Infectious Organisms: Bacteria, Viruses, Fungi, Parasites and Prions
Infectious organisms are biological agents capable of entering a host, surviving or replicating, interacting with tissues and causing infection. An infection may be asymptomatic, colonising, local, invasive, disseminated or fatal. Not every microbe is pathogenic: the normal microbiota can protect against invasion, while disease depends on the agent, dose, route, virulence, host susceptibility and immune response.
Learning outcomes
- Define infectious organism, pathogen, colonisation, infection, disease, virulence and opportunistic infection.
- Compare bacteria, viruses, fungi, protozoa, helminths, ectoparasites and prions by structure, replication and clinical behaviour.
- Recognise important bacterial, viral, fungal and parasitic patterns relevant to emergency presentations.
- Explain how toxins, adhesins, capsules, biofilms, intracellular survival, antigenic variation and immune evasion cause disease.
- Select specimen types and first-line diagnostic approaches without confusing colonisation with invasive infection.
- Use antimicrobial-stewardship principles and identify situations that require isolation, public-health notification or urgent referral.
1. Core definitions
| Term | Meaning | Example/clinical implication |
|---|---|---|
| Microorganism/microbe | A microscopic living organism or infectious entity; includes bacteria, fungi, protozoa and some parasites. | Many are harmless or beneficial; classification alone does not prove disease. |
| Pathogen | An organism or agent able to cause disease under particular host and environmental conditions. | Pathogenicity is the capacity to cause disease; it differs from severity. |
| Colonisation | Presence and multiplication on/in a host without tissue invasion or disease. | Nasopharyngeal carriage of bacteria may not require antibiotics. |
| Infection | Entry and multiplication/interaction of an infectious agent in a host, with or without symptoms. | Laboratory detection must be interpreted with signs, site and host factors. |
| Infectious disease | Clinical dysfunction or tissue injury caused by infection and host response. | Pneumonia, meningitis, sepsis and malaria are diseases, not merely positive cultures. |
| Virulence | Degree of damage or severity produced by a pathogen in a particular host. | Toxin production, invasion and immune evasion can increase virulence. |
| Opportunistic pathogen | An organism that causes disease when barriers or immunity are impaired. | Candida, Pseudomonas or Pneumocystis may be dangerous in selected hosts. |
| Pathogenicity island/virulence factor | Gene or product that supports adhesion, invasion, toxin production, immune evasion or nutrient acquisition. | Virulence may be gained through mutation, plasmids, phages or horizontal gene transfer. |
2. The major classes at a glance
| Class | Cellular status | How it multiplies | Typical treatment class | Examples |
|---|---|---|---|---|
| Bacteria | Prokaryotic cells with DNA, ribosomes and a membrane/cell wall. | Binary fission; some form spores or survive intracellularly. | Antibacterials selected by syndrome, susceptibility and local guidance. | Staphylococcus, Streptococcus, Enterobacterales, Mycobacterium. |
| Viruses | Acellular particles containing DNA or RNA in a capsid, sometimes an envelope. | Obligate intracellular replication using host and viral machinery. | Vaccines/prevention, supportive care and selected antivirals. | Influenza, HIV, hepatitis viruses, herpesviruses, SARS-CoV-2. |
| Fungi | Eukaryotic yeasts, moulds or dimorphic organisms. | Budding, fragmentation or spores; hyphae may invade tissue. | Antifungals; source control and immune restoration are often critical. | Candida, Cryptococcus, Aspergillus, dermatophytes. |
| Protozoa | Unicellular eukaryotic parasites. | Asexual and/or sexual life-cycle stages, often in vectors or hosts. | Antiprotozoal drugs and supportive/complication management. | Plasmodium, Entamoeba, Giardia, Trypanosoma. |
| Helminths | Multicellular parasitic worms. | Egg, larval and adult stages; some require intermediate hosts. | Anthelmintics, surgery or treatment of inflammatory complications. | Schistosoma, Taenia, Ascaris, hookworm. |
| Ectoparasites | Arthropods living on the skin or hair. | Egg/nymph/adult or other arthropod life cycles. | Topical/oral antiparasitic therapy and environmental control. | Scabies mites, lice, ticks, fleas. |
| Prions | Abnormally folded infectious proteins without DNA or RNA. | Template-directed misfolding of host prion protein. | No proven curative antimicrobial; strict infection-control and specialist care. | Creutzfeldt–Jakob disease and related transmissible spongiform encephalopathies. |
3. Bacteria
3.1 Structure and physiology
Bacteria are prokaryotic cells with a nucleoid, 70S ribosomes, cytoplasmic membrane and a cell wall of variable composition. They lack a membrane-bound nucleus and mitochondria. Their small size, rapid generation and ability to exchange genes allow rapid adaptation.
| Feature | Clinical significance |
|---|---|
| Cell wall | Peptidoglycan provides shape and is a target for beta-lactams and glycopeptides. Gram staining reflects wall/envelope structure. |
| Gram-positive envelope | Thick peptidoglycan with teichoic acids; examples include Staphylococcus, Streptococcus and Enterococcus. |
| Gram-negative envelope | Thin peptidoglycan plus outer membrane containing lipopolysaccharide; endotoxin can drive systemic inflammation. |
| Capsule/slime layer | Reduces phagocytosis and supports adherence; important in pneumococcus, meningococcus, Klebsiella and others. |
| Flagella/pili/fimbriae | Motility, adhesion and conjugative gene transfer; urinary and intestinal colonisation often depends on adhesins. |
| Biofilm | Organised community in extracellular matrix on devices or tissues; reduces antimicrobial penetration and immune clearance. |
| Spores | Highly resistant survival forms in Bacillus and Clostridium; require rigorous decontamination and environmental control. |
| Intracellular survival | Some organisms survive in macrophages or epithelial cells, changing specimen collection and drug penetration requirements. |
3.2 Shapes and arrangements
- Cocci: Staphylococci form clusters; streptococci and enterococci form chains/pairs; Neisseria are diplococci.
- Bacilli: Rods include Enterobacterales, Pseudomonas, Bacillus, Clostridium and mycobacteria.
- Curved/spiral organisms: Vibrio, Campylobacter, Helicobacter, Treponema and Borrelia require specific culture or molecular methods.
- Intracellular or wall-deficient organisms: Chlamydia, Rickettsia, Mycoplasma and Coxiella have distinctive diagnostic and treatment considerations.
3.3 Bacterial disease mechanisms
| Mechanism | Example effect |
|---|---|
| Adhesion | Fimbriae/adhesins attach to respiratory, urinary or intestinal epithelium. |
| Invasion | Enzymes, secretion systems and motility breach barriers and enter tissue/blood. |
| Exotoxins | Secreted proteins produce specific effects such as neurotoxicity, enteric secretion or cytolysis. |
| Endotoxin/LPS | Activates innate immunity, cytokines, vasodilation, capillary leak and potentially septic shock. |
| Immune evasion | Capsules, antigenic variation, intracellular residence, IgA protease and complement resistance prolong infection. |
| Tissue destruction and inflammation | Direct cytotoxicity plus host neutrophil/immune response cause abscess, necrosis or organ dysfunction. |
3.4 Clinically important bacterial patterns
- Pyogenic infection: fever, neutrophilia, pus, abscess, cellulitis, pneumonia or meningitis.
- Sepsis: infection-associated organ dysfunction due to dysregulated host response; the organism may be in blood or only at a focus.
- Intracellular/slow-growing infection: tuberculosis, brucellosis, rickettsial disease and atypical pneumonia may require special specimens, prolonged culture or molecular tests.
- Toxin-mediated illness: clinical disease can persist after the organism is absent because toxin effects continue.
- Device-associated infection: biofilms produce persistent, relapsing infection and may require device removal/source control.
4. Viruses
4.1 Structure
Viruses contain a DNA or RNA genome enclosed in a protein capsid; some have a lipid envelope derived from host membranes. Envelope proteins determine receptor binding and entry but are vulnerable to drying, detergents, heat and solvents. Non-enveloped viruses are often more environmentally stable.
| Viral feature | Clinical implication |
|---|---|
| Genome type | DNA or RNA, single- or double-stranded, positive- or negative-sense, segmented or non-segmented; determines replication strategy and mutation rate. |
| Envelope | Enveloped viruses often spread through close contact, droplets or fluids and are susceptible to detergents; exceptions and route-specific rules apply. |
| Receptor tropism | Receptor distribution determines which cells/organs can be infected. |
| Latency/persistence | Herpesviruses can remain dormant and reactivate; hepatitis/HIV persistence causes chronic disease. |
| Antigenic variation | Mutation, reassortment or recombination can permit immune escape and outbreaks. |
| Oncogenic potential | Some viruses alter cell-cycle control or chronic inflammation, contributing to cancer risk. |
4.2 Replication cycle
- Attachment: viral ligand binds a host-cell receptor or co-receptor.
- Entry/uncoating: fusion, endocytosis or membrane penetration releases the genome.
- Genome expression: viral and host enzymes transcribe/translate early proteins.
- Genome replication and assembly: nucleic acid and structural proteins form new virions.
- Release: lysis, budding or exocytosis spreads infection to new cells/hosts.
4.3 Viral injury and disease
- Direct cytopathic effect, apoptosis or necrosis can destroy infected cells.
- Immune-mediated injury may exceed direct viral injury, as in some hepatitis or severe respiratory disease.
- Persistent infection can produce fibrosis, immune exhaustion, malignancy or reactivation.
- Viraemia can disseminate infection to the brain, placenta, liver, marrow or other organs.
5. Fungi
Fungi are eukaryotic organisms with a nucleus, mitochondria, ergosterol-containing membrane and a cell wall rich in chitin/glucans. They may be environmental, commensal or invasive pathogens.
| Form | Features | Clinical pattern |
|---|---|---|
| Yeast | Unicellular, budding forms; some produce pseudohyphae. | Candida mucosal disease, bloodstream infection or deep-organ infection. |
| Mould | Filamentous hyphae forming a mycelium; spores aid dissemination. | Aspergillus, mucormycosis and dermatophyte disease. |
| Dimorphic fungi | Yeast/mould form changes with temperature or environment. | May cause pulmonary and disseminated disease after inhalation. |
| Dermatophytes | Keratin-loving moulds affecting skin, hair and nails. | Tinea and onychomycosis; usually superficial but persistent. |
5.1 Invasive fungal disease
Risk increases with neutropenia, advanced HIV, transplantation, corticosteroids, diabetes, severe burns, prolonged ICU stay, broad-spectrum antibiotics and indwelling devices. Invasive disease may cause pulmonary nodules, hypoxia, CNS lesions, disseminated sepsis or necrotic skin lesions. Diagnosis often combines culture, microscopy, antigen/PCR and imaging; a negative test does not always exclude disease.
6. Parasites
Parasites are organisms that obtain nutrients or shelter from a host. Human disease is caused by protozoa, helminths and ectoparasites. Life cycles, intermediate hosts, vectors and tissue stages determine clinical disease and diagnostic specimens.
| Group | Characteristics | Examples/clinical syndromes |
|---|---|---|
| Protozoa | Single-celled eukaryotes; trophozoite and cyst/oocyst stages are common. | Malaria, amoebic dysentery, giardiasis, trypanosomiasis, leishmaniasis. |
| Nematodes | Roundworms; eggs/larvae/adults may inhabit gut, blood or tissues. | Ascaris, hookworm, Strongyloides, filariasis. |
| Cestodes | Segmented tapeworms; humans may host adult or larval stages. | Taenia infection, cysticercosis, hydatid disease. |
| Trematodes | Flukes with complex life cycles often involving snails or food. | Schistosomiasis, liver and lung fluke disease. |
| Ectoparasites | Arthropods live on skin/hair and may transmit other pathogens. | Scabies, lice, ticks and fleas. |
6.1 Parasite-related injury
- Direct tissue invasion, obstruction or nutrient theft.
- Haemolysis and microvascular obstruction, as in severe malaria.
- Granulomatous inflammation around eggs or larvae, as in schistosomiasis.
- Allergic/eosinophilic responses and anaphylaxis after cyst leakage.
- Chronic fibrosis, portal hypertension, anaemia or malnutrition.
7. Prions
Prions are abnormal, misfolded forms of a host protein that can induce normal prion protein to adopt the abnormal conformation. They contain no DNA or RNA, are resistant to ordinary sterilisation approaches and cause progressive neurodegenerative disease with spongiform change.
- Human prion disease may be sporadic, inherited or acquired through medical/food exposure.
- Clinical features include rapidly progressive dementia, myoclonus, ataxia, visual or psychiatric symptoms and akinetic mutism, depending on subtype.
- Diagnosis uses clinical course, MRI, EEG, CSF biomarkers and specialised testing; definitive diagnosis may require neuropathology.
- There is no proven curative antimicrobial. Infection prevention requires specialist protocols for high-risk tissues and instruments.
8. Normal microbiota and opportunistic disease
The microbiota competes with pathogens, produces metabolites, supports barrier function and trains immunity. Disease can follow disruption of these relationships.
| Situation | Mechanism | Example |
|---|---|---|
| Barrier breach | Skin, mucosa, gut or airway integrity is lost. | Wound infection, peritonitis, catheter-associated bacteraemia. |
| Microbiome disruption | Antibiotics or hospital exposure reduce colonisation resistance. | Clostridioides difficile colitis or Candida overgrowth. |
| Immune deficiency | Neutropenia, HIV, steroid therapy or inherited defects permit unusual invasion. | Invasive mould, Pneumocystis, disseminated TB. |
| Altered anatomy/function | Obstruction, stasis, devices or aspiration permit organisms to persist. | Obstructive pyelonephritis, aspiration pneumonia, biofilm infection. |
| High inoculum/virulence | Large exposure or toxin/invasion factors overwhelm local defences. | Foodborne intoxication, meningococcal sepsis, necrotising infection. |
9. Virulence factors and host damage
| Virulence strategy | How it works | Possible clinical effect |
|---|---|---|
| Adhesion | Surface proteins bind host receptors and resist mechanical clearance. | Colonisation of airway, urinary tract or gut. |
| Invasion | Enzymes, secretion systems, motility or cytoskeletal manipulation breach tissue. | Cellulitis, abscess, enteritis, bacteraemia. |
| Capsule/antiphagocytic surface | Blocks complement deposition or phagocyte uptake. | Invasive pneumococcal, meningococcal or Klebsiella disease. |
| Biofilm | Matrix shelters organisms from antibiotics and immune cells. | Catheter, prosthetic-joint and chronic wound infection. |
| Toxin production | Exotoxins or endotoxin alter nerves, gut secretion, membranes or cytokines. | Paralysis, diarrhoea, shock, necrosis. |
| Antigenic variation | Changes surface antigens or hides in cells. | Reinfection, chronicity, immune escape. |
| Nutrient acquisition | Siderophores or host-molecule capture obtain iron and other nutrients. | Survival in blood and tissue despite host sequestration. |
10. Clinical diagnosis by organism class
| Suspected class | Useful first approaches | Specimen/interpretation cautions |
|---|---|---|
| Bacteria | Gram stain, culture and susceptibility; blood cultures for sepsis; targeted NAAT/antigen tests. | Collect before antibiotics when safe; avoid superficial swabs for deep infection; distinguish colonisation/contamination. |
| Viruses | NAAT/PCR, antigen, serology or viral culture in selected settings; imaging and clinical syndrome remain important. | Use the correct site, swab/transport medium and timing; antibodies may reflect past infection or vaccination. |
| Fungi | Microscopy, culture, histopathology, antigen, beta-D-glucan or fungal PCR depending on syndrome. | Colonisation is common; a positive respiratory culture may not prove invasive disease. |
| Protozoa/helminths | Blood film/rapid antigen/NAAT, stool microscopy/concentration, serology or tissue imaging. | Life-cycle timing and repeat samples matter; eosinophilia is supportive but not universal. |
| Ectoparasites | Skin/hair examination, dermoscopy, scraping, microscopy or direct identification. | Treat close contacts/environment where indicated; assess for vector-borne co-infection. |
| Prions | Neurologic examination, MRI, EEG, CSF biomarkers and specialist referral. | Routine culture/PCR does not diagnose prion disease; follow high-risk tissue precautions. |
10.1 Specimen principles
- Choose the specimen closest to the disease process: blood for bloodstream infection, CSF for meningitis, lower-respiratory material for pneumonia/TB, tissue/aspirate for abscess and stool for enteric disease.
- Use aseptic collection and adequate volume; label site, timing and prior therapy.
- Transport rapidly under the validated condition; a poor specimen cannot be rescued by a sophisticated assay.
- Interpret results with pre-test probability, imaging and host status; a positive molecular test may detect residual nucleic acid after viable infection has resolved.
11. Treatment and antimicrobial stewardship
Treatment depends on organism, site, severity, host factors, local resistance and source control. Antibiotics do not treat viruses, and antifungals/antiparasitics are not interchangeable.
| Principle | Application |
|---|---|
| Stabilise first | Airway, breathing, circulation, sepsis recognition, fluids/vasopressors, glucose and seizure control take priority in emergencies. |
| Obtain appropriate specimens | Blood cultures or site specimens before antimicrobials when this does not delay life-saving therapy. |
| Start empiric therapy when indicated | Use syndrome-, severity- and local-guideline-based treatment; do not wait for a result in suspected bacterial meningitis, septic shock or other time-critical infection. |
| De-escalate | Review cultures/NAAT, narrow therapy, adjust dose to renal/hepatic function and stop when infection is excluded or course completed. |
| Source control | Drain abscesses, remove infected devices, relieve obstruction, debride necrotic tissue and address perforation when required. |
| Prevent resistance | Correct drug, dose, route and duration; avoid unnecessary antibiotics and use infection-prevention measures. |
WHO defines antimicrobial resistance as bacteria, viruses, fungi and parasites no longer responding to antimicrobial medicines. Resistance is selected by antimicrobial exposure and spreads through organisms, people, animals and environments. Stewardship and diagnostics are therefore part of pathology and emergency care.
12. Emergency presentations: clues and red flags
| Presentation | Organism classes to consider | Urgent actions |
|---|---|---|
| Septic shock | Bacteria most common; fungi, viruses or parasites in selected hosts. | Resuscitate, cultures, prompt appropriate antimicrobials, lactate/organ assessment and source control. |
| Meningitis/encephalitis | Bacteria, viruses, fungi, parasites or prions depending on time course/host. | Isolation when indicated, urgent CSF/blood pathway, empiric therapy and specialist input. |
| Severe pneumonia/hypoxia | Bacteria, viruses, fungi, TB or mixed infection. | Oxygen/ventilation, imaging, appropriate respiratory specimens, isolation and empiric treatment as indicated. |
| Necrotising soft-tissue infection | Toxin-producing or mixed bacteria. | Immediate surgical review, broad empiric therapy, resuscitation and debridement. |
| Severe malaria/haemolysis | Plasmodium species. | Urgent smear/rapid testing, glucose, haemoglobin, renal assessment, antimalarial therapy and complication management. |
| Immunocompromised fever | Bacteria, fungi, viruses, mycobacteria and parasites. | Neutrophil count, cultures, urgent broad but rational treatment and early infectious-disease/microbiology advice. |
13. Prevention and infection control
- Hand hygiene, respiratory etiquette, environmental cleaning and safe injection practices interrupt many routes.
- Vaccination reduces disease from selected bacteria and viruses and protects vulnerable populations.
- Food/water safety, vector control, deworming programmes where indicated and safe animal contact reduce exposure.
- Standard precautions apply to all specimens; transmission-based precautions are added when a pathogen or syndrome warrants them.
- Antimicrobial stewardship preserves treatment effectiveness and reduces selection of resistant organisms.
- Early notification is essential for diseases with outbreak, occupational, public-health or bioterrorism implications.
14. Integrated cases
Case 1: Fever with shock
A patient has fever, hypotension, confusion and a suspected urinary source. Obtain blood/urine specimens promptly without delaying resuscitation, start guideline-based empiric therapy, assess lactate/organ function and relieve obstruction if present. A positive culture must be interpreted with contamination and colonisation in mind.
Case 2: Meningitis
Fever, neck stiffness and altered consciousness require an urgent bacterial/viral pathway. Draw blood cultures, perform safe neuroimaging/LP decisions, start empiric therapy when indicated and use appropriate isolation. CSF cell count, chemistry, Gram stain, culture and molecular tests complement—not replace—clinical judgement.
Case 3: Neutropenic fever
Neutropenia removes a major barrier to bacterial and fungal invasion. Treat as time-critical, collect cultures, examine skin/lines/lungs, evaluate for mould risk and reassess daily for de-escalation or escalation.
Case 4: Chronic cough and weight loss
Consider tuberculosis and other chronic infections. Send appropriate sputum/respiratory specimens for smear/NAAT/culture using the correct biosafety and transport route; apply airborne precautions and notify the relevant programme.
15. Examination-ready summary
- Pathogens include bacteria, viruses, fungi, protozoa, helminths, ectoparasites and prions.
- Colonisation is not the same as infection, and infection is not always symptomatic disease.
- Bacteria are prokaryotic cells; viruses are obligate intracellular particles; fungi are eukaryotic; parasites have complex host life cycles; prions are infectious misfolded proteins.
- Virulence factors include adhesion, invasion, capsules, biofilms, toxins, antigenic variation and immune evasion.
- Correct specimen, timing, transport and interpretation are as important as the test itself.
- Stabilise emergencies, obtain specimens when safe, start time-critical empiric therapy, pursue source control and de-escalate with results.
- Antimicrobial resistance affects bacteria, viruses, fungi and parasites; stewardship and infection prevention are essential.
16. Quick self-test
- Define colonisation, infection, disease, pathogenicity and virulence.
- Why can a positive culture fail to prove invasive infection?
- Compare bacteria and viruses in cellular organisation and replication.
- What is the difference between an exotoxin and endotoxin?
- Why are capsules and biofilms important virulence factors?
- List the three main parasite groups that cause human disease.
- What makes fungi eukaryotic and clinically distinctive?
- Why can prion disease not be managed like a bacterial infection?
- How can normal microbiota become opportunistic pathogens?
- Which specimen is usually more useful for a deep abscess: superficial swab or aspirated tissue/fluid, and why?
- What are the emergency principles in suspected septic shock?
- Why should antibiotics not be used for uncomplicated viral infection?
- How does antimicrobial resistance arise and spread?
- When should public-health or specialist laboratory advice be sought?
- Why must test results be interpreted with pre-test probability and host factors?
Answer guide
1. Colonisation is presence without disease; infection is entry/multiplication; disease is clinical dysfunction; pathogenicity is capacity to cause disease; virulence is degree of damage. 2. It may reflect colonisation or contamination rather than the disease focus. 3. Bacteria are living prokaryotic cells dividing by binary fission; viruses are acellular DNA/RNA particles that replicate inside host cells. 4. Exotoxins are secreted proteins with specific effects; endotoxin is mainly LPS from Gram-negative outer membrane that drives innate inflammation. 5. They resist phagocytosis and antibiotics/immune clearance. 6. Protozoa, helminths and ectoparasites. 7. They have nuclei, mitochondria, ergosterol membranes and chitin/glucan walls; invasive disease is common in immunocompromised hosts. 8. It is an infectious misfolded protein without nucleic acid and needs specialised infection-control/diagnostic pathways. 9. Barrier breach, antibiotics, immune deficiency, obstruction, devices or high inoculum. 10. Aspirate/tissue samples the disease process and avoids superficial colonisers. 11. Resuscitation, cultures when feasible, prompt empiric antimicrobials, organ assessment and source control. 12. Antibiotics act on bacterial targets and do not treat viruses; unnecessary use selects resistance and harms microbiota. 13. Genetic change/selection plus transmission of resistant organisms or genes. 14. Suspected high-consequence/outbreak pathogens, prion disease, unusual organisms, severe immunocompromise or specialised tests. 15. A result may represent past infection, carriage, contamination or residual nucleic acid and must fit the syndrome.
Authoritative resources and further reading
- NCBI Bookshelf: Medical Microbiology
- NCBI: How Infection Works
- CDC: review of pathogen classes and transmission
- CDC: parasite groups
- WHO: antimicrobial resistance
- WHO: Antimicrobial Resistance Diagnostic Initiative
- WHO: food safety and infectious agents
Clinical caution: Organism prevalence, resistance patterns and empiric regimens vary by country, facility and patient group. Use current Ugandan and facility guidelines, microbiology advice and antimicrobial stewardship policy.
