DCM 3101 • LWA 1 • Sub-topic 1.2
Principles of infectious disease
Infection is the establishment of a foreign organism in or on a host. It may remain as colonisation, progress to tissue injury and clinical disease, or become an opportunistic or endogenous infection when host defences are impaired. The clinical student must understand the organism, the host response and the transmission context together.
- Classify infectious agents and relate their biology to clinical disease.
- Explain normal flora, colonisation resistance and endogenous infection.
- Describe the six links in the chain of infection.
- Explain pathogenicity, virulence factors, toxins, invasion, biofilm and intracellular survival.
- Relate innate and adaptive responses to fever, inflammation, organ dysfunction and recovery.
1. Infection is an interaction, not only the presence of an organism
Colonisation may occur without overt tissue injury. Infectious disease occurs when the interaction between pathogen and host produces damage and clinical illness. Communicable disease is transmitted between hosts; endogenous disease arises from organisms already colonising the patient. Opportunistic infection occurs when natural defence is compromised by HIV, malnutrition, malignancy, immunosuppressive medicine, invasive devices or other conditions.
2. Groups of infectious agents
| Agent | Key biology | Clinical principle |
|---|---|---|
| Prions | Abnormally folded proteins without nucleic acid; induce abnormal folding of normal host protein. | Cause transmissible spongiform encephalopathies and are not treated like bacteria or viruses. |
| Viruses | Contain DNA or RNA in a capsid, sometimes with a lipid envelope; depend on host cells for replication. | Enveloped viruses are generally less environmentally stable; non-enveloped viruses often survive better on surfaces. |
| Bacteria | Prokaryotes that can synthesise proteins and nucleic acids; Gram-positive and Gram-negative cell walls differ. | Capsules, plasmids, flagella, spores and endotoxin influence disease and treatment. |
| Fungi | Eukaryotes occurring as yeasts, moulds or dimorphic forms; membranes contain ergosterol and walls contain chitin or glucan. | Superficial, systemic and opportunistic disease differ in host risk and therapy. |
| Protozoa | Unicellular eukaryotes, often with complex life cycles or vectors. | Travel, water, food, vector and immune status guide diagnosis. |
| Helminths | Multicellular parasites including nematodes, trematodes and cestodes. | Clinical disease reflects tissue migration, adult burden, eggs and host immune response. |
3. Koch’s postulates and their limits
Classical postulates linked a microorganism to a disease by finding it in cases, isolating it, reproducing disease in a susceptible host and recovering it again. They remain historically important but do not apply fully to organisms that cannot be cultured, agents that require specific host cells, members of normal flora or diseases with multiple causes. Modern evidence also uses molecular detection, serology, epidemiology and experimental models.
4. Normal human flora and colonisation resistance
Humans carry large communities of resident and transient microorganisms. Resident flora survive and replicate at a body site; transient flora remain briefly. Normal flora can be mutualistic, commensal or parasitic depending on the interaction. They contribute vitamins, occupy attachment sites, lower local pH, produce bacteriocins and stimulate protective antibodies. Antibiotics, surgery, immune suppression and barrier damage can cause overgrowth, translocation or cross-infection.
Normal flora cause illness when they overgrow at their usual site, move into a normally sterile site, or are transferred to another susceptible person. Examples include vaginal thrush after antibiotics, urinary infection from enteric flora, dental caries and device-associated infection.
5. Pathogenicity, infectivity and virulence
- Pathogenicity is the capacity to cause disease; infectivity is the capacity to establish infection; virulence is the degree of harm.
- Primary pathogens can cause disease in healthy hosts; opportunistic pathogens generally require impaired defence.
- Virulence factors include adhesins, capsules, motility, invasins, enzymes, toxins, antigenic variation, immune evasion and mechanisms that acquire nutrients.
- Plasmids, bacteriophages, mutation, recombination and horizontal gene transfer can change pathogenicity and antimicrobial resistance.
6. How pathogens establish disease
- Adherence: adhesins bind host receptors and determine tissue tropism.
- Colonisation: the organism survives local pH, oxygen, nutrients, mucus, flow and competing flora.
- Invasion: organisms cross epithelium, enter tissue or exploit wounds, devices and injections.
- Multiplication and dissemination: pathogens spread through contiguous tissue, lymph, blood, nerves or vectors.
- Tissue injury: direct cytotoxicity, nutrient theft, obstruction, invasion, toxins or immune-mediated damage.
- Persistence: latency, intracellular survival, biofilm and antigenic change permit chronic or recurrent disease.
7. Toxins and microbial injury
Endotoxin is chiefly a component of Gram-negative outer membrane lipopolysaccharide released during bacterial damage or lysis and causes broad inflammatory effects. Exotoxins are proteins released by living bacteria and often produce specific effects on target cells. Toxin-mediated disease may be severe even when the organism is no longer present at the site of injury.
8. Intracellular pathogens and biofilm
Viruses replicate inside cells. Some bacteria, parasites and fungi survive within macrophages or other cells after phagocytosis. Biofilms are communities embedded in an extracellular matrix on teeth, prostheses, catheters and other surfaces; organisms in biofilms communicate, exchange genes and become less accessible to immune cells and antimicrobials. Device removal or source control may therefore be as important as drug choice.
9. Host defence
| Defence | Examples | Clinical importance |
|---|---|---|
| Physical and chemical barriers | Skin, mucosa, mucus, cilia, cough, gastric acid, bile, urine flow | Breaks, burns, catheters, obstruction and aspiration increase risk. |
| Normal flora | Competition, pH change, bacteriocins and immune priming | Antibiotics can remove colonisation resistance. |
| Innate immunity | Neutrophils, macrophages, complement, NK cells, pattern receptors and cytokines | Fast response; excessive activation can injure tissue. |
| Adaptive immunity | Antibodies, B cells, T cells, memory and cellular cytotoxicity | Specific protection; impaired cellular or humoral immunity changes pathogens. |
10. Host response can help and harm
Clinical manifestations reflect both microbial virulence and the host response. Cytokines and antimicrobial factors help contain infection but may damage tissue. Excess inflammation can cause fever, hypotension, capillary leak, thrombosis, acute lung injury and organ dysfunction. Immune reconstitution inflammatory syndrome illustrates how recovery of immune function can paradoxically worsen inflammation against a persisting pathogen.
11. Fever and systemic inflammation
Microbial and endogenous pyrogens stimulate monocytes and macrophages to release cytokines such as IL-1, TNF and IL-6. These alter hypothalamic thermoregulation through prostaglandin E2. Rigors occur when the body attempts to raise its core temperature. Fever should be interpreted with age, immune status, antipyretic use, perfusion and organ function; absence of fever does not exclude severe infection.
12. The six links in the chain of infection
Communicable transmission requires an agent, reservoir, portal of exit, mode of transmission, portal of entry and susceptible host. Prevention works by breaking any link. For a respiratory infection, ventilation and masks affect transmission; vaccination and prophylaxis protect the host; treatment reduces the reservoir and communicability.
- Do not equate a positive culture with disease without assessing colonisation and contamination.
- Ask whether tissue injury is caused directly by the organism, by a toxin or by the immune response.
- Consider devices, biofilm, obstruction and source control when infection persists.
- Match the suspected organism and site to the host’s immune defect and exposure history.
13. Principles at the bedside
- Identify the syndrome and severity before naming an organism.
- Obtain a good specimen before antimicrobials when safe, without delaying resuscitation.
- Use local guidance and antimicrobial stewardship; narrow, stop or change treatment when evidence returns.
- Protect the patient, staff and community with standard precautions and transmission-based measures.
- Reassess response, complications and the possibility that the diagnosis is non-infectious.
References
- SlideShare: 15 Principles of Infectious Disease
- Davidson’s Principles and Practice of Medicine.
- WHO resources on infection prevention and antimicrobial resistance.
DCM 3101 • LWA 1 • Sub-topic 1.2
Infectious-disease terminology
Infectious-disease vocabulary allows a clinician to describe the agent, host, source, timing, transmission and public-health importance of a case precisely. A student doctor should be able to define a term, use it in a case note, distinguish it from a similar term and explain it in plain language to a patient.
- Define infection, colonisation, contamination, infestation and infectious disease.
- Use case, carrier, reservoir, host, communicable and contagious correctly.
- Distinguish sporadic, endemic, hyperendemic, holoendemic, outbreak, epidemic and pandemic.
- Explain nosocomial, opportunistic, iatrogenic, zoonotic, eradication and surveillance.
- Apply epidemiological terms to a case definition, case-control study and cohort study.
1. Infection and its clinical states
| Term | Definition | Clinical use |
|---|---|---|
| Infection | Entry and development or multiplication of an infectious agent in a human or animal host, with or without symptoms. | Infection may be asymptomatic; disease is not required. |
| Colonisation | Organisms are present and may multiply at a body site without tissue invasion or clinical injury. | Nasal Staphylococcus aureus carriage is not automatically infection. |
| Subclinical infection | Infection without recognisable symptoms, but with biological evidence or an immune response. | It may still contribute to transmission. |
| Latent infection | The agent persists in a relatively inactive state and may reactivate later. | Latent tuberculosis can reactivate with immunosuppression. |
| Clinical or manifest infection | Infection produces signs and symptoms that can be recognised clinically. | Pneumonia, meningitis and malaria are manifest infections. |
| Contamination | Presence of an infectious agent on a body surface, object, instrument, food, water or specimen without establishing infection. | A contaminated culture or surface can lead to a false conclusion. |
| Infestation | Lodgement, development and reproduction of arthropods or other parasites on the body or clothing. | Lice and scabies mites are infestations; malaria is an infection. |
2. Agent, pathogen and host vocabulary
- Infectious agent/pathogen: a bacterium, virus, fungus, protozoan, helminth, prion or other organism capable of causing infection or disease.
- Pathogenicity: the ability of an organism to cause disease. Virulence describes the degree of harm produced once disease occurs.
- Infectivity: the ability to enter, survive and multiply in a host. A highly infectious organism establishes itself readily.
- Invasiveness: the ability to enter tissues, cross barriers and spread beyond the initial site.
- Toxigenicity: the ability to produce toxins that damage cells locally or at a distant site.
- Host: a person or animal that provides lodgement for an infectious agent under natural conditions.
- Definitive or primary host: the host in which a parasite reaches maturity or undergoes sexual reproduction.
- Intermediate or secondary host: the host in which a larval or asexual stage develops.
- Transport host: an organism in which an agent remains alive but does not develop.
- Susceptible host: a person at risk of acquiring infection or developing disease because protective barriers or immunity are inadequate.
3. Reservoir, source and portals
| Term | Meaning | Examples |
|---|---|---|
| Reservoir | The person, animal, arthropod, plant, soil, water or substance in which an agent normally lives and multiplies. | Humans for measles, cattle for some zoonoses, soil for Clostridium spores. |
| Source of infection | The person, animal, object or substance from which the host actually acquires the agent. | A contaminated meal, a mosquito, a patient’s respiratory secretions or a needle. |
| Portal of exit | The route by which the agent leaves its reservoir. | Respiratory tract, stool, urine, blood, skin lesion, genital secretion or placenta. |
| Portal of entry | The opening through which an agent enters the susceptible host. | Mucous membranes, inhalation, broken skin, injection site, urinary catheter or placenta. |
| Vector | A living carrier that transmits an agent biologically or mechanically. | Anopheles mosquito, tick, tsetse fly or housefly. |
4. Cases, carriers and case definitions
A case is a person in a population or study group identified as having the disease, disorder or condition under investigation. A case definition is a standard set of clinical, laboratory, person, place and time criteria used to decide whether someone is counted. It should be simple, practical and objective, while balancing sensitivity against specificity.
- Possible case: compatible clinical features with limited evidence.
- Probable case: compatible features plus epidemiological or preliminary laboratory support.
- Confirmed case: definitive laboratory or other accepted confirmation.
- Primary case: the first case introduced into the population being studied.
- Index case: the first case to come to the investigator’s attention; it may not be the primary case.
A carrier is an infected person or animal that harbours and can shed an agent without obvious illness. An incubatory carrier sheds during incubation; a convalescent carrier continues shedding during recovery; a healthy carrier sheds without having recognised disease. Carriers are epidemiologically important because they may transmit infection while appearing well.
5. Communicability and related terms
- Communicable disease: illness caused by an agent or its products that can be transmitted directly or indirectly between people, animals and the environment.
- Contagious disease: a communicable disease readily spread by direct contact or close personal contact; not every communicable disease is equally contagious.
- Non-communicable infection: disease caused by an organism already colonising the host or acquired from an endogenous source rather than passed between hosts.
- Period of communicability: the time during which an infected host can transmit the agent.
- Incubation period: interval from acquisition to first symptoms; it is not necessarily the same as the period of infectiousness.
- Generation interval: time from infection in one case to infection in a person they infect.
6. Population patterns
| Pattern | Meaning | Example or interpretation |
|---|---|---|
| Sporadic | Irregular, infrequent cases without a predictable pattern. | Occasional isolated cases of a rare disease. |
| Endemic | Constant baseline presence in a geographic area or population without ongoing importation. | Malaria may be endemic in a region. |
| Hyperendemic | Persistently high incidence or prevalence, often affecting many age groups. | High sustained transmission despite ongoing control. |
| Holoendemic | Very high infection beginning early in life; adults may show less clinical disease because of partial immunity. | Classically described for intense malaria transmission. |
| Outbreak | A localised occurrence of cases above expectation; the term is often used to minimise public alarm. | Cases linked to one school, ward, meal or village. |
| Epidemic | Occurrence clearly in excess of expected levels in a community or region. | A sudden rise in cholera above the baseline. |
| Pandemic | An epidemic spreading across countries or continents and affecting a large population. | Global spread of a novel influenza strain. |
| Exotic disease | A disease imported into a country where it does not ordinarily occur. | An imported case of a tropical infection. |
7. Zoonoses and animal-population terms
A zoonosis is an infection naturally transmissible between vertebrate animals and humans. An epizootic is an outbreak or epidemic in an animal population; an enzootic disease is constantly present in an animal population. Important zoonoses include rabies, anthrax, brucellosis, Rift Valley fever, bovine tuberculosis, salmonellosis and hydatidosis. Ask about animal contact, occupation, slaughtering, bites, milk, meat, animal births and unusual animal deaths.
8. Special clinical and health-care terms
| Term | Definition | Why it matters |
|---|---|---|
| Nosocomial or health-care-associated infection | Infection originating during care in a hospital or health facility and not present or incubating at admission. | Includes surgical-site infection, catheter-associated UTI, hospital pneumonia and occupational transmission. |
| Opportunistic infection | Infection by organisms normally harmless or controlled, becoming pathogenic when host defences are impaired. | Consider HIV, immunosuppressive drugs, malignancy, malnutrition and devices. |
| Iatrogenic disease | An adverse health effect generated by a professional activity, medicine, procedure or health-care system. | Examples include drug reaction, line infection and procedure-related injury. |
| Superinfection | A new infection occurring during or after treatment of another infection, often with resistant or overgrown organisms. | Review antibiotics, devices and immune status. |
| Eradication | Permanent reduction of worldwide transmission to zero so routine control measures are no longer needed. | It is absolute; elimination in a defined area is different. |
| Surveillance | Continuous systematic collection, analysis, interpretation and feedback of health data for action. | Surveillance guides outbreak detection and control. |
9. Epidemiological study terms
- Case-control study: begin with disease status, compare exposures in cases and controls, and estimate association commonly with an odds ratio. It is useful for rare diseases and outbreaks but is vulnerable to recall and selection bias.
- Cohort study: begin with exposure status, follow exposed and unexposed groups, and compare incidence or risk. It establishes temporality better but may require time and resources.
- Morbidity: illness, disease or deviation from a state of health, measured by incidence, prevalence, disability or service use.
- Mortality: deaths in a population, often expressed as a rate or ratio.
- Incidence: new cases occurring in a population during a specified period.
- Prevalence: all existing cases at a point or during a period.
- Attack rate: proportion of an exposed or at-risk group that becomes ill during an outbreak.
- Infection is not the same as disease; colonisation is not the same as invasion.
- A reservoir is the usual habitat; the source is where the host acquired the agent.
- An index case is first detected, not necessarily first infected.
- Endemic describes expected presence; epidemic describes excess occurrence.
- Eradication is global; elimination is usually geographic.
10. Applying terminology to a clinical note
Write precisely: “A 24-year-old student is a probable case of acute watery diarrhoea in an outbreak linked to a shared meal. The likely vehicle is contaminated food; the suspected reservoir is human or environmental; stool culture is pending. The patient is not yet a confirmed case.” This sentence separates evidence, uncertainty, source and public-health action.
References
- SlideShare: Infectious disease terminology
- Uganda Clinical Guidelines, Ministry of Health.
- WHO resources on surveillance and outbreak investigation.
DCM 3101 • LWA 1 • Sub-topic 1.2
Concepts in infectious disease
Infectious disease is illness caused by a biological agent or its products interacting with a susceptible host. The agent may be a bacterium, virus, fungus, protozoan, helminth or, in selected settings, an ectoparasite or prion. Infection does not always mean disease: a person can carry an organism without symptoms, while disease occurs when the interaction produces tissue injury, functional disturbance or a clinically important immune response.
- Define infection, infectious disease, colonisation, contamination, infestation, endemic, epidemic, pandemic, sporadic, outbreak and pathogenesis.
- Explain the agent–host–environment model and the chain of infection.
- Relate entry, multiplication, dissemination, tissue injury and host response to clinical presentation.
- Take an exposure-focused history, identify danger signs and choose purposeful investigations.
- Apply prevention, infection-prevention-and-control and public-health principles in a clinical setting.
1. Core definitions
| Term | Meaning | Clinical example or implication |
|---|---|---|
| Infection | Entry and multiplication of an infectious agent in a host, with or without symptoms. | Asymptomatic HIV infection is still infection, even when the patient feels well. |
| Infectious disease | Clinical illness caused by an agent or by the host response to it. | Pneumonia may result from direct microbial injury and inflammatory exudate. |
| Colonisation | Presence and growth of organisms on a body surface without tissue invasion or disease. | Nasal carriage of Staphylococcus aureus is not the same as invasive infection. |
| Contamination | Accidental presence of organisms on an object, specimen, wound or surface. | A contaminated urine sample can produce a misleading culture. |
| Infestation | External or internal occupation by larger parasites, usually arthropods or helminths. | Scabies is an ectoparasitic infestation; schistosomiasis is a helminthic infection. |
| Pathogen | An agent capable of causing disease under suitable conditions. | Pathogenicity is the ability to cause disease; virulence is the degree of damage caused. |
| Reservoir | The usual habitat in which an agent lives and multiplies. | Humans, animals, soil, water and equipment may act as reservoirs. |
| Incubation period | Time from exposure or entry to the first symptoms. | It helps estimate the likely exposure and informs contact tracing. |
| Period of communicability | Time during which an infected person can transmit the agent to another host. | It may begin before symptoms and persist after apparent recovery. |
| Case fatality | Proportion of diagnosed cases that die from the disease. | It reflects severity and access to care, not only organism biology. |
2. Patterns of occurrence in populations
- Sporadic: cases occur irregularly and infrequently without a predictable pattern.
- Endemic: a disease is consistently present at an expected baseline in a population or geographic area. Endemic does not mean harmless.
- Hyperendemic: persistently high transmission or prevalence in a population.
- Outbreak: more cases than expected in a defined place, group or period; the threshold may be one unusual case of a rare disease.
- Epidemic: occurrence above the expected level in a community, region or population.
- Pandemic: sustained transmission across multiple countries or continents affecting large populations.
- Cluster: an aggregation in time or place that may signal common exposure, even before an outbreak is confirmed.
- Elimination and eradication: elimination reduces transmission to zero in a defined area; eradication removes global transmission and the natural reservoir.
- Do not label every cluster an epidemic before comparing it with the expected baseline.
- Ask who is affected, where, when, by what exposure and whether transmission is continuing.
- Notify the appropriate public-health authority for diseases requiring urgent reporting.
3. The agent–host–environment model
Disease usually arises from an interaction rather than from the agent alone. The agent contributes infective dose, route, toxins, enzymes, capsule, adherence factors, antigenic variation, resistance and survival outside the host. The host contributes age, immunity, vaccination, nutrition, pregnancy, genetics, skin and mucosal barriers, microbiome, comorbidities and access to care. The environment contributes climate, crowding, sanitation, water, vectors, health-care practices, occupation, housing, conflict, travel and the availability of prevention.
| Component | Questions during clinical reasoning | Examples |
|---|---|---|
| Agent | What organism is plausible? Is it toxin-producing, resistant or unusually virulent? | Mycobacterium tuberculosis, Plasmodium falciparum, HIV, Salmonella Typhi |
| Host | Why this patient and why now? What barriers or immune defects are present? | HIV, diabetes, malnutrition, extremes of age, pregnancy, steroids |
| Environment | What exposure or system allowed transmission? | Unsafe water, crowding, vector habitat, health-care device, occupational exposure |
4. The chain of infection
Transmission can be interrupted at multiple links. The chain is: infectious agent → reservoir → portal of exit → mode of transmission → portal of entry → susceptible host. A patient-centred plan should identify which link is active and which intervention is feasible.
| Link | Examples | Ways to break the link |
|---|---|---|
| Agent | Bacterium, virus, fungus, protozoan, helminth | Appropriate antimicrobial therapy, sterilisation, disinfection, safe prescribing |
| Reservoir | Human case or carrier, animal, soil, water, food, equipment | Case finding, treatment, environmental cleaning, safe food and water |
| Portal of exit | Respiratory droplets, blood, stool, urine, genital secretions, skin lesions | Respiratory hygiene, wound covering, safe sharps and body-fluid precautions |
| Transmission | Contact, droplet, airborne, vehicle, vector, blood-borne, sexual, vertical | Hand hygiene, PPE, ventilation, isolation, condoms, vector control, safe injections |
| Portal of entry | Respiratory tract, mucosa, broken skin, placenta, injection site | Vaccination, barrier methods, aseptic technique, protective equipment |
| Susceptible host | Non-immune, immunosuppressed, malnourished, very young or old | Vaccination, prophylaxis, nutrition, chronic disease control, prompt diagnosis |
5. Modes of transmission
- Direct contact: transfer during skin-to-skin contact, sexual contact or exposure to lesions.
- Indirect contact: contaminated instruments, surfaces, linen or hands carry the agent.
- Droplet: larger respiratory particles travel a short distance during cough, sneeze or close conversation.
- Airborne: small particles or droplet nuclei remain suspended and may travel farther in poorly ventilated spaces.
- Vehicle-borne: food, water, blood, medications or other materials carry the agent.
- Vector-borne: mosquitoes, ticks, flies or other vectors transmit an agent biologically or mechanically.
- Vertical: transmission from mother to child during pregnancy, delivery or breastfeeding.
6. Pathogenesis: how exposure becomes disease
Pathogenesis is the sequence by which an agent establishes infection, evades or alters host defences, damages tissue and produces signs and symptoms. It often includes exposure, adherence, entry, multiplication, invasion or toxin release, dissemination, host inflammatory response, tissue injury and either clearance, persistence, latency or death.
Fever, swelling, cough, diarrhoea and organ dysfunction may reflect direct microbial injury, toxins, immune-complex disease, cytokine-mediated inflammation, tissue hypoxia or a combination. This distinction matters because killing the organism alone may not immediately reverse inflammation or organ damage.
7. Host defence and susceptibility
First-line barriers include intact skin, mucous membranes, cilia, cough, gastric acid, normal flora and antimicrobial peptides. Innate immunity responds rapidly through neutrophils, macrophages, complement, natural killer cells and inflammatory mediators. Adaptive immunity uses antibodies, T lymphocytes and immunological memory. A defect at any level changes the likely organisms and presentation.
| Risk factor | Mechanism | Clinical consequences |
|---|---|---|
| HIV or other cellular immune deficiency | Reduced T-cell coordination of macrophage and cytotoxic responses | Opportunistic infections, atypical presentations, recurrent disease |
| Diabetes | Impaired neutrophil function, vascular disease and tissue glucose changes | Skin, urinary, pulmonary and invasive infections; poor wound healing |
| Malnutrition | Reduced barrier integrity and immune-cell production | Severe, prolonged or recurrent infection |
| Splenectomy or absent splenic function | Reduced clearance of encapsulated bacteria | Rapid invasive sepsis, especially with pneumococcus |
| Corticosteroids and cytotoxic drugs | Suppression of inflammation or lymphocyte proliferation | Blunted fever and opportunistic or disseminated infection |
| Extremes of age and pregnancy | Immune and physiological changes | Different severity, drug choices and prevention needs |
8. Clinical presentation and stages of infection
Many infections pass through exposure, incubation, a prodrome, acute illness, decline and convalescence, but the pattern varies. Incubation is followed by early non-specific symptoms such as fever, malaise, myalgia or headache. Localising symptoms then suggest the organ system. Some patients remain asymptomatic, some develop a chronic or latent infection, and some deteriorate rapidly with sepsis or organ failure.
Severity is not defined by temperature alone. Assess perfusion, mental state, respiratory effort, oxygenation, urine output, hydration, pain, nutritional status and organ function. Older adults, immunosuppressed patients and people taking antipyretics may have serious infection without high fever.
9. Exposure-focused infectious-disease history
- Timing and place of onset; travel or movement through endemic areas.
- Household, school, workplace and health-care contacts; similar illness in others.
- Food, water, street foods, unpasteurised products and recent diarrhoea in contacts.
- Animals, insect bites, farming, caves, slaughterhouses and occupational exposures.
- Sexual exposure, pregnancy possibility, needles, transfusion, tattoos and medical procedures.
- Vaccination history, previous infection, prophylaxis, HIV status and tuberculosis contact.
- Recent antibiotics, adherence, hospitalisation and resistant-organism history.
- Housing, crowding, ventilation, sanitation, access to clean water and ability to isolate.
10. Diagnosis: specimen before treatment when safe
Start with a problem representation and a ranked differential. Obtain the correct specimen from the correct site at the correct time, before antimicrobials when this will not delay life-saving treatment. Label accurately and document antibiotics already taken. Interpret a test in context: a positive culture may represent contamination or colonisation, while a negative result may follow poor sampling, early disease or prior treatment.
| Question | Examples of useful investigations |
|---|---|
| Is there systemic inflammation or organ dysfunction? | Full blood count, renal function, liver function, glucose, lactate where indicated, urinalysis and observations. |
| What organism is present? | Blood cultures, urine or stool culture, sputum or swab testing, microscopy, antigen tests, nucleic-acid tests and parasite films. |
| Where is the focus? | Chest radiograph, ultrasound, CT, MRI, echocardiography or focused examination. |
| Could this be an alternative non-infectious condition? | Medication review, malaria testing where relevant, imaging, autoimmune or metabolic studies guided by the differential. |
11. Principles of management
- Recognise and treat immediate threats: airway, breathing, circulation, consciousness, seizures, hypoglycaemia, severe dehydration and shock.
- Apply standard precautions and additional isolation measures based on the suspected mode of transmission.
- Use local guidelines and antimicrobial stewardship: choose the narrowest effective agent, correct dose and route, review cultures, adjust for renal/hepatic function and de-escalate or stop when infection is not supported.
- Provide source control when needed, such as drainage of an abscess, removal of an infected device or treatment of obstruction.
- Support the host with oxygen when indicated, fluids carefully, nutrition, analgesia, antipyretics, glucose control and thrombosis or pressure-injury prevention where appropriate.
- Monitor response and complications; document review time, escalation triggers and pending results.
Suspect severe infection when there is new organ dysfunction, shock, altered mental state, respiratory failure, oliguria, severe hypoxaemia, bleeding, jaundice or rapidly worsening condition. Escalate early, obtain cultures where this does not delay treatment, begin locally recommended resuscitation and antimicrobial management, and involve senior help.
12. Prevention and control
| Level | Interventions |
|---|---|
| Primary prevention | Vaccination, safe water and food, sanitation, ventilation, condoms, vector control, hand hygiene, safe injection and occupational protection. |
| Secondary prevention | Screening, contact tracing, early diagnosis, isolation, post-exposure prophylaxis and prompt treatment. |
| Tertiary prevention | Prevent disability, relapse, transmission from chronic disease, drug toxicity and long-term organ damage. |
| Health-care infection prevention | Hand hygiene, standard precautions, PPE, aseptic procedures, sterilisation, environmental cleaning, sharps safety and surveillance of health-care-associated infection. |
13. Public-health response to a suspected outbreak
- Verify the diagnosis and confirm that cases exceed the expected baseline.
- Construct a case definition and line list with person, place, time, symptoms, exposure, specimen and outcome.
- Notify the responsible surveillance team and coordinate laboratory support.
- Describe the outbreak by time, place and person; draw an epidemic curve where possible.
- Generate and test hypotheses, identify the source and interrupt transmission.
- Communicate clearly with patients and the community, address misinformation and protect confidentiality.
- Continue active surveillance, document lessons and strengthen prevention after the event.
14. Clinical summary for the student doctor
When an infectious disease is possible, ask: What is the syndrome? What exposure explains it? Which agent is plausible? How sick is the patient? What specimen will answer the question? Which link in transmission can I break today? What treatment is immediately necessary, and how will I know it is working? The strongest answer integrates bedside assessment, microbiology, pharmacology, epidemiology, infection prevention and communication.
- Infection may be asymptomatic; disease is the clinical consequence.
- Use agent–host–environment and chain-of-infection models to organise reasoning.
- Endemic, epidemic and pandemic describe patterns, not severity.
- Collect a good specimen and interpret results in clinical context.
- Stabilisation, source control, rational antimicrobials and prevention must proceed together.
References
- Doctors Revision Uganda: DCM 3101 curriculum
- Uganda Clinical Guidelines, Ministry of Health.
- Davidson’s Principles and Practice of Medicine, 23rd edition.
- Harrison’s Principles of Internal Medicine.
- WHO resources on infection prevention and control, surveillance and antimicrobial resistance.
