 6: Merozoites lyse Hepatocytes → Infect RBCs & Multiply
o 7: Merozoites → Form Gametocytes → Sucked up by Anopheles Mosquito
- Incubation:
o Between 2wks and several months

https://www.cdc.gov/dpdx/malaria/index.html

- Pathogenesis:
o RBC Invasion and Lysis →
§ Release of Pyrogens → Fever
§ Extravascular haemolysis – (in spleen)
• →Haemoglobinuria
• →Anaemia
§ Headache
o RBC’s Become ‘Sticky’ → Adhere to Endothelium → Capillaries Clogged → Tissue Hypoxia →
Multiorgan Failure
§ Cerebral Malaria
§ Pulmonary Oedema
§ Renal Failure
o Immune Complex Deposition (Type III Hypersensitivity):
§ Glomerulonephritis
§ Arthritis
- Symptoms:
o (The Common Symptoms):
§ Episodic Fever (6-8hrs) – Due to consecutive Waves of Merozoites Escaping from RBCs &
Reinfecting Other RBCs
• May be ‘Tertian’ (Every 2nd day) or ‘Quartan’ (Every 3rd day)
§ Vomiting/Headache/Diarrhoea
o “Complicated Malaria” (Acute) – Exclusively by P-Falciparum (80% of Cases; 90% of Deaths):
§ Severe Headache/Nausea/Vomiting
§ Cerebral Ischaemia/Hallucinations
§ Severe Anaemia (Hb of 10-20)
§ Haemoglobinuria (+ Renal Failure)
§ Hepatomegaly/Splenomegaly
§ Hypoglycaemia/Acidosis
§ Seizures/Coma
§ Death (Fatality Rate ≈20% with Treatment; 100% without treatment)(Within hours/days)
§ Treated with Artemisinins – Target Gametocytes in the blood (kills active infection)
o “Uncomplicated Malaria” (Chronic) – With P-Vivax & P-Ovale:
§ Headache
§ Fever, Chills, Sweating (Fever may be periodic)
§ Muscle Fatigue/Joint Pain
§ Dry Cough
§ Splenomegaly/Haemolytic Anaemia/Jaundice
§ Nausea/Vomiting
§ (Relapses can occur months/years after exposure – Due to Latent Hypnozoites in Liver)
§ Treated with Primaquine - Targets Hypnozoites in Liver (Preventing recurrence of P Vivax)
- Diagnosis:
o Symptomatic Diagnosis – (Classical Symptoms + Endemic Area ≈ Malaria)
o Old way - Microscopic Examination of Blood (Thick & Thin Films)(Still highly Effective)
o New way – RDTs (Rapid Diagnostic Tests) – Antigen Tests Similar to Pregnancy Test
- Possible Treatments:
o Gametocidal Drugs:
§ Artemethers – Target Gametocytes in the blood (The form that’s infective to mosquitoes)
§ (Single Dose Primaquine is also effective)
o Drugs Targeting Hypnozoites – (in the Liver):
§ Primaquine - Targets Hypnozoites in Liver (Which can lie dormant and cause
recurrences)→Preventing recurrence of P Vivax
o Vaccine Development:
§ Some currently in trial phases and offer partial protection:
• Seem to be showing partial protection, but not total prevention
• Short lived nature of natural immunity
• Parasites’ able to mutate
- Genetic Protection Against Malaria:
o Sickle Cell Trait (heterozygotes) is Protective from Malaria:
§ In a Sickle Cell carrier, Infected Sickle RBCs rupture prematurely → Plasmodium is Unable to
Reproduce
§ ↓O2 → ↓Plasmodium Growth
§ ↑Macrophage Phagocytosis of the Infected Sickle Cells (Eliminates the parasites in the sickle
cell population)
o Others:
§ Lack of the Duffy Antigen (A RBC surface receptor which makes a RBC susceptible to P-Vivax)
§ G6-phosphate dehydrogenase deficiency
§ Thalassemia
- Immunity to Malaria:
o Immunes:
§ After Repeated exposure over many years in an endemic area
§ →Malaria episodes are brief and rarely severe
o Non-immunes:
§ Infants/children
§ Travellers from non-malarious areas
§ →Very symptomatic
§ →Susceptible to severe, life-threatening malaria
o Loss of Immunity to Malaria:
§ Pregnant women
§ Previously immune residing outside of endemic areas
§ →also susceptible to severe, life-threatening malaria
- Disease Prevention:
o Prophylactic Drugs
o Mosquito Nets & Repellents
o Indoor Residual Spraying (Insecticides) in houses
o Vector Control (DDT Spraying, Poisoning Breeding Grounds)
o Public Education about Disease Epidemiology

LEISHMANIASIS:
- Vector:
o Transmitted Via Ectoparasites (Namely Sandflies)
- Pathogen:
o Leishmania Parasites
o 2 Forms in Lifecycle:
§ Amastigotes – In man (mostly Intracellular)
§ Promastigotes – In the Sandfly
- Disease:
o Visceral Leishmaniosis – AKA- Kala Azar:
§ Fever
§ Weight loss
§ Anaemia
§ Swelling of liver & spleen
§ Patient Turns Black
o Cutaneous Leishmaniosis:
§ Nodular & Ulcerated Skin Lesions
o Mucocutaneous Leishmaniosis:
§ Destructive Nasopharyngeal Lesions

https://en.wikipedia.org/wiki/File:Leishmaniasis_ulcer.jpg

https://www.cdc.gov/parasites/leishmaniasis/biology.html
ARBOVIRUSES:
- Aetiology:
o Alphaviruses:
§ Ross River Virus - Alphavirus - Mosquitoes - Fever + Rash + Arthritis
§ Barmah Forest Virus - Alphavirus - Mosquitoes - Indistinguishable from RRV
o Flaviviruses:
§ Dengue (4x Serotypes) - Flavivirus - Aedes Aegypti - Haemorrhagic Fevers
§ Murray Valley Encephalitis - Flavivirus - Mosquitoes - Encephalitic Fevers
- Pathogenesis:
o 1: Bite of an arthropod → Infection
o 2: Virus may replicate in the endothelium and lymphatics
o 3: Viraemia and infection of Target Organs → Fever and malaise (Often due to cytokines)
o 4: Adaptive Immunity to Viral Infections is Cell Mediated (Tc-Cells, NK-Cells)
o 5: Long-Term Immunity to Re-Infection is via Humoral Response (Antibodies & Complement)
§ Prevent Re-Infection by neutralising free viruses in blood & preventing Fusion with Cells
o 3x Typical Presentations:
§ ROSS RIVER VIRUS & BARMAH FOREST VIRUS:
• (Fever)
• *Rash (Maculopapular) (On Trunk)
• *Arthritis (Symmetrical Polyarthritis)
• Lethargy
• (Barmah Forest – Indistinguishable from RRV)
§ DENGUE FEVER:
• (Fever)
• *Rash (Haemorrhagic/Petechial – due to DIC → Thrombocytopenia)
• *Myalgia (“Breakbone Fever” – Severe Muscle Pain)
• (+/- Vom, Diarr, Abdo Pain)
• If 2nd Infection with Different Serotype → Dengue Haemorrhagic Fever/Shock (DHF)
o Severe Bleeding
o Leaky Capillaries
o Shock
§ MURRAY VALLEY ENCEPHALITIS:
• (Fever)
• *CNS Involvement → Headache, Neck Rigidity, Nausea, Convulsions, ALOC
• ~20% Mortality; 50% of survivors have significant neurological disabilities
- Diagnosis:
o Serology for Ab’s Test
o PCR for viral Ag’s

- Treatment:
o Supportive Treatment
ROSS RIVER VIRUS (RRV)
- Causative Organism:
o Ross River Virus
o (RRV is an Alphavirus)
- Vectors:
o Aedes Vigilax – Breeds in stagnant Salt Water (Mudflats/Mangroves/Tidal Flats/Etc)
o Culex Annulirostris – Breeds in freshwater pools/ponds/wetlands/lakes/dams/etc)

- Reservoir Hosts:
o Kangaroos & Wallabies

- Symptoms: (Similar to “Barmah Forest Disease”)
o 95% Polyarthritis in small, joints, fingers, hands, feet & wrist
o 30-50% suffer fever
o Maculopapular Rash (Red/Raised – but not itchy)
o Arthralgia (sore joints)
o Nausea, myalgia, anorexia & lethargy
o Symptoms can last from 30 weeks to 2 years (Especially Arthritic Symptoms)
- Infections are Epidemic/Seasonal:
o Seasonal Rainfall (affects breeding environment of vector)
o Lunar influences on the tides → flooded marshlands (affects breeding environment of vector)
o Temperature & Humidity changes

DENGUE VIRUS:
o Dengue Virus (A Flavivirus)
o 4x Serotypes:
§ (Ie: Different epitopes on the envelope → Specific for adaptive responses)
- Vector:
o Aedes Aegypti
§ Urban Environment (Pots/Gutters/Puddles/Around the house)
§ Infective Vector radius of ~200m from breeding ground

- General:
o It is Extremely Common
o Its Incidence is Increasing
- Presentation: - (Note: Most present Before Immune Response)
o Typical Presentation:
§ Fever & Malaise (Death warmed up/“Breakbone Fever”)
§ Polyarthritis (Muscle & Joint Pain)
§ Hemorrhagic Rash
o Dengue Haemorrhagic Fever (DHF):
§ Severe Bleeding
§ Leaky Capillaries
§ Shock
o Children may suffer from Dengue Haemorrhagic Shock Syndrome (DHSS)(DSS):
§ A result of Immune Enhancement due to a Second Infection with a different Serotype
o (The Dengue Pyramid):
§ Some infected will be Sub-Clinical
§ Most infected will be Clinically Obvious
§ Some will have Dengue Haemorrhagic Fever (DHF)
§ A few will have Dengue Shock Syndrome (Rare, but high mortality rate)

- Pathophysiology:
o →Dengue Haemorrhagic Fever (DHF):
§ 1: Primary Infection →Production of Antibody to Non-Neutralising Epitopes
§ 2: Secondary Infection →Binding of Ab to Non-Neutralising Epitopes →↑Fc-Mediated
Uptake of Dengue Virus by Macrophages
• 3: →Activated Macrophages →Massive Cytokine Production (Especially TNFα, TNFβ
and IFNγ)
• 4: Cytokines + Complement → ↑Vessel Permeability → Vascular Leakage &
Haemorrhage
o →Dengue Shock Syndrome (DSS):
§ Due to Immune Enhancement following a second infection with a different Dengue Serotype
§ Secondary Infection→Binding of Ab to Non-Neutralising Epitopes →↑Fc-Mediated Uptake
of Dengue Virus by Macrophages
• →Activated Macrophages → Massive Cytokine Production (Especially TNFα, TNFβ
and IFNγ)
• Cytokines + Complement → ↑Vessel Permeability → Vascular Leakage &
Haemorrhage → If Severe →SHOCK!
- Disease Progression & Diagnostic Tests:
o - (Note: Most present Before Immune Response)
§ Note:Early negative serology is irrelevant because there may not be antibodies yet
§ Note: Also difficult to distinguish between Antibodies against different serotypes
o *- Dengue Non-Structural Protein 1 (NS1) (detected via ELISA)
§ RDT’s Available
o - High IgG Titre to Flaviviruses
o - Dengue Virus Antigens (detected via PCR)

- Epidemiology & Transmission:
o Endemic and epidemic where vectors present:
§ Vector = Aedes Aegypti (Mosquito)
• Urban Environment (Pots/Gutters/Puddles/Around the house)
• Infective Vector radius of ~200m from breeding ground
§ Reservoir Host = Monkeys
o Events Leading to Dengue Epidemic:
§ 1: Viraemic Individual
§ 2: Community must have Aedes Aegypti
§ 3: Extrinsic Incubation Period (Time from infection of vector, to when it can transmit it to
others)
§ 4: Intrinsic Incubation (Time from infection of human host, to onset of symptoms)
§ 5: First Cases
§ (Note: Cycle takes 13-21 Days – Hence it may take several weeks for a Dengue Outbreak to
be recognised in Townsville)

- Treatment:
o Fluid therapy (usually very effective)
o (Avoid Aspirin or Brufen – Ie: Stuff that makes bleeding worse)
o NO Vaccines present

YELLOW FEVER:
o Yellow Fever Virus (A Flavivirus)
- Vector:
o Aedes Aegypti
§ Urban Environment (Pots/Gutters/Puddles/Around the house)
§ Infective Vector radius of ~200m from breeding ground
- Pathophysiology:
o Virus Infects Viral Organs (Especially the Liver):
§ →Liver Necrosis →Jaundice
o The virus also damages the kidney and heart
- Presentation:
o Characterised by Jaundice
o High case fatality rate
- Transmission
o Urban cycle:
§ Requires man to man transmission
o Sylvatic cycle:
§ Involves other animals/environment (Especially monkeys)

https://ubth.org/yellow-fever-symptoms-prevention/
MURRAY VALLEY ENCEPHALITIS:
• Causative Organism:
o Murray Valley Virus
o (A Flavivirus)
• Vector:
o Culex Annulirostris – Breeds in freshwater pools/ponds/wetlands/lakes/dams/etc
o (Reservoir Host = Water Birds)

• Potentially Fatal CNS infection:
o Virus crosses the Blood Brain Barrier during initial Viraemia
- → CD8-Tc-Cells invade the CNS → Attack infected Glial Cells → Damages brain
o Note: Knockout Mice with No Cell-Mediated Immunity (Tc-Cell Cytotoxins: Perforins/Granzymes),
do not get Encephalitis associated with Infection. Why?
- Lack of CD8-Tc-Cell Cytotoxic Enzymes → No cytotoxicity of Tc-Cells → No cell-mediated
damage of Virally-Infected Glial Cells in the brain → NO Encephalitis
• Presentation:
o Fever
o Headaches
o Nausea & Vomiting
• Severity of brain damage varies:
o Complete Recovery
o Mild Residual Neurological Symptoms
o Severe Neurological Damage
o Death
• Prognosis of Encephalitis:
o ~20% fatal
o ~50% of survivors have significant neurological disabilities
• Distribution in Australia:
o Requires Culex Annulirostris (Which breeds in freshwater/ponds/etc)
o Endemic in Wet, Tropical Areas of the Northern Territory:
§ Eg: Kimberly
o (Epidemic in NQ & Murray Valley) – An Epidemic Requires:
§ Very wet summer
§ Massive growth of the organism
§ Susceptible individuals & reservoir & amplificatory hosts & Migratory Birds
§ Continuous channels of water

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