Toxin production/tissue damage – exotoxins or endotoxins causing direct cellular
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Toxin production/tissue damage – exotoxins or endotoxins causing direct cellular injury or triggering damaging inflammatory responses.
Dissemination – spread from the primary site via blood, lymphatics, or nerves to
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Dissemination – spread from the primary site via blood, lymphatics, or nerves to cause local or systemic disease.
Target protection/overproduction – overproduction of the target enzyme to
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Target protection/overproduction – overproduction of the target enzyme to overwhelm drug inhibition. Genetic basis: acquired resistance occurs via spontaneous chromosomal mutation, o horizontal gene transfer (conjugation via plasmids, transduction via bacteriophages transformation by uptake of free DNA), often involving transposons and integrons tha facilitate spread of resistance genes. 26B(i). ESBLs (Extended-Spectrum Beta-Lactamases) Enzymes produced by certain Gram-negative bacteria (commonly E. coli, Klebsiell pneumoniae) that hydrolyse and confer resistance to penicillins, and extended spectrum cephalosporins (e.g., ceftriaxone, cefotaxime, ceftazidime) and monobactam (aztreonam), but not carbapenems or cephamycins. ESBL production is typicall plasmid-mediated and inhibited in vitro by clavulanic acid, which forms the basis o laboratory detection (double-disc synergy test). Treatment of ESBL-producing infections usually requires carbapenems. 26B(ii). Multidrug resistance in tuberculosis management Multidrug-resistant TB (MDR-TB): Mycobacterium tuberculosis resistant to at leas isoniazid and rifampicin, the two most potent first-line anti-TB drugs. Extensively drug-resistant TB (XDR-TB): MDR-TB with additional resistance to an fluoroquinolone and at least one second-line injectable agent (or, per updated WHO definitions, resistance to fluoroquinolones and bedaquiline or linezolid). Management principles: use of a combination regimen of at least 4–5 effectiv second-line drugs (e.g., bedaquiline, linezolid, clofazimine, cycloserine fluoroquinolones) for a prolonged duration (previously 18–24 months; newer WHO recommended all-oral shorter regimens are now 6–9 months), guided by drug susceptibility testing, with directly observed therapy (DOT) to ensure adherence and prevent further resistance amplification.
Arenaviridae — Lassa fever virus, Lymphocytic choriomeningitis virus
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Arenaviridae — Lassa fever virus, Lymphocytic choriomeningitis virus
Outcome – clinical disease, subclinical/latent infection, carrier state, or clearance
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Outcome – clinical disease, subclinical/latent infection, carrier state, or clearance by host defences.
Reduced drug uptake/permeability – altered porin channels reducing entry of
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Reduced drug uptake/permeability – altered porin channels reducing entry of drug (common in Gram-negative bacilli).
Filoviridae — Ebola virus, Marburg virus
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Filoviridae — Ebola virus, Marburg virus
Diagnosis of viral infections (HIV viral load, Hepatitis B/C viral load, SARS-CoV-2
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Diagnosis of viral infections (HIV viral load, Hepatitis B/C viral load, SARS-CoV-2 detection).
Detection of drug-resistance genes (e.g., rpoB mutation for rifampicin resistance in
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Detection of drug-resistance genes (e.g., rpoB mutation for rifampicin resistance in TB — GeneXpert MTB/RIF).
Distinguish between vaginitis and cervicitis (aetiology,
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Distinguish between vaginitis and cervicitis (aetiology, pathogenesis, laboratory diagnosis) Definition: - Vaginitis: inflammation of the vaginal mucosa, presenting with abnorma discharge, odour, itching, and irritation. - Cervicitis: inflammation of the uterin cervix (endocervix), often asymptomatic or presenting with mucopurulent discharg and post-coital bleeding. Aetiology: | Feature | Vaginitis | Cervicitis | |—|—|—| | Common causes | Candid albicans, Trichomonas vaginalis, bacterial vaginosis (Gardnerella vaginalis + anaerobes) | Neisseria gonorrhoeae, Chlamydia trachomatis, Herpes simplex virus | Nature of organisms | Often endogenous flora overgrowth or protozoal | Classi sexually transmitted pathogens | | Site infected | Squamous epithelium of vagina Columnar epithelium of endocervix | Pathogenesis: - Vaginitis results from disruption of the normal vaginal flor (lactobacilli) allowing overgrowth of pathogens, or direct protozoal/fungal invasion o squamous epithelium, causing epithelial irritation and inflammatory exudate. Cervicitis results from pathogens (especially obligate intracellular organisms lik Chlamydia, or Gonococcus) infecting the columnar epithelial cells of the endocervix triggering a purulent or mucopurulent inflammatory response; it can ascend to caus pelvic inflammatory disease. Laboratory diagnosis: - Vaginitis: wet mount microscopy (clue cells for bacteria vaginosis, motile trichomonads, pseudohyphae/budding yeast for candidiasis), vagina pH, whiff test (KOH) for bacterial vaginosis, Gram stain (Nugent score), culture on Sabouraud dextrose agar for Candida. - Cervicitis: endocervical swab for Gram stain (intracellular Gram-negative diplococci for gonorrhoea), nucleic acid amplification tes (NAAT) for Chlamydia trachomatis and N. gonorrhoeae, culture on Thayer Martin/modified New York City medium for gonococcus.
Essay on Under-One Vaccinations in Nigeria Nigeria’s National Programme on Immunization (NPI), aligned with the WHO
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Essay on Under-One Vaccinations in Nigeria Nigeria’s National Programme on Immunization (NPI), aligned with the WHO Expanded Programme on Immunization (EPI), provides scheduled vaccines to children under one year to prevent the major childhood killer diseases. Objectives: reduce infant and under-five mortality and morbidity from vaccine preventable diseases (VPDs); achieve herd immunity. Schedule (Nigeria routine immunization, birth–9 months): - At birth: BCG (Bacille Calmette-Guérin, against tuberculosis), Oral Polio Vaccine 0 (OPV0), Hepatiti B birth dose. - 6 weeks: OPV1, Pentavalent vaccine 1 (Diphtheria, Pertussis, Tetanus Hepatitis B, Haemophilus influenzae type b), Pneumococcal Conjugate Vaccine (PCV1), Inactivated Polio Vaccine (IPV, one dose in schedule), Rotavirus vaccine 1. - 10 weeks: OPV2, Pentavalent 2, PCV2, Rotavirus 2. - 14 weeks: OPV3, Pentavalent 3 PCV3, IPV. - 9 months: Measles vaccine 1, Yellow fever vaccine, Vitamin A supplementation, Meningococcal A conjugate vaccine (MenA, where introduced). Vaccine-preventable diseases targeted: tuberculosis, poliomyelitis, diphtheria pertussis, tetanus, hepatitis B, H. influenzae type b disease, pneumococcal disease rotavirus diarrhoea, measles, yellow fever. Challenges in Nigeria: poor cold-chain infrastructure, vaccine hesitancy and misinformation, insecurity limiting access in some regions, inadequate funding and health worker shortages, poor birth registration affecting tracking, and urban-rura disparities in coverage. Strategies to improve coverage: routine immunization strengthening, periodi Supplementary Immunization Activities (SIAs) for polio and measles, health education/social mobilization, Reaching Every Ward (REW) strategy, and public-privat partnerships (e.g., GAVI support).
Steps in establishment of an infectious process
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Steps in establishment of an infectious process
Exposure/contact – pathogen encounters the host via a portal of entry (respiratory
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Exposure/contact – pathogen encounters the host via a portal of entry (respiratory gastrointestinal, genitourinary, skin/mucosa, transplacental).
Adherence – attachment of the organism to host cells via adhesins, pili/fimbriae, or
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Adherence – attachment of the organism to host cells via adhesins, pili/fimbriae, or surface proteins.
Colonisation – multiplication of the organism at the site of entry, evading initial
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Colonisation – multiplication of the organism at the site of entry, evading initial host defences (mucus, normal flora, secretory IgA).
Invasion – penetration of epithelial barriers into deeper tissue, often facilitated by
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Invasion – penetration of epithelial barriers into deeper tissue, often facilitated by invasins, toxins, or enzymes (hyaluronidase, collagenase).
Evasion of host immune defences – mechanisms such as capsule formation (anti
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Evasion of host immune defences – mechanisms such as capsule formation (anti phagocytic), antigenic variation, intracellular survival, IgA protease production, biofilm formation.
Principle and procedure of Gram staining Principle: Gram staining is a differential staining technique that exploits difference
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Principle and procedure of Gram staining Principle: Gram staining is a differential staining technique that exploits difference in bacterial cell wall structure. Gram-positive bacteria have a thick peptidoglycan laye that retains the crystal violet-iodine complex despite decolourisation with alcohol/acetone, staining purple. Gram-negative bacteria have a thin peptidoglycan layer and an outer lipopolysaccharide membrane that is disrupted by the decolouriser releasing the crystal violet-iodine complex; they then take up the counterstain (safranin), staining pink/red. Procedure: 1. Fixation: prepare a thin smear of the specimen on a glass slide, air-dry and heat-fix by passing through a flame. 2. Primary stain: flood the smear with crysta violet for 30–60 seconds; rinse with water. 3. Mordant: apply Gram’s iodine for 30–6 seconds (forms crystal violet-iodine complex within the cell wall); rinse with water. 4 Decolourisation: apply acetone/alcohol briefly (a few seconds) until no more purpl colour washes off; rinse immediately with water — this is the critical differentiating step. 5. Counterstain: apply safranin for 30–60 seconds; rinse with water. 6. Dry and examine under oil-immersion microscopy (×100). Interpretation: Gram-positive organisms appear purple/blue; Gram-negativ organisms appear pink/red. Morphology (cocci, bacilli, arrangement) is also noted.
Principles to reduce spread of infection in the hospital
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Principles to reduce spread of infection in the hospital environment
Standard precautions applied to all patients regardless of diagnosis (hand
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Standard precautions applied to all patients regardless of diagnosis (hand hygiene, use of personal protective equipment, safe injection practices, respiratory hygiene/cough etiquette).
Hand hygiene – the single most effective measure; the WHO “5 Moments for Hand
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Hand hygiene – the single most effective measure; the WHO “5 Moments for Hand Hygiene.”
Transmission-based precautions (contact, droplet, airborne) for patients with
Standard Answer:
Transmission-based precautions (contact, droplet, airborne) for patients with known/suspected transmissible infections.
Environmental cleaning and disinfection of surfaces, equipment, and linen.
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Environmental cleaning and disinfection of surfaces, equipment, and linen.
Sterilisation of reusable instruments according to their risk classification
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Sterilisation of reusable instruments according to their risk classification (critical, semi-critical, non-critical).
Safe waste management – segregation and disposal of sharps and infectious
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Safe waste management – segregation and disposal of sharps and infectious waste.
Isolation of infectious patients in single rooms or cohort wards where
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Isolation of infectious patients in single rooms or cohort wards where appropriate.
Antimicrobial stewardship to reduce selection pressure for resistant organisms.
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Antimicrobial stewardship to reduce selection pressure for resistant organisms.
Surveillance of hospital-acquired infections and outbreak detection.
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Surveillance of hospital-acquired infections and outbreak detection.
Staff education and training on infection prevention and control (IPC) policies.
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Staff education and training on infection prevention and control (IPC) policies.
Vaccination of healthcare workers (e.g., Hepatitis B, influenza).
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Vaccination of healthcare workers (e.g., Hepatitis B, influenza).
Adequate ventilation of clinical areas, especially for airborne pathogens.
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Adequate ventilation of clinical areas, especially for airborne pathogens.
MRSA (Methicillin-Resistant Staphylococcus aureus)
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MRSA (Methicillin-Resistant Staphylococcus aureus) Definition: Staphylococcus aureus strains that have acquired resistance to methicillin and all other beta-lactam antibiotics (penicillins, cephalosporins, carbapenems), excep newer anti-MRSA agents. Mechanism of resistance: acquisition of the mecA gene (carried on the mobil genetic element Staphylococcal Cassette Chromosome mec, SCCmec), which encode an altered penicillin-binding protein (PBP2a) with low affinity for beta-lactams allowing cell wall synthesis to continue despite the presence of these drugs. Types: - Hospital-acquired MRSA (HA-MRSA): affects hospitalised, often immunocompromised patients; associated with invasive devices and prolonged hospita stay. - Community-acquired MRSA (CA-MRSA): affects otherwise health individuals in the community, often carries Panton-Valentine leukocidin (PVL) toxin causes skin/soft tissue infections and necrotising pneumonia. Clinical significance: causes skin and soft tissue infections, bacteraemia endocarditis, pneumonia, osteomyelitis, and surgical site infections; associated with higher morbidity, mortality, and treatment cost than methicillin-sensitive strains. Laboratory diagnosis: culture and sensitivity testing; cefoxitin disc diffusion tes (surrogate for methicillin resistance); PCR detection of mecA/mecC gene; automated susceptibility systems. Treatment: vancomycin, teicoplanin, linezolid, daptomycin, or clindamycin depending on susceptibility; local abscess drainage where indicated. Control: contact precautions, hand hygiene, screening of high-risk patients decolonisation protocols (nasal mupirocin, chlorhexidine washes), antimicrobia stewardship.
Essay on Sepsis Definition: Sepsis is life-threatening organ dysfunction caused by a dysregulated hos
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Essay on Sepsis Definition: Sepsis is life-threatening organ dysfunction caused by a dysregulated hos response to infection (Sepsis-3 definition). Septic shock is a subset of sepsis with circulatory and cellular/metabolic abnormalities profound enough to substantiall increase mortality (persisting hypotension requiring vasopressors to maintain MAP ≥65 mmHg, and serum lactate >2 mmol/L despite adequate fluid resuscitation). Aetiology: any infectious source — commonly Gram-negative bacilli (E. coli Klebsiella, Pseudomonas), Gram-positive cocci (S. aureus, Streptococcus pneumoniae) and fungi in immunocompromised patients. Common sources: pneumonia, urinar tract infection, intra-abdominal infection, skin/soft tissue infection, catheter-related bloodstream infection. Pathogenesis: microbial components (endotoxin/LPS, exotoxins, peptidoglycan trigger pattern recognition receptors (Toll-like receptors) on immune cells, releasing pro-inflammatory cytokines (TNF-α, IL-1, IL-6). This causes widespread endothelia injury, increased vascular permeability, activation of coagulation (leading t disseminated intravascular coagulation), microvascular thrombosis, and tissu hypoperfusion, resulting in multi-organ dysfunction. A compensatory anti-inflammator response can also cause immunosuppression, predisposing to secondary infections. Clinical features: fever or hypothermia, tachycardia, tachypnoea, altered menta status, hypotension, oliguria, mottled skin, and signs referable to the primary source o infection. Diagnosis: clinical suspicion + qSOFA (quick SOFA: respiratory rate ≥22/min, altered mentation, systolic BP ≤100 mmHg) for rapid bedside screening; full SOFA score fo organ dysfunction; blood cultures (before antibiotics), full blood count, serum lactate renal and liver function tests, coagulation profile, imaging/cultures to identify source. Management (Surviving Sepsis Campaign “Hour-1 bundle”): 1. Measure serum lactate. 2. Obtain blood cultures before antibiotics. 3. Administer broad-spectrum antibiotics within one hour. 4. Begin rapid administration of 30 mL/kg crystalloid fo hypotension or lactate ≥4 mmol/L. 5. Apply vasopressors (norepinephrine first-line) i hypotensive during/after fluid resuscitation to maintain MAP ≥65 mmHg. 6. Sourc control (drainage of abscess, removal of infected device, debridement). 7. Supportiv care: oxygenation/ventilation, renal replacement therapy if needed, glycaemic control stress ulcer and VTE prophylaxis. Complications: acute respiratory distress syndrome, acute kidney injury disseminated intravascular coagulation, multi-organ failure, death.
Diagnosis of sexually transmitted infections (gonorrhoea, chlamydia).
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Diagnosis of sexually transmitted infections (gonorrhoea, chlamydia).
Sterilization — definition and classification of hospital items
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Sterilization — definition and classification of hospital items Definition: Sterilization is the process by which all forms of microbial life, including bacterial spores, are completely destroyed or removed from an item or surface. Classification (Spaulding classification) based on risk of infection transmission: Category Definition Method of Examples processing Critical items Enter sterile tissue or Sterilization (steam Surgical instruments, the vascular system autoclave, ethylene needles, implants, oxide, or dry heat) catheters Semi-critical items Contact mucous High-level disinfection Endoscopes, membranes or non- (or sterilization) laryngoscope blades, intact skin vaginal specula Non-critical items Contact intact skin Low-level disinfection Blood pressure cuffs, only stethoscopes, bed rails
Classes of antimicrobial agents (with examples)
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Classes of antimicrobial agents (with examples) Class Mechanism Examples Beta-lactams (Penicillins, Inhibit cell wall Amoxicillin, Ceftriaxone Cephalosporins, Carbapenems) (peptidoglycan) synthesis Glycopeptides Inhibit cell wall synthesis Vancomycin, Teicoplanin Aminoglycosides Inhibit protein synthesis (30S Gentamicin, Amikacin ribosomal subunit) Tetracyclines Inhibit protein synthesis (30S Doxycycline, Tetracycline subunit) Macrolides Inhibit protein synthesis (50S Erythromycin, Azithromycin subunit) Fluoroquinolones Inhibit DNA Ciprofloxacin, Levofloxacin gyrase/topoisomerase IV Sulphonamides/Folate Inhibit folic acid synthesis Cotrimoxazole antagonists (sulfamethoxazole- trimethoprim) Nitroimidazoles DNA damage in Metronidazole, Tinidazole anaerobes/protozoa Antifungals (Azoles, Polyenes) Disrupt fungal cell membrane Fluconazole, Amphotericin B (ergosterol) Antivirals Inhibit viral replication Acyclovir, Zidovudine enzymes
Koch’s postulates and their limitations Koch’s postulates (criteria to establish a causal link between a microorganism and
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Koch’s postulates and their limitations Koch’s postulates (criteria to establish a causal link between a microorganism and disease): 1. The organism must be found in abundance in all organisms suffering from the disease, but not in healthy individuals. 2. The organism must be isolated from diseased host and grown in pure culture. 3. The cultured organism should caus disease when introduced into a healthy, susceptible host. 4. The organism must be re isolated from the experimentally infected host and identified as identical to the origina causative agent. Limitations: - Some pathogens cannot be cultured in vitro (e.g., Mycobacterium leprae, Treponema pallidum). - Some organisms cause disease only in specific hosts making animal models unsuitable (host specificity). - Asymptomatic carriers exist — the organism may be present without causing disease. - Some diseases have multipl causative agents (polymicrobial infections), violating postulate 1. - Some agents caus several different disease presentations (e.g., Streptococcus pyogenes). - Ethica constraints prevent deliberate infection of human volunteers for many pathogens. Viruses require living cells (not simple culture media) for propagation, which wa unknown in Koch’s era. - Latent/slow viral infections (e.g., prions, some herpesviruses may not fulfil the postulates temporally.
Classification of emerging and re-emerging infections (with
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Classification of emerging and re-emerging infections (with examples) Emerging infections: newly identified or newly evolved pathogens/diseases, o diseases whose incidence has increased in the last two decades. - Examples: HIV/AIDS SARS-CoV-2 (COVID-19), Ebola virus disease, Nipah virus, Zika virus, avian influenz (H5N1). Re-emerging infections: previously known diseases that had declined significantl but have reappeared or increased in incidence/geographic range. - Examples Tuberculosis (multidrug-resistant strains), Cholera, Dengue fever, Yellow fever Diphtheria, Measles (due to declining vaccination coverage). Classification by mechanism of emergence: 1. Genetic/microbial adaptation antigenic drift/shift (influenza), antimicrobial resistance (MDR-TB). 2. Ecologica changes – deforestation, climate change, urbanisation bringing humans into contac with new reservoirs (Lassa fever, Nipah virus). 3. Human demographics/behaviour travel, migration, sexual behaviour (HIV). 4. International travel and commerce rapid global spread (SARS-CoV-2). 5. Breakdown of public health measures – war poverty, reduced vaccination coverage (measles, diphtheria resurgence). 6. Animal to-human spillover (zoonoses) – most emerging infections originate from anima reservoirs.
Steps in the management of sepsis See the Surviving Sepsis Campaign Hour-1 bundle (detailed under Question 7): 1
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Steps in the management of sepsis See the Surviving Sepsis Campaign Hour-1 bundle (detailed under Question 7): 1 Measure lactate (repeat if initial >2 mmol/L). 2. Obtain blood cultures prior t antibiotics. 3. Administer broad-spectrum antibiotics. 4. Rapid crystalloid fluid resuscitation (30 mL/kg) for hypotension/lactate ≥4 mmol/L. 5. Vasopressors fo persistent hypotension despite fluids (target MAP ≥65 mmHg). 6. Identify and contro the source of infection (drainage/debridement/device removal). 7. Ongoing reassessment of fluid status and tissue perfusion. 8. Supportive organ car (mechanical ventilation, renal replacement therapy, glycaemic control) as needed. 9 De-escalation of antibiotics once culture/sensitivity results are available.
Identification of organisms directly from clinical specimens without need for
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Identification of organisms directly from clinical specimens without need for culture, reducing turnaround time.
Epidemiological typing/strain identification during outbreak investigation.
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Epidemiological typing/strain identification during outbreak investigation.
Detection of antimicrobial resistance genes (e.g., mecA for MRSA).
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Detection of antimicrobial resistance genes (e.g., mecA for MRSA).
Standard and Transmission-based precautions Standard precautions: the basic level of infection control applied to the care of ALL
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Standard and Transmission-based precautions Standard precautions: the basic level of infection control applied to the care of ALL patients regardless of suspected or confirmed infection status, based on the principl that blood, body fluids, secretions, excretions (except sweat), non-intact skin, and mucous membranes may contain transmissible infectious agents. - Two components hand hygiene and use of personal protective equipment (gloves, gown, mask eye protection). (Others include safe injection practices and safe handling o contaminated equipment/linen.) Transmission-based precautions: additional precautions used for patients known o suspected to be infected with pathogens spread by specific routes, used in addition t standard precautions. - Contact precautions: gloves and gown; components — singl room/cohorting and dedicated equipment. (e.g., MRSA, C. difficile). - Drople precautions: surgical mask when within 1–2 metres of patient; components — patien placement in single room and mask for patient during transport. (e.g., meningococca meningitis, influenza). - Airborne precautions: N95/FFP respirator; components — negative-pressure isolation room and limiting susceptible staff exposure. (e.g tuberculosis, measles, chickenpox).
Syndromic management of sexually transmitted infections
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Syndromic management of sexually transmitted infections Syndromic management treats STIs based on recognisable groups of symptoms and signs (syndromes) rather than waiting for laboratory confirmation, allowing immediat treatment. Three key syndromes and causative organisms:
Urethral discharge syndrome
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Urethral discharge syndrome Neisseria gonorrhoeae Chlamydia trachomatis
Vaginal discharge syndrome
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Vaginal discharge syndrome Trichomonas vaginalis Candida albicans (and bacterial vaginosis organisms such as Gardnerella vaginalis)
Genital ulcer disease syndrome
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Genital ulcer disease syndrome Treponema pallidum (syphilis) Haemophilus ducreyi (chancroid) (Herpes simplex virus is also a major cause.)
Factors determining if a pathogen can establish disease in the
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Factors determining if a pathogen can establish disease in the host
Portal of entry – appropriateness of the site of exposure for that organism.
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Portal of entry – appropriateness of the site of exposure for that organism.
Infectious dose – minimum number of organisms required to establish infection.
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Infectious dose – minimum number of organisms required to establish infection.
Virulence factors of the organism – adhesins, toxins, capsule, invasins, enzymes
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Virulence factors of the organism – adhesins, toxins, capsule, invasins, enzymes
Ability to evade host defences – resistance to phagocytosis, complement,
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Ability to evade host defences – resistance to phagocytosis, complement, antibody.
Host immune status – immunocompetence, prior immunity/vaccination.
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Host immune status – immunocompetence, prior immunity/vaccination.
Integrity of host physical/anatomical barriers – skin, mucosa, cilia, normal
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Integrity of host physical/anatomical barriers – skin, mucosa, cilia, normal flora.
Host genetic susceptibility – receptor polymorphisms, HLA type.
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Host genetic susceptibility – receptor polymorphisms, HLA type.
Environmental factors – temperature, pH, oxygen tension at the site.
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Environmental factors – temperature, pH, oxygen tension at the site.
Presence of underlying disease/comorbidities – diabetes, malnutrition,
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Presence of underlying disease/comorbidities – diabetes, malnutrition, immunosuppression.
Microbial competition – status of normal/commensal flora at the site.
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Microbial competition – status of normal/commensal flora at the site.
Quality in the laboratory and core components of a quality
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Quality in the laboratory and core components of a quality system Definition: Quality in the laboratory refers to the accuracy, reliability, timeliness, and reproducibility of test results, ensuring they are fit for clinical use and support correc patient management. Core components of a laboratory quality system (WHO/CLSI “Quality System Essentials”): 1. Organisation and personnel (trained, competent staff) 2. Equipmen (calibration and maintenance) 3. Purchasing and inventory (reagent/suppl management) 4. Process control (including internal and external qualit assessment/proficiency testing) 5. Information management 6. Documents and record
Occurrence/incident management (non-conforming event management) 8
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Occurrence/incident management (non-conforming event management) 8 Assessment (internal and external audits) 9. Process improvement (continuous qualit improvement) 10. Customer service 11. Facilities and safety
Quantification of pathogen load to monitor treatment response (viral load
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Quantification of pathogen load to monitor treatment response (viral load monitoring).
Efflux pumps – active extrusion of the antibiotic from the bacterial cell before it
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Efflux pumps – active extrusion of the antibiotic from the bacterial cell before it reaches its target.
Bypass of the metabolic pathway – acquisition of an alternative, resistant
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Bypass of the metabolic pathway – acquisition of an alternative, resistant enzyme pathway (e.g., alternative folate synthesis pathway).
Sequential Organ Failure Assessment (SOFA) score Purpose: SOFA is a scoring system used to track a patient’s status during their stay in
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Sequential Organ Failure Assessment (SOFA) score Purpose: SOFA is a scoring system used to track a patient’s status during their stay in an intensive care unit and to determine the extent of a person’s organ function or rat of failure; it is used in the Sepsis-3 definition (an acute increase of ≥2 points reflect organ dysfunction associated with sepsis). Organ systems assessed (each scored 0–4): 1. Respiratory – PaO₂/FiO₂ ratio 2 Coagulation – platelet count 3. Liver – serum bilirubin 4. Cardiovascular – mean arterial pressure/vasopressor requirement 5. Central nervous system – Glasgow Coma Scale 6. Renal – serum creatinine or urine output Total score ranges 0–24; higher scores correlate with increased mortality. qSOFA (respiratory rate ≥22/min, altered mentation, systolic BP ≤100 mmHg) is a rapid bedside screening tool used outside the ICU to identify patients at risk who need ful SOFA assessment.
Pathophysiology of infectious diseases — host-parasite
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Pathophysiology of infectious diseases — host-parasite relationship Host-parasite relationships can be classified as: - Commensalism: organism benefits, host unaffected (normal flora). - Mutualism: both host and organism benefi (e.g., gut flora aiding digestion/vitamin K synthesis). - Parasitism: organism benefit at the host’s expense, causing disease. Pathophysiological process: Disease results from the interplay between th pathogen’s virulence and the host’s defence mechanisms. 1. Pathogen adheres and colonises a body surface, overcoming physical/chemical barriers and competing with normal flora. 2. It evades innate immune defences (phagocytes, complement, natura killer cells) via mechanisms like capsules, biofilms, or intracellular survival. 3. It ma produce toxins (exotoxins damaging specific cells; endotoxins/LPS triggering systemi inflammatory responses) or enzymes causing direct tissue damage. 4. The host mount an inflammatory and adaptive immune response (antibody and cell-mediated), which while protective, may itself contribute to tissue damage (immunopathology) — e.g., in tuberculosis granuloma formation or post-streptococcal glomerulonephritis. 5. Th outcome depends on the balance between pathogen virulence and host defence clearance, chronic/latent infection, or progressive disease and death.
Determinants of pathogenicity
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Determinants of pathogenicity
Adhesion factors – fimbriae/pili, adhesins that mediate attachment to host cells.
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Adhesion factors – fimbriae/pili, adhesins that mediate attachment to host cells.
Invasiveness – ability to penetrate and spread within host tissue (invasins,
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Invasiveness – ability to penetrate and spread within host tissue (invasins, spreading enzymes like hyaluronidase, collagenase, streptokinase).
Toxigenicity – production of exotoxins (secreted, highly specific, e.g., diphtheria
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Toxigenicity – production of exotoxins (secreted, highly specific, e.g., diphtheria toxin) and endotoxins (lipopolysaccharide of Gram-negative bacteria, triggering systemic inflammation).
Capsule – anti-phagocytic property allowing evasion of host immune clearance
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Capsule – anti-phagocytic property allowing evasion of host immune clearance (e.g., Streptococcus pneumoniae).
Antigenic variation – alteration of surface antigens to evade host antibody
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Antigenic variation – alteration of surface antigens to evade host antibody response (e.g., Neisseria gonorrhoeae pilin variation, influenza antigenic drift/shift)
Intracellular survival – resistance to phagolysosomal killing (e.g., Mycobacterium
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Intracellular survival – resistance to phagolysosomal killing (e.g., Mycobacterium tuberculosis, Salmonella typhi).
Enzyme production – coagulase, catalase, IgA protease, which help evade or
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Enzyme production – coagulase, catalase, IgA protease, which help evade or damage host defences.
Biofilm formation – protects bacteria from antibiotics and host immune cells.
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Biofilm formation – protects bacteria from antibiotics and host immune cells.
Infectious dose – minimum number of organisms needed to initiate infection.
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Infectious dose – minimum number of organisms needed to initiate infection.
Host susceptibility factors – nutritional status, immune status, genetic factors.
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Host susceptibility factors – nutritional status, immune status, genetic factors.
Staining techniques and organisms identified
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Staining techniques and organisms identified Staining technique Principle Organisms identified Gram stain Differential stain based on cell Staphylococcus aureus (Gram- wall structure positive cocci), Escherichia coli (Gram-negative bacilli) Ziehl-Neelsen (acid-fast) Acid-fastness of mycolic acid- Mycobacterium tuberculosis, stain rich cell wall resists Mycobacterium leprae decolourisation with acid- alcohol India ink stain Negative staining Cryptococcus neoformans demonstrating capsule against dark background Giemsa stain Romanowsky stain for blood Plasmodium species, parasites and cell morphology Trypanosoma species Albert’s/Methylene blue Demonstrates metachromatic Corynebacterium diphtheriae stain granules (Any three of the above are acceptable answers.)
Uses of nucleic acid amplification techniques (NAAT) in medical
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Uses of nucleic acid amplification techniques (NAAT) in medical microbiology
Rapid, sensitive detection of fastidious or slow-growing organisms (e.g.,
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Rapid, sensitive detection of fastidious or slow-growing organisms (e.g., Mycobacterium tuberculosis, Chlamydia trachomatis).
Essay on the infectious process of communicable diseases
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Essay on the infectious process of communicable diseases A communicable disease is one that is transmissible from an infected host (human animal or environmental reservoir) to a susceptible host, either directly or indirectly. Chain of infection (essential elements): 1. Infectious agent – the causativ pathogen (bacteria, virus, fungus, parasite). 2. Reservoir – the habitat where th organism normally lives, grows, and multiplies (human, animal, or environmental). 3 Portal of exit – route by which the pathogen leaves the reservoir (respiratory tract faeces, blood, genital secretions). 4. Mode of transmission – direct (contact, droplet or indirect (airborne, vehicle-borne via food/water/fomites, vector-borne). 5. Portal o entry – route by which the pathogen enters a new host (respiratory tract gastrointestinal tract, mucous membranes, skin breaks, parenteral). 6. Susceptible host – an individual lacking effective immunity to the pathogen. Stages of the infectious process in the individual: exposure → incubation period (organism multiplying, no symptoms) → prodromal stage (non-specific symptoms) → clinical illness (specific signs/symptoms) → convalescence/recovery, or progression t complications/death, or a carrier state. Control is achieved by breaking any link in the chain: eliminating the reservoir interrupting transmission (sanitation, vector control, PPE), protecting portals o entry/exit, and increasing host resistance (vaccination, nutrition).
Outbreak — definition, reasons for investigation, and steps in
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Outbreak — definition, reasons for investigation, and steps in management Definition: An outbreak is the occurrence of cases of disease in excess of what i normally expected in a defined community or geographical area over a particula period of time. (Also called an epidemic; two or more linked cases can constitute an outbreak for rare diseases.) Reasons why an outbreak must be investigated: 1. To identify the causative agen and source of infection. 2. To determine the mode of transmission and prevent furthe spread. 3. To identify populations at risk and implement control measures. 4. T evaluate and strengthen existing prevention/control programmes. 5. To provid opportunity for training and research. Steps in outbreak management/investigation: 1. Confirm the existence of an outbreak (compare with baseline/expected rates). 2. Verify the diagnosis (clinical and laboratory confirmation). 3. Establish a case definition and actively search for and count cases. 4. Describe the outbreak in terms of person, place, and time (descriptiv epidemiology). 5. Develop and test hypotheses regarding source and mode o transmission (analytical epidemiology — case-control or cohort studies). 6. Implemen control and prevention measures (often started early, in parallel with investigation). 7 Communicate findings to stakeholders and the public. 8. Maintain ongoing surveillanc to monitor the effectiveness of control measures.
Major categories of measures for controlling biological risks in
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Major categories of measures for controlling biological risks in the laboratory
Administrative controls – biosafety policies, standard operating procedures,
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Administrative controls – biosafety policies, standard operating procedures, biosafety committees, training, risk assessment.
Engineering controls – biosafety cabinets, negative pressure rooms, HEPA
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Engineering controls – biosafety cabinets, negative pressure rooms, HEPA filtration, autoclaves.
Personal protective equipment (PPE) – gloves, gowns, respirators, eye
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Personal protective equipment (PPE) – gloves, gowns, respirators, eye protection.
Safe work practices – proper handling and disposal of sharps, decontamination of
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Safe work practices – proper handling and disposal of sharps, decontamination of spills, hand hygiene.
Waste management – segregation, autoclaving/incineration of biohazardous
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Waste management – segregation, autoclaving/incineration of biohazardous waste.
Immunisation of laboratory personnel where applicable (e.g., Hepatitis B).
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Immunisation of laboratory personnel where applicable (e.g., Hepatitis B).
Biosafety levels (BSL 1–4) – matching containment level to the risk group of the
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Biosafety levels (BSL 1–4) – matching containment level to the risk group of the organism handled.
Post-exposure protocols – incident reporting and prophylaxis where indicated.
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Post-exposure protocols – incident reporting and prophylaxis where indicated.
Rapid diagnostic test (RDT) Definition: A rapid diagnostic test is a point-of-care diagnostic tool designed to giv
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Rapid diagnostic test (RDT) Definition: A rapid diagnostic test is a point-of-care diagnostic tool designed to giv quick results (usually within 15–30 minutes) without need for sophisticated laborator equipment, typically based on immunochromatographic (lateral flow) technolog detecting antigens or antibodies. Principle: A sample (blood, serum, urine) is applied to a test strip/cassette; if th target antigen or antibody is present, it binds to labelled antibodies/antigens and migrates along the strip, producing a visible coloured line at the test line (and control line confirming the test is functioning). Examples: Malaria RDT (detects Plasmodium histidine-rich protein-2 or lactat dehydrogenase), HIV RDT (detects antibodies), Hepatitis B surface antigen RDT pregnancy test (hCG), SARS-CoV-2 antigen test. Advantages: rapid, simple to perform, requires minimal training, no need fo electricity or laboratory infrastructure, useful in resource-limited/field settings. Limitations: generally lower sensitivity than laboratory-based methods (PCR/ELISA) cannot quantify pathogen load, risk of false negatives/positives, quality can be affected by storage conditions. 26A. Mechanisms of resistance in acquired antimicrobial resistance
Enzymatic inactivation/modification of the drug – e.g., beta-lactamases
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Enzymatic inactivation/modification of the drug – e.g., beta-lactamases hydrolysing beta-lactam ring; aminoglycoside-modifying enzymes.
Alteration of the drug target – e.g., altered penicillin-binding proteins (PBP2a in
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Alteration of the drug target – e.g., altered penicillin-binding proteins (PBP2a in MRSA), mutated DNA gyrase (fluoroquinolone resistance), altered ribosomal binding sites.
Definitions with examples (i) Exanthem: A widespread skin rash, usually of infectious origin, often accompanied
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Definitions with examples (i) Exanthem: A widespread skin rash, usually of infectious origin, often accompanied by systemic symptoms such as fever. Examples: measles, rubella, varicell (chickenpox), roseola infantum (HHV-6). (ii) Enanthem: A rash or lesion occurring on mucous membranes (rather than skin) often accompanying an exanthem. Examples: Koplik’s spots (measles), herpangin lesions (Coxsackievirus), oral lesions in hand-foot-and-mouth disease (Coxsackieviru A16). (iii) Antigenic drift: Gradual, minor accumulation of point mutations in the gene encoding surface antigens (haemagglutinin/neuraminidase) of influenza virus, leading to small antigenic changes over time. Responsible for seasonal influenza epidemics Examples: yearly variation in influenza A(H3N2), A(H1N1), and influenza B strains. (iv) Antigenic shift: Abrupt, major change in the influenza A surface antigen resulting from reassortment of genome segments between two different influenza A strains co-infecting the same host (e.g., a human and an avian/swine strain), producing a novel subtype to which the population has little or no immunity — the cause o pandemics. Examples: H1N1 (1918 “Spanish flu,” 2009 pandemic), H2N2 (1957 “Asian flu”), H3N2 (1968 “Hong Kong flu”).
Definitions (a) Normal flora: The community of microorganisms (bacteria, fungi) that reside on
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Definitions (a) Normal flora: The community of microorganisms (bacteria, fungi) that reside on and within the body surfaces of healthy individuals (skin, gut, respiratory tract genitourinary tract) without normally causing disease; may be resident (permanent) o transient. (b) Virulence: The degree or intensity of pathogenicity of an organism, i.e., th quantitative measure of the severity of disease it is capable of causing, often expressed in terms such as LD₅₀ (lethal dose for 50% of a population) or ID₅₀ (infectious dose fo 50%). (c) Pathogenicity: The qualitative ability of an organism to cause disease in a host. (d) Infectious process: The sequence of events by which a pathogen enters a host establishes itself, multiplies, and produces disease, encompassing adherence colonisation, invasion, immune evasion, and tissue damage.
Diagnostic techniques, appropriate specimens, and clinical
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Diagnostic techniques, appropriate specimens, and clinical conditions (2024 mock) Diagnostic technique Appropriate specimen Clinical condition Gram stain and culture Sputum Bacterial pneumonia Ziehl-Neelsen stain/GeneXpert Sputum Pulmonary tuberculosis Blood culture Venous blood Bacteraemia/sepsis Wet mount/thick-thin blood Peripheral blood Malaria film (Giemsa) ELISA/rapid test for HBsAg Serum Hepatitis B infection
Basis of microbial pathogenicity (2024 mock) Microbial pathogenicity is based on the interplay of: 1. Ability to colonise the host
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Basis of microbial pathogenicity (2024 mock) Microbial pathogenicity is based on the interplay of: 1. Ability to colonise the host adherence to epithelial surfaces via specific adhesins/pili, competing successfully with normal flora. 2. Ability to invade host tissue – production of invasins and spreading factors (hyaluronidase, collagenase, streptokinase) enabling penetration beyond th initial site. 3. Ability to evade host immune defences – capsule formation (anti phagocytic), antigenic variation, intracellular survival, complement resistance, IgA protease production. 4. Toxin production – exotoxins (specific, potent, often enzymatic, e.g., diphtheria toxin, cholera toxin) and endotoxins (lipopolysaccharide o Gram-negative cell walls, triggering systemic inflammatory cascade and septic shock)
Genetic determinants – virulence genes often clustered on pathogenicity islands
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Genetic determinants – virulence genes often clustered on pathogenicity islands plasmids, or bacteriophages, allowing horizontal transfer of virulence traits between strains. 6. Host factors – susceptibility, immune status, and the adequacy of the host’ response also determine whether colonisation progresses to overt disease. Ultimately, pathogenicity reflects a dynamic balance between microbial virulenc factors and host defence mechanisms; the same organism may be harmless in one hos and cause severe disease in another depending on this balance.
Enveloped vs naked (non-enveloped) viruses
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Enveloped vs naked (non-enveloped) viruses Feature Enveloped viruses Naked (non-enveloped) viruses Outer structure Lipid bilayer envelope derived Capsid (protein coat) only, no from host cell membrane, lipid membrane studded with viral glycoproteins Stability in environment Less stable; susceptible to More stable; resistant to desiccation, detergents, heat, drying, detergents, and harsh lipid solvents environmental conditions Transmission Typically require direct Can survive on fomites, contact with body fluids, transmitted via faecal-oral respiratory droplets (moist route, water, food environments) Release from cell Bud through host cell Usually released by cell lysis membrane (often without lysing cell) Sensitivity to disinfectants Sensitive to alcohol, Resistant to many detergents, bile disinfectants, bile, gastric acid Examples HIV, Influenza virus, Poliovirus, Rotavirus, Herpesviruses, Hepatitis B and Adenovirus, Hepatitis A virus, C, Coronaviruses Papillomavirus
RNA virus vs DNA virus
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RNA virus vs DNA virus Feature RNA virus DNA virus Genome Single- or double-stranded Single- or double-stranded RNA DNA (mostly dsDNA) Site of replication Usually cytoplasm (exception: Usually nucleus (exception: Orthomyxoviruses, Poxviruses replicate in Retroviruses replicate partly in cytoplasm) nucleus) Replication enzyme RNA-dependent RNA Uses host DNA polymerase polymerase (own or host- (mostly), some carry their own derived); Retroviruses use reverse transcriptase Mutation rate High (RNA polymerase lacks Low (host DNA polymerase has proofreading), leading to proofreading function), more greater genetic genetically stable variability/antigenic variation Examples Influenza virus, HIV, Poliovirus, Herpesviruses, Hepatitis B Measles virus, SARS-CoV-2, virus, Adenovirus, Hepatitis C virus Papillomavirus, Poxvirus 3–4. Essay on HIV infection (i) Morphology: HIV is a spherical, enveloped RNA retrovirus (family Retroviridae genus Lentivirus), approximately 100–120 nm in diameter. It has an outer lipid envelope studded with glycoprotein spikes (gp120 attached non-covalently t transmembrane gp41). Beneath the envelope is a matrix protein (p17), enclosing cone-shaped capsid (p24) that contains two copies of single-stranded positive-sens RNA genome, along with the enzymes reverse transcriptase, integrase, and protease. (ii) Mode of transmission: - Sexual contact (vaginal, anal, oral) — commonest rout globally. - Blood-borne: transfusion of infected blood/blood products, sharing o needles/syringes (injecting drug use), occupational needle-stick injury. - Vertica (mother-to-child): transplacental, during delivery, or through breastfeeding. (iii) Laboratory diagnosis: - Screening: rapid diagnostic test (immunochromatographic) and ELISA detecting antibodies to HIV-1/HIV-2, o combined antigen (p24)/antibody assays (4th generation). - Confirmation: Western blot or a second, different rapid test/ELISA per national algorithm. - Virological tests HIV RNA PCR (viral load) — used for early infant diagnosis and monitoring treatmen response; proviral DNA PCR for infants under 18 months (maternal antibody interfere with antibody-based tests). - Immune monitoring: CD4+ T-cell count to asses degree of immunosuppression and guide opportunistic infection prophylaxis. (iv) Clinical presentation: - Acute retroviral syndrome (2–4 weeks post-exposure) fever, lymphadenopathy, sore throat, rash, myalgia — a self-limiting mononucleosis-lik illness. - Clinical latency: asymptomatic period lasting years, with ongoing vira replication and gradual CD4 decline. - Symptomatic HIV/AIDS: opportunisti infections (oral/oesophageal candidiasis, Pneumocystis jirovecii pneumonia tuberculosis, cryptococcal meningitis, cytomegalovirus retinitis), AIDS-defining malignancies (Kaposi’s sarcoma, non-Hodgkin lymphoma), wasting syndrome, and HIV associated neurocognitive disorders. (v) Treatment: Combination Antiretroviral Therapy (cART), typically two nucleosid reverse transcriptase inhibitors (NRTIs) plus an integrase strand transfer inhibito (INSTI) — e.g., Tenofovir + Lamivudine + Dolutegravir (TLD), the current WHO preferred first-line regimen. Other drug classes include non-nucleoside revers transcriptase inhibitors (NNRTIs) and protease inhibitors, used in alternative o second-line regimens. Treatment is lifelong, aims to achieve durable viral suppression and is initiated in all HIV-positive individuals regardless of CD4 count (“treat all strategy). (vi) Prevention and control: - Consistent condom use and safer sexual practices. Pre-exposure prophylaxis (PrEP) and post-exposure prophylaxis (PEP) with antiretrovirals. - Prevention of mother-to-child transmission (PMTCT) programmes — maternal ART, safe delivery practices, infant prophylaxis, and safer infant feeding. Screening of blood and blood products before transfusion. - Harm reduction for peopl who inject drugs (needle/syringe exchange programmes). - Voluntary medical mal circumcision (reduces female-to-male transmission risk). - Health education and behaviour change communication. - Universal precautions in healthcare settings. (vii) Complications: opportunistic infections, AIDS-defining malignancies, wasting syndrome, HIV-associated nephropathy, HIV-associated neurocognitive disorder immune reconstitution inflammatory syndrome (IRIS) following ART initiation, and increased risk of cardiovascular disease. 5a. Classification of viruses Viruses are classified using several schemes: 1. Nucleic acid type: DNA viruses v RNA viruses. 2. Strandedness: single-stranded (ss) vs double-stranded (ds). 3 Baltimore classification (based on mode of mRNA synthesis) — seven classes: - Clas I: dsDNA viruses (e.g., Herpesviruses) - Class II: ssDNA viruses (e.g., Parvovirus) Class III: dsRNA viruses (e.g., Rotavirus) - Class IV: positive-sense ssRNA viruses (e.g Poliovirus, Coronavirus) - Class V: negative-sense ssRNA viruses (e.g., Influenza virus Rabies virus) - Class VI: ssRNA viruses that replicate through a DNA intermediat (Retroviruses, e.g., HIV) - Class VII: dsDNA viruses that replicate through an RNA intermediate (e.g., Hepatitis B virus) 4. Presence/absence of envelope: enveloped v naked. 5. Capsid symmetry: icosahedral, helical, or complex. 6. Size and morphology. 7. Site of replication: nuclear vs cytoplasmic. 8. Family, genus species — formal taxonomic classification (e.g., family Herpesviridae, genu Simplexvirus, species HSV-1). 5b. Infections associated with Varicella Zoster Virus VZV (a member of the Herpesviridae family, subfamily Alphaherpesvirinae) causes tw distinct clinical entities: 1. Varicella (chickenpox) — the primary infection, typicall in childhood; presents with fever and a generalised, pruritic vesicular rash appearing in successive crops (“dew drops on a rose petal”), with lesions at different stage simultaneously. 2. Herpes zoster (shingles) — reactivation of latent virus (which persists in dorsal root/cranial nerve ganglia after primary infection), presenting as painful, unilateral vesicular rash in a dermatomal distribution, more common in th elderly and immunocompromised. Complications include post-herpetic neuralgia ophthalmic zoster (with risk of vision loss), and disseminated zoster in immunocompromised patients. 6–7. Antigenic drift and antigenic shift in Influenza virus Antigenic drift: Gradual accumulation of point mutations in the genes encoding th haemagglutinin (HA) and neuraminidase (NA) surface glycoproteins, due to the error prone nature of the viral RNA polymerase (lacking proofreading). This produces mino antigenic changes over time, allowing the virus to partially evade pre-existing population immunity, and is responsible for seasonal influenza epidemics, necessitating annual reformulation of the influenza vaccine. Antigenic shift: An abrupt, major change in HA and/or NA occurring when tw different influenza A strains (e.g., a human strain and an avian or swine strain) co infect the same host cell and their genome segments reassort (influenza has segmented genome), producing a novel virus subtype. Because the population ha little or no pre-existing immunity to the new subtype, antigenic shift can caus pandemics (e.g., 1918 H1N1, 1957 H2N2, 1968 H3N2, 2009 H1N1 pandemic) Antigenic shift only occurs in Influenza A (which infects multiple species), no Influenza B or C.
Essay on Lassa Fever Aetiology: Caused by Lassa virus, a single-stranded, enveloped RNA virus of th
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Essay on Lassa Fever Aetiology: Caused by Lassa virus, a single-stranded, enveloped RNA virus of th family Arenaviridae. Epidemiology: Endemic in West Africa (Nigeria, Sierra Leone, Liberia, Guinea). Th natural reservoir/host is the multimammate rat (Mastomys natalensis), which shed the virus in urine and faeces without becoming ill itself. Nigeria records recurren seasonal outbreaks, typically peaking in the dry season (November–April). Pathogenesis: Transmission to humans occurs via inhalation or ingestion o aerosolised/contaminated rodent excreta, or through contact with broken skin/mucou membranes; person-to-person transmission occurs via direct contact with blood secretions, or contaminated materials of an infected person (including in healthcar settings). The virus initially replicates at the site of entry, then disseminates via th lymphatics and bloodstream, infecting multiple organs. It causes widespread endothelial and hepatocyte damage, increased vascular permeability, and impaired coagulation, leading to haemorrhagic manifestations and multi-organ dysfunction in severe cases, related in part to viral suppression of the host innate immune respons (interferon evasion). Clinical features: Incubation period 6–21 days. Onset is usually gradual with fever malaise, headache, sore throat, and myalgia. Progression may include retrosterna pain, vomiting, diarrhoea, abdominal pain, and in severe cases: facial oedema, mucosa bleeding (gums, conjunctivae), pleural effusion, and shock. Sensorineural hearing los is a notable complication, occurring in a proportion of both severe and mild cases Case fatality is roughly 1% overall in the community but much higher (15–20%) among hospitalised severe cases. Laboratory diagnosis: Reverse transcriptase-PCR (RT-PCR) for viral RNA (gold standard, especially in the acute phase); ELISA for IgM/IgG antibodies; viral cultur (requires biosafety level 4 facilities, rarely done clinically). Prevention: Rodent control (proper food storage, eliminating rodent access to homes) community hygiene education, isolation and barrier nursing of suspected/confirmed cases, use of personal protective equipment by healthcare workers, safe buria practices, and prompt case reporting/contact tracing. There is currently no licensed vaccine. Treatment: Early administration of intravenous Ribavirin has been shown to reduc mortality, particularly when given within the first six days of illness; supportive car (fluid/electrolyte balance, management of shock and bleeding) is essential.
Prevention of poliomyelitis
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Prevention of poliomyelitis
Bunyavirales (order, multiple families) — Crimean-Congo haemorrhagic fever
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Bunyavirales (order, multiple families) — Crimean-Congo haemorrhagic fever virus, Rift Valley fever virus, Hantavirus
Vaccination — the cornerstone of prevention:
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Vaccination — the cornerstone of prevention: Oral Polio Vaccine (OPV): live-attenuated trivalent/bivalent vaccine, induces mucosal (intestinal) immunity, used in routine immunization and mass campaigns; risk of rare vaccine-associated paralytic polio and circulating vaccine-derived poliovirus. Inactivated Polio Vaccine (IPV): injectable, induces humoral immunity, no risk of vaccine-derived virus, included in routine schedules alongside OPV in the polio endgame strategy.
Supplementary Immunization Activities (SIAs) — mass campaigns/National
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Supplementary Immunization Activities (SIAs) — mass campaigns/National Immunization Days to boost population immunity and interrupt transmission.
Surveillance — Acute Flaccid Paralysis (AFP) surveillance to detect cases
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Surveillance — Acute Flaccid Paralysis (AFP) surveillance to detect cases promptly.
Environmental surveillance — testing sewage/wastewater for poliovirus
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Environmental surveillance — testing sewage/wastewater for poliovirus circulation.
Good sanitation and hygiene — safe water supply and proper faecal waste
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Good sanitation and hygiene — safe water supply and proper faecal waste disposal to interrupt faecal-oral transmission.
Health education on hand hygiene and safe food/water practices.
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Health education on hand hygiene and safe food/water practices.
Global Polio Eradication Initiative coordination — outbreak response, cross-
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Global Polio Eradication Initiative coordination — outbreak response, cross- border collaboration.
Varicella Zoster — two disease entities (pathogenesis and
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Varicella Zoster — two disease entities (pathogenesis and clinical manifestations) (See also Question 5b above.) VZV causes: Varicella (chickenpox) — primary infection. - Pathogenesis: virus enters via th respiratory tract/conjunctiva, replicates in regional lymph nodes, causes a primar viraemia seeding the reticuloendothelial system, followed by a secondary viraemia tha disseminates virus to the skin, producing the characteristic vesicular rash. The viru then establishes latency in dorsal root and cranial nerve ganglia. - Clinica manifestations: prodrome of fever and malaise, followed by a generalised pruriti rash progressing from macules → papules → vesicles (“dewdrop on a rose petal”) → pustules → crusts, with lesions in different stages present simultaneously; lesions ma involve mucous membranes. Usually self-limiting in healthy children; can be severe in adults, neonates, and immunocompromised patients (risk of varicella pneumonia encephalitis). Herpes Zoster (shingles) — reactivation of latent virus. - Pathogenesis: reactivation occurs when cell-mediated immunity to VZV declines (ageing, immunosuppression stress), allowing the latent virus in sensory ganglia to replicate and travel along th sensory nerve to the corresponding dermatome. - Clinical manifestations: unilateral dermatomal pain (often preceding the rash), followed by a vesicular rash confined t the affected dermatome; complications include post-herpetic neuralgia, ophthalmi zoster (Hutchinson’s sign, risk of keratitis/vision loss), Ramsay Hunt syndrom (geniculate ganglion involvement with facial palsy and ear vesicles), and disseminated zoster in the immunocompromised. 11–12. Herpesviridae family — members and general characteristics; pathophysiology of two members Members of the Herpesviridae family (human herpesviruses): 1. Herpes Simple Virus type 1 (HHV-1) 2. Herpes Simplex Virus type 2 (HHV-2) 3. Varicella Zoster Viru (HHV-3) 4. Epstein-Barr Virus (HHV-4) 5. Cytomegalovirus (HHV-5) 6. Human Herpesvirus 6 and 7 (roseola) 7. Kaposi’s Sarcoma-associated Herpesvirus (HHV-8) General characteristics: - Large, enveloped, double-stranded DNA viruses with icosahedral capsid. - Replicate in the nucleus of the host cell. - Share the hallmar biological property of establishing latency after primary infection, with the capacit for reactivation later in life, often triggered by immunosuppression or stress. Transmitted by close/direct contact with infected secretions. - Cause a wide range o diseases from mucocutaneous lesions to congenital infection and malignancy. Pathophysiology of two members: (a) Herpes Simplex Virus (HSV-1 and HSV-2): Enters through mucosal surfaces o breaks in skin, replicates locally in epithelial cells causing vesicular lesions, then travels retrograde along sensory nerve axons to establish latency in sensory gangli (trigeminal ganglion for HSV-1, sacral ganglia for HSV-2). Reactivation (triggered b stress, UV light, immunosuppression, fever) causes recurrent lesions at or near th original site. HSV-1 classically causes orolabial herpes and can cause herpe encephalitis (temporal lobe); HSV-2 classically causes genital herpes and neonata herpes (acquired during vaginal delivery). (b) Epstein-Barr Virus (EBV): Transmitted via saliva (“kissing disease”); infect oropharyngeal epithelial cells initially, then B-lymphocytes via the CD21 receptor causing polyclonal B-cell proliferation controlled by cytotoxic T-cells (producing th atypical lymphocytes seen in blood films). Causes infectious mononucleosis (fever pharyngitis, lymphadenopathy, splenomegaly), establishes lifelong latency in memor B-cells, and is associated with malignancies including Burkitt’s lymphoma nasopharyngeal carcinoma, and post-transplant lymphoproliferative disease, as well a being implicated in some cases of hairy leukoplakia in HIV patients. 13–14. Classification and general characteristics of Influenza viruses Classification: Influenza viruses belong to the family Orthomyxoviridae, and ar classified into three main types based on antigenic differences in nucleoprotein and matrix protein: - Influenza A: infects humans and a wide range of animals (birds pigs); subtyped by haemagglutinin (H1–H18) and neuraminidase (N1–N11) surfac antigens (e.g., H1N1, H3N2); responsible for pandemics (undergoes both antigeni drift and shift). - Influenza B: infects humans (and seals) only; divided into tw lineages (Victoria and Yamagata); undergoes antigenic drift only, causes seasona epidemics, generally milder than A. - Influenza C: infects humans and pigs; cause mild upper respiratory illness, not associated with epidemics. - (Influenza D primaril affects cattle.) General characteristics: - Enveloped, single-stranded, negative-sense, segmented RNA viruses (8 gene segments for types A and B). - Surface glycoproteins haemagglutinin (mediates attachment to sialic acid receptors) and neuraminidas (facilitates release of new virions). - Segmented genome allows genetic reassortmen (basis of antigenic shift). - Transmitted via respiratory droplets; causes seasona epidemics and occasional pandemics.
Viruses causing exanthems
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Viruses causing exanthems
Measles virus — measles (rubeola): erythematous maculopapular rash,
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Measles virus — measles (rubeola): erythematous maculopapular rash, cephalocaudal spread, with Koplik’s spots as enanthem.
Rubella virus — rubella (German measles): milder pink maculopapular rash,
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Rubella virus — rubella (German measles): milder pink maculopapular rash, associated with congenital rubella syndrome if acquired in pregnancy.
Varicella Zoster virus — chickenpox: vesicular rash in successive crops.
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Varicella Zoster virus — chickenpox: vesicular rash in successive crops.
Human Herpesvirus 6 — roseola infantum (exanthem subitum): high fever
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Human Herpesvirus 6 — roseola infantum (exanthem subitum): high fever followed by rash as fever resolves.
(Parvovirus B19 causes erythema infectiosum/“fifth disease” — also acceptable.)
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(Parvovirus B19 causes erythema infectiosum/“fifth disease” — also acceptable.)
Concise note on one exanthem-causing infection Measles (Rubeola) - Aetiology: Measles virus, family Paramyxoviridae, genu
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Concise note on one exanthem-causing infection Measles (Rubeola) - Aetiology: Measles virus, family Paramyxoviridae, genu Morbillivirus — a single-stranded, negative-sense, enveloped RNA virus. Pathogenesis: Transmitted via respiratory droplets/airborne spread; virus infect respiratory epithelium and disseminates via lymphatics and blood (primary and secondary viraemia) to skin, respiratory tract, and other organs, causing characteristi multinucleated giant cell formation and immune suppression (predisposing t secondary bacterial infections). - Clinical presentation: prodrome of fever, cough coryza, conjunctivitis, and Koplik’s spots (enanthem on buccal mucosa), followed by an erythematous maculopapular rash beginning on the face/behind ears and spreading cephalocaudally. Complications include otitis media, pneumonia, encephalitis, and subacute sclerosing panencephalitis (a rare, delayed, fatal complication).
Essay on classification of viruses (See Question 5a above for the full classification schema — nucleic acid type
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Essay on classification of viruses (See Question 5a above for the full classification schema — nucleic acid type strandedness, Baltimore classification, envelope status, capsid symmetry, and taxonomic family/genus/species.) 18–19. Structural proteins and glycoproteins of HIV; functional and structural proteins Structural proteins/glycoproteins of HIV: 1. gp120 — surface envelop glycoprotein; binds to CD4 receptor on host T-helper cells and co-receptor (CCR5/CXCR4). 2. gp41 — transmembrane glycoprotein; mediates fusion of vira envelope with host cell membrane. 3. p17 (matrix protein) — lines the inner surfac of the viral envelope. 4. p24 (capsid protein) — forms the cone-shaped cor enclosing the viral genome; used as a diagnostic marker (p24 antigen testing). 5. p7 (nucleocapsid protein) — binds and protects the viral RNA genome. Functional (enzymatic/regulatory) proteins of HIV: 1. Reverse transcriptase — transcribes viral RNA into proviral DNA. 2. Integrase — integrates proviral DNA int the host cell genome. 3. Protease — cleaves polyprotein precursors into matur functional viral proteins. 4. Tat — transactivates viral gene transcription. 5. Rev — regulates export of viral mRNA from the nucleus.
Classes of antiretroviral drugs
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Classes of antiretroviral drugs
Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs) — e.g.,
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Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs) — e.g., Tenofovir, Lamivudine, Zidovudine — inhibit reverse transcriptase by acting as faulty DNA chain terminators.
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) — e.g., Efavirenz,
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Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) — e.g., Efavirenz, Nevirapine — bind directly to and inhibit reverse transcriptase at a site distinct from the active site.
Flaviviridae — Yellow fever virus, Dengue virus
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Flaviviridae — Yellow fever virus, Dengue virus
Integrase Strand Transfer Inhibitors (INSTIs) — e.g., Dolutegravir, Raltegravir
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Integrase Strand Transfer Inhibitors (INSTIs) — e.g., Dolutegravir, Raltegravir — block integration of viral DNA into the host genome. (Also acceptable: Protease Inhibitors — e.g., Lopinavir/ritonavir, Atazanavir — inhibit the viral protease enzyme; Entry/Fusion inhibitors — e.g., Maraviroc, Enfuvirtide.)
Biology, infectious process, and pathology of SARS-CoV-2
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Biology, infectious process, and pathology of SARS-CoV-2 Biology: SARS-CoV-2 is an enveloped, single-stranded, positive-sense RNA virus of th family Coronaviridae, with a large genome (~30 kb), the largest among RNA viruses. I has a characteristic crown-like appearance on electron microscopy due to club-shaped spike (S) glycoprotein projections, along with membrane (M), envelope (E), and nucleocapsid (N) structural proteins. Infectious process: Transmission occurs mainly via respiratory droplets and aerosols and to a lesser extent via contact with contaminated surfaces. The spike protein bind to the angiotensin-converting enzyme 2 (ACE2) receptor on host respiratory epithelia cells (and other ACE2-expressing tissues), with priming by the host protease TMPRSS facilitating membrane fusion and cell entry. The viral RNA genome is translated and replicated using the viral RNA-dependent RNA polymerase, and new virions assembl and are released via exocytosis. Pathology: Initial infection of upper respiratory epithelium may progress to lowe respiratory tract involvement, causing diffuse alveolar damage, type II pneumocyt injury, and hyaline membrane formation (histologically resembling ARDS). Sever disease is associated with a dysregulated host immune response (“cytokine storm” with elevated IL-6, TNF-α, and other inflammatory mediators, endothelial dysfunction and a pro-thrombotic state predisposing to microvascular and macrovascula thrombosis. Extrapulmonary manifestations (cardiac, renal, neurological gastrointestinal) reflect both direct viral cytopathic effect (via ACE2-expressing cells in these organs) and immune-mediated injury.
Essay on classification of viruses (As per Question 5a/17 — full classification by nucleic acid, Baltimore scheme
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Essay on classification of viruses (As per Question 5a/17 — full classification by nucleic acid, Baltimore scheme envelope, symmetry, and taxonomy.) 23/32. Satellitism in Haemophilus influenzae Definition: Satellitism is a laboratory phenomenon in which colonies of Haemophilu influenzae grow larger in the immediate vicinity of colonies of Staphylococcus aureu (or other organisms) streaked on the same blood agar plate, with colony siz diminishing with increasing distance from the S. aureus streak. Basis: H. influenzae requires two growth factors present in blood — Factor X (haemin required for cytochrome synthesis) and Factor V (NAD, required for oxidation reduction reactions) — which are not readily available on unheated blood (sheep) aga because Factor V is inactivated by an NADase in sheep red blood cells, and th bacteria cannot lyse the intact red cells to release Factor X. Staphylococcus aureu growing on the same plate haemolyses red blood cells (releasing Factor X) and, mor importantly, secretes Factor V (NAD) into the surrounding medium, thereby “feeding the nearby H. influenzae colonies and allowing them to grow — hence “satellite colonies clustering around the staphylococcal streak. On chocolate agar (heated blood agar), both factors are already freely available, so satellitism is not seen, and H influenzae grows uniformly. 24–25. Pseudomonas aeruginosa Morphology: Gram-negative, aerobic, non-fermenting, motile (polar flagellum bacillus; produces a characteristic fruity (grape-like) odour and blue-green pigment (pyocyanin and pyoverdin) on culture media. Virulence factors: 1. Pili/fimbriae — mediate adherence to host epithelium. 2 Exotoxin A — inhibits host protein synthesis (similar mechanism to diphtheria toxin via ADP-ribosylation of elongation factor-2). 3. Pyocyanin — pigment that generate reactive oxygen species, damaging host tissue. 4. Elastase and proteases — degrad host tissue components and immune proteins. 5. Lipopolysaccharide (endotoxin) — triggers systemic inflammatory response. 6. Alginate/biofilm production — protect against phagocytosis, antibiotics, and host clearance (notably in cystic fibrosis lung infection). 7. Type III secretion system — injects effector toxins directly into hos cells. Diseases: Nosocomial infections including ventilator-associated pneumonia, catheter associated urinary tract infections, burn wound infections, malignant otitis externa (in diabetics), keratitis (contact lens wearers), ecthyma gangrenosum (in neutropenic/immunocompromised patients), and chronic pulmonary infection in cysti fibrosis patients. Laboratory diagnosis: Culture on MacConkey/blood agar showing non-lactos fermenting colonies with a characteristic grape-like odour and blue-green pigment oxidase-positive; identification confirmed biochemically or by automated systems. Treatment: Anti-pseudomonal beta-lactams (piperacillin-tazobactam, ceftazidime cefepime, meropenem/imipenem), aminoglycosides (gentamicin, amikacin tobramycin), fluoroquinolones (ciprofloxacin), and polymyxins (colistin) for multidrug resistant strains; combination therapy is often used for serious infections. Anti-pseudomonal antibiotics by class: 1. Anti-pseudomonal penicillins — Piperacillin (with tazobactam) 2. Anti-pseudomonal cephalosporins — Ceftazidime Cefepime 3. Carbapenems — Meropenem, Imipenem 4. Aminoglycosides — Gentamicin, Amikacin, Tobramycin 5. Fluoroquinolones — Ciprofloxacin, Levofloxacin Prevention: strict infection control practices, hand hygiene, minimising invasiv device duration, water system maintenance in hospitals, and wound care.
Human Papillomavirus (HPV) infection — types, transmission,
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Human Papillomavirus (HPV) infection — types, transmission, risk factors, clinical manifestations, diagnosis, prevention Types: HPV is a non-enveloped, double-stranded DNA virus (family Papillomaviridae with over 100 genotypes, classified by oncogenic potential: - Low-risk types (e.g HPV 6, 11) — cause benign genital warts (condylomata acuminata) and laryngea papillomas. - High-risk (oncogenic) types (e.g., HPV 16, 18, and others) — associated with cervical, anal, vulvar, penile, and oropharyngeal cancers. Transmission: primarily through direct skin-to-skin or mucosal contact during sexua activity (vaginal, anal, oral); vertical transmission from mother to infant during delivery can cause recurrent respiratory papillomatosis. Risk factors: early age at first intercourse, multiple sexual partners immunosuppression (including HIV infection), smoking, high parity, co-infection with other STIs, and lack of vaccination. Clinical manifestations: genital warts (low-risk types); cervical intraepithelia neoplasia (CIN) progressing to invasive cervical cancer (high-risk types), usually afte a long latency period; also associated with vulvar, vaginal, anal, penile, and oropharyngeal cancers. Diagnosis: Papanicolaou (Pap) smear cytology for cervical screening; HPV DNA testing (molecular/NAAT); colposcopy with biopsy for histological confirmation o dysplasia/malignancy; visual inspection with acetic acid (VIA) in low-resource settings Prevention: HPV vaccination (bivalent, quadrivalent, or nonavalent vaccines targeting high-risk and/or low-risk types), ideally given before sexual debut (recommended around ages 9–14); routine cervical cancer screening (Pap smear/HPV testing) condom use (reduces but does not eliminate risk given skin-to-skin transmission) reduction of risk factors.
Bacillary vs Amoebic Dysentery (tabular comparison)
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Bacillary vs Amoebic Dysentery (tabular comparison) Feature Bacillary Dysentery Amoebic Dysentery Causative organism Shigella species (also Entamoeba histolytica Salmonella, invasive E. coli) Onset Acute, sudden Usually more gradual/insidious Stool character Frequent, small-volume stools Stool with blood and mucus, with blood and mucus, often less watery, “anchovy sauce” with tenesmus appearance in liver abscess- related cases Fever Common, often high-grade Usually low-grade or absent Microscopy Numerous pus cells Few pus cells, characteristic (neutrophils), few red cells haematophagous trophozoites with ingested RBCs Pathology Mucosal ulceration limited to Flask-shaped ulcers, can colon, inflammatory invade deeper and spread to liver (amoebic liver abscess) Diagnosis Stool culture, Gram stain Stool microscopy (trophozoites/cysts), serology, antigen detection Treatment Antibiotics (e.g., ciprofloxacin, Metronidazole/tinidazole ceftriaxone) + fluid (tissue), followed by a luminal replacement agent (e.g., paromomycin)
Markers of Hepatitis B virus infection and diagnostic values
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Markers of Hepatitis B virus infection and diagnostic values Marker Diagnostic significance HBsAg (surface antigen) First marker to appear; indicates current infection (acute or chronic) Anti-HBs (surface antibody) Indicates immunity — either from resolved infection or successful vaccination HBeAg (e antigen) Marker of active viral replication and high infectivity Anti-HBe Indicates reduced viral replication/seroconversion, generally lower infectivity IgM anti-HBc (core antibody) Indicates recent/acute infection (within the “window period” when HBsAg may be undetectable) IgG anti-HBc Indicates past exposure (either resolved infection or chronic infection), persists lifelong HBV DNA Direct marker of viral load, used to assess replication activity and monitor treatment Schematic pattern over time: - Acute infection: HBsAg rises first → HBeAg and HBV DNA appear (high infectivity) → IgM anti-HBc appears during acute illness → HBsAg declines and disappears → “window period” (HBsAg negative, anti-HBs not ye positive, IgM anti-HBc positive) → anti-HBs and anti-HBe appear indicating recovery/immunity, IgG anti-HBc persists. - Chronic infection: HBsAg persist beyond 6 months, with variable HBeAg/anti-HBe and HBV DNA levels depending on replicative phase; anti-HBs remains negative. - Vaccination: only anti-HBs is positiv (all other markers negative).
Viral haemorrhagic fever families with examples
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Viral haemorrhagic fever families with examples
Diagnostic modalities, clinical reasoning, and treatment of
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Diagnostic modalities, clinical reasoning, and treatment of Lassa fever (See also Question 8.) Clinical reasoning: Suspect Lassa fever in a patient from/travelling through an endemic West African region presenting with gradual-onset fever unresponsive t antimalarials and antibiotics, especially with sore throat, retrosternal pain proteinuria, facial swelling, or bleeding tendencies, particularly during outbrea seasons or with a history of rodent exposure or contact with a confirmed case. Diagnostic modalities: RT-PCR for viral RNA (most reliable in the acute febril phase, first 1–2 weeks); ELISA for IgM (recent infection) and IgG (past exposure antibodies; full blood count and liver function tests (elevated AST is a marker o severity); viral culture in reference laboratories with BSL-4 capacit (research/confirmatory use only). Treatment: Early intravenous Ribavirin (most effective within the first six days o symptom onset) reduces mortality significantly; supportive management include careful fluid and electrolyte management, blood product support for haemorrhage management of shock, and treatment of complications; strict barrier nursing/isolation to prevent nosocomial spread.
Structural and functional proteins of HIV (See Question 18–19 above.)
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Structural and functional proteins of HIV (See Question 18–19 above.)
Mumps Aetiology: Mumps virus, a single-stranded, negative-sense RNA virus of the famil
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Mumps Aetiology: Mumps virus, a single-stranded, negative-sense RNA virus of the famil Paramyxoviridae, genus Rubulavirus. Pathogenesis: Transmitted via respiratory droplets and direct contact with saliva virus replicates in the upper respiratory tract epithelium and regional lymph nodes followed by viraemia that disseminates the virus to the salivary glands (particularl parotid) and other tissues (testes, ovaries, pancreas, meninges, inner ear) which possess receptors favouring viral tropism. Clinical spectrum: - Classic presentation: fever, malaise, and painful parotiti (unilateral or bilateral parotid gland swelling). - Complications: orchitis (in post pubertal males, may cause testicular atrophy but rarely infertility), oophoritis pancreatitis, aseptic meningitis/encephalitis, and sensorineural hearing loss (usuall unilateral). - A significant proportion of infections may be subclinical. Diagnosis: primarily clinical; confirmed by RT-PCR or viral culture from saliva/ora fluid, or serology (IgM antibody, or rising IgG titre in paired sera). Treatment: supportive — analgesics/antipyretics, adequate hydration, rest; no specifi antiviral therapy. Prevention: MMR (Measles-Mumps-Rubella) live attenuated vaccine, given pe routine childhood immunization schedule; isolation of cases during the infectiou period.
Lag phase: Cells adapt to the new environment — synthesising enzymes, RNA, and
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Lag phase: Cells adapt to the new environment — synthesising enzymes, RNA, and other molecules needed for division — with little or no increase in cell number. Duration depends on the condition of the inoculum and the medium.
Log (exponential) phase: Cells divide at a constant maximal rate characteristic of
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Log (exponential) phase: Cells divide at a constant maximal rate characteristic of the organism and medium, with the population doubling at regular intervals (generation time); cells are metabolically most active and most susceptible to antibiotics acting on cell wall/protein synthesis during this phase.
Stationary phase: Rate of cell division equals rate of cell death, so the total viable
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Stationary phase: Rate of cell division equals rate of cell death, so the total viable count plateaus, due to depletion of nutrients, accumulation of toxic metabolic waste products, and reduced oxygen availability; some bacteria begin spore formation and secondary metabolite (e.g., toxin, antibiotic) production here.
Death (decline) phase: Nutrient exhaustion and toxin accumulation cause the
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Death (decline) phase: Nutrient exhaustion and toxin accumulation cause the death rate to exceed the division rate, with viable cell numbers declining logarithmically. (A diagram would plot log₁₀ viable count on the y-axis against time on the x-axis showing the characteristic sigmoid curve with the four phases labelled sequentially.)
Cross-section of the bacterial cell envelope and medical
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Cross-section of the bacterial cell envelope and medical importance of each part Layers (from innermost to outermost) and their medical importance:
Cytoplasmic (plasma) membrane — phospholipid bilayer regulating transport;
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Cytoplasmic (plasma) membrane — phospholipid bilayer regulating transport; site of action of polymyxins (colistin), which disrupt membrane integrity.
Peptidoglycan (murein) layer — provides structural rigidity and shape; target of
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Peptidoglycan (murein) layer — provides structural rigidity and shape; target of beta-lactam antibiotics (penicillins, cephalosporins) and glycopeptides (vancomycin); thickness differs between Gram-positive (thick) and Gram-negative (thin) bacteria, forming the basis of the Gram stain.
Periplasmic space (Gram-negative only) — contains hydrolytic enzymes and beta-
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Periplasmic space (Gram-negative only) — contains hydrolytic enzymes and beta- lactamases that can inactivate antibiotics before they reach their target.
Outer membrane (Gram-negative only) — contains lipopolysaccharide (LPS), the
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Outer membrane (Gram-negative only) — contains lipopolysaccharide (LPS), the endotoxin responsible for septic shock; also contains porins that regulate antibiotic entry (loss of porins is a resistance mechanism).
Capsule/glycocalyx (in some organisms) — polysaccharide layer that is anti-
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Capsule/glycocalyx (in some organisms) — polysaccharide layer that is anti- phagocytic, a major virulence factor, and the basis of polysaccharide vaccines (e.g., pneumococcal, meningococcal vaccines).
Flagella — organs of motility; also act as an antigen (H antigen) used in serotyping
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Flagella — organs of motility; also act as an antigen (H antigen) used in serotyping (e.g., Salmonella).
Pili/Fimbriae — mediate adherence to host cells (virulence factor) and, in the case
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Pili/Fimbriae — mediate adherence to host cells (virulence factor) and, in the case of sex pili, genetic exchange (conjugation, spread of resistance genes).
Differences between Gram-positive and Gram-negative cell walls
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Differences between Gram-positive and Gram-negative cell walls Feature Gram-positive Gram-negative Peptidoglycan layer Thick (multilayered) Thin (single layer) Outer membrane Absent Present, containing lipopolysaccharide (LPS/endotoxin) Periplasmic space Minimal/absent Present, prominent Teichoic acid Present (embedded in Absent peptidoglycan) Lipopolysaccharide (endotoxin) Absent Present — responsible for septic shock Gram stain result Retains crystal violet — stains Decolourised, takes up purple safranin — stains pink/red Susceptibility to Generally more susceptible Generally less susceptible lysozyme/penicillin (outer membrane acts as barrier) 5/25. Classification of Mycobacteria species (with examples)
Tuberculous mycobacteria (Mycobacterium tuberculosis complex) — M.
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Tuberculous mycobacteria (Mycobacterium tuberculosis complex) — M. tuberculosis, M. bovis, M. africanum — cause tuberculosis.
Non-tuberculous (atypical) mycobacteria — M. avium-intracellulare complex,
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Non-tuberculous (atypical) mycobacteria — M. avium-intracellulare complex, M. kansasii, M. fortuitum — cause opportunistic pulmonary or disseminated disease, particularly in immunocompromised hosts.
Leprosy bacillus — Mycobacterium leprae — causes leprosy (Hansen’s disease);
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Leprosy bacillus — Mycobacterium leprae — causes leprosy (Hansen’s disease); notably cannot be cultured on artificial media. (Runyon classification of non-tuberculous mycobacteria by growth rate and pigmen production is also acceptable as a supplementary classification.)
Laboratory diagnosis of syphilis Causative organism: Treponema pallidum (a spirochaete that cannot be cultured on
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Laboratory diagnosis of syphilis Causative organism: Treponema pallidum (a spirochaete that cannot be cultured on artificial media). Direct detection methods: - Dark-field microscopy — direct visualisation of motil spirochaetes from a chancre/lesion exudate (most useful in primary syphilis). - PCR — detects treponemal DNA from lesion swabs. Serological tests (used for screening and confirmation): 1. Non-treponema (screening) tests: VDRL (Venereal Disease Research Laboratory) and RPR (Rapid Plasma Reagin) — detect antibodies (reagin) against cardiolipin-lecithin-cholestero antigen; sensitive but non-specific (false positives occur in pregnancy, autoimmun disease, other infections); used for screening and monitoring treatment respons (titres decline with successful treatment). 2. Treponemal (confirmatory) tests TPHA (Treponema Pallidum Haemagglutination Assay), FTA-ABS (Fluorescen Treponemal Antibody Absorption), and treponemal-specific EIA/CLIA — more specific confirm true infection, but remain positive for life even after treatment (not useful fo monitoring cure). Diagnostic algorithm: typically a non-treponemal screening test is confirmed with treponemal test (or vice versa, in the “reverse algorithm”), as neither test alone is both sensitive and specific.
Mycetoma Definition: A chronic, progressive, granulomatous subcutaneous infection, classicall
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Mycetoma Definition: A chronic, progressive, granulomatous subcutaneous infection, classicall affecting the foot (“Madura foot”), characterised by the triad of tumefaction (swelling) multiple sinus tracts, and discharge containing characteristic grains. Aetiology: Two forms based on causative organism: - Eumycetoma — caused by fung (e.g., Madurella mycetomatis). - Actinomycetoma — caused by aerobic actinomycete (bacteria) such as Nocardia species, Actinomadura, and Streptomyces somaliensis. Transmission: traumatic inoculation of the organism into subcutaneous tissue typically through minor skin injury from contaminated soil or plant material (common in barefoot agricultural workers in tropical regions, hence more common on the foot). Clinical features: painless, slowly progressive subcutaneous swelling with multipl discharging sinuses draining grains (the colour and consistency of the grains help differentiate fungal from actinomycete causes); can progress to involve bone, causing deformity. Laboratory diagnosis: microscopic examination of grains (crushed and stained) culture on appropriate media, histopathology, and imaging (X-ray/MRI) for bon involvement. Treatment: Actinomycetoma responds to prolonged antibiotic therapy (e.g combination of sulphonamides/co-trimoxazole with an aminoglycoside such a streptomycin or amikacin); Eumycetoma requires prolonged antifungal therapy and often surgical debridement/amputation in advanced cases.
Acute Post-Streptococcal Glomerulonephritis: can follow either pharyngeal o
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Acute Post-Streptococcal Glomerulonephritis: can follow either pharyngeal o skin (impetigo) streptococcal infection with specific “nephritogenic” strains; caused by deposition of antigen-antibody immune complexes in the glomerular basemen membrane, triggering complement activation and inflammation. Presents with haematuria (smoky/cola-coloured urine), oedema, hypertension, and reduced urin output, typically 1–3 weeks after the preceding infection; generally self-limiting in children with supportive management (management of fluid balance and blood pressure), though it can occasionally progress to chronic kidney disease, more so in adults.
Classification of pathogenic Treponemes (with diseases)
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Classification of pathogenic Treponemes (with diseases)
Treponema pallidum subspecies pallidum — causes venereal syphilis.
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Treponema pallidum subspecies pallidum — causes venereal syphilis.
Treponema pallidum subspecies pertenue — causes yaws (a non-venereal,
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Treponema pallidum subspecies pertenue — causes yaws (a non-venereal, tropical skin/bone disease).
Classification of bacteria based on oxygen and temperature
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Classification of bacteria based on oxygen and temperature requirements Based on oxygen requirement: 1. Obligate aerobes — require oxygen for growth (e.g., Mycobacterium tuberculosis, Pseudomonas aeruginosa). 2. Obligate anaerobe — grow only in the absence of oxygen, killed by exposure to it (e.g., Clostridium tetani Bacteroides fragilis). 3. Facultative anaerobes — can grow with or without oxygen (e.g., Escherichia coli, Staphylococcus aureus). 4. Microaerophiles — requir reduced oxygen concentration for optimal growth (e.g., Helicobacter pylori Campylobacter jejuni). 5. Aerotolerant anaerobes — do not use oxygen but can tolerate its presence (e.g., some Lactobacillus species). Based on temperature requirement: 1. Psychrophiles — grow optimally at low temperatures (0–20°C). 2. Mesophiles — grow optimally at moderate temperature (20–45°C), including most human pathogens which grow best at 37°C (bod temperature). 3. Thermophiles — grow optimally at high temperatures (45–80°C). 9/31. Essay on E. coli Morphology: Gram-negative, non-sporing, facultatively anaerobic bacillus, motil (peritrichous flagella), a member of the family Enterobacteriaceae, ferments lactos (distinguishing it from many other enteric pathogens on MacConkey agar). Virulence factors: 1. Fimbriae/pili (adhesins, e.g., P fimbriae in uropathogeni strains). 2. Endotoxin (LPS) — triggers systemic inflammatory response in bacteraemia. 3. Exotoxins — e.g., heat-labile and heat-stable enterotoxins (ETEC) Shiga-like (Vero) toxin (EHEC/STEC), causing haemolytic uraemic syndrome. 4 Capsule (K antigen) — anti-phagocytic, important in neonatal meningitis (K1 strains)
Siderophores — iron-acquisition systems enhancing survival in the host.
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Siderophores — iron-acquisition systems enhancing survival in the host. Laboratory features: Gram-negative bacillus; lactose fermenter (pink colonies on MacConkey agar); indole-positive, methyl red-positive, Voges-Proskauer-negative citrate-negative (IMViC pattern); grows readily on routine media. Diseases associated: Urinary tract infection (commonest cause), neonatal meningiti and sepsis, traveller’s diarrhoea (Enterotoxigenic E. coli), haemorrhagic colitis and haemolytic uraemic syndrome (Enterohaemorrhagic E. coli, e.g., O157:H7), wound infections, and intra-abdominal sepsis. Treatment: guided by culture and sensitivity; commonly used agents includ nitrofurantoin/fosfomycin for uncomplicated UTI, and beta-lactams, fluoroquinolones or carbapenems (for ESBL-producing strains) for more invasive disease; antibiotics ar avoided in EHEC infection due to risk of increasing toxin release and precipitating haemolytic uraemic syndrome.
Cholera — aetiology, pathogenesis, clinical presentation,
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Cholera — aetiology, pathogenesis, clinical presentation, laboratory diagnosis, treatment Aetiology: Vibrio cholerae (serogroups O1 and O139), a Gram-negative, curved (comma-shaped) bacillus with a single polar flagellum. Pathogenesis: Transmitted via the faecal-oral route (contaminated water/food). Afte surviving gastric acidity (facilitated by a large infectious dose or reduced gastric acid) the organism colonises the small intestinal mucosa without invading it, and produce cholera toxin, an AB-type exotoxin. The A subunit ADP-ribosylates a G-protein permanently activating adenylate cyclase, raising intracellular cAMP, which drive massive efflux of chloride and water into the intestinal lumen via the CFTR channel causing profuse watery diarrhoea. Clinical presentation: sudden onset of profuse, painless, watery diarrhoea (“rice water stools”), often with vomiting; can lead to rapid, severe dehydration hypovolaemic shock, metabolic acidosis, and hypokalaemia if untreated; can caus death within hours in severe cases. Laboratory diagnosis: dark-field microscopy of fresh stool showing characteristi darting motility; stool culture on selective media (Thiosulphate Citrate Bile Salt Sucrose — TCBS — agar, yielding yellow colonies); rapid dipstick antigen tests for field use; serotyping/PCR for confirmation and outbreak investigation. Treatment: Aggressive fluid and electrolyte replacement is the cornerstone — ora rehydration solution for mild-moderate cases, intravenous fluids (e.g., Ringer’s lactate for severe dehydration/shock; antibiotics (e.g., doxycycline, azithromycin, o ciprofloxacin) shorten duration of illness and reduce organism shedding but ar adjunctive to rehydration, not a substitute for it.
Mechanisms of acquired resistance; ESBLs; MDR-TB (See General Section, Question 26, for full detail on mechanisms of acquired
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Mechanisms of acquired resistance; ESBLs; MDR-TB (See General Section, Question 26, for full detail on mechanisms of acquired resistance, ESBLs, and MDR-TB management.)
Periodontal infection Definition: Inflammatory disease affecting the supporting structures of the teeth
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Periodontal infection Definition: Inflammatory disease affecting the supporting structures of the teeth (gingiva, periodontal ligament, alveolar bone, cementum), caused by dental plaqu bacteria. Aetiology: Polymicrobial, dominated by anaerobic Gram-negative bacteria including Porphyromonas gingivalis, Tannerella forsythia, Aggregatibacte actinomycetemcomitans, and Treponema denticola (“red complex” organisms) organised within dental plaque biofilm. Risk factors: poor oral hygiene, smoking, diabetes mellitus, immunosuppression hormonal changes (pregnancy), genetic susceptibility, and certain medications causing gingival overgrowth. Types of periodontal infections: 1. Gingivitis — reversible inflammation limited t the gingiva, without loss of attachment. 2. Periodontitis — progressive inflammation extending to the periodontal ligament and alveolar bone, with irreversible attachmen loss and pocket formation. 3. Necrotising periodontal disease — severe, rapidl destructive form, often in immunocompromised individuals. Laboratory investigations: clinical periodontal probing (pocket depth, attachmen loss), radiographs to assess bone loss, microbial culture/PCR of subgingival plaque in selected cases. Treatment: mechanical plaque removal (scaling and root planing), oral hygien education, adjunctive antimicrobials (local or systemic) in selected cases, and surgica intervention for advanced disease. Prevention: regular oral hygiene (brushing, flossing), routine dental check-ups smoking cessation, and control of systemic risk factors (e.g., diabetes). Complications: tooth mobility and loss, alveolar bone loss, and systemic association (periodontitis has been linked to increased cardiovascular risk and adverse pregnanc outcomes).
Treponema pallidum subspecies endemicum — causes endemic syphilis (bejel).
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Treponema pallidum subspecies endemicum — causes endemic syphilis (bejel).
Treponema carateum — causes pinta (a skin-limited treponematosis).
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Treponema carateum — causes pinta (a skin-limited treponematosis).
Helicobacter pylori infection Morphology: Gram-negative, spiral/curved, microaerophilic bacillus with multipl
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Helicobacter pylori infection Morphology: Gram-negative, spiral/curved, microaerophilic bacillus with multipl flagella, producing abundant urease — a key feature exploited for diagnosis. Mode of transmission: oral-oral or faecal-oral route; typically acquired in childhood with higher prevalence in areas of poor sanitation/overcrowding. Risk factors: low socioeconomic status, overcrowding, poor sanitation, and childhood acquisition within families. Laboratory diagnosis: - Invasive (endoscopy-based): rapid urease test (biops urease test), histology, culture, PCR of gastric biopsy. - Non-invasive: urea breath tes (using labelled carbon), stool antigen test, serology (indicates exposure, no necessarily active infection). Diseases associated: chronic gastritis, peptic ulcer disease (gastric and duodenal) gastric adenocarcinoma, and gastric MALT (mucosa-associated lymphoid tissue lymphoma. Pathogenesis involves urease-mediated neutralisation of gastric acid enabling survival, flagellar motility enabling penetration of the mucus layer, adhesin for attachment to gastric epithelium, and the CagA/VacA virulence factors causing epithelial damage and chronic inflammation. Treatment: Eradication therapy — typically triple therapy (a proton pump inhibito plus two antibiotics, e.g., amoxicillin and clarithromycin) or quadruple therap (bismuth-based, especially where clarithromycin resistance is a concern) for 10–14 days. Complications: peptic ulcer perforation/bleeding, gastric outlet obstruction, gastri carcinoma, and MALT lymphoma.
African Histoplasmosis Aetiology: Caused by Histoplasma capsulatum var. duboisii (distinct from the classi
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African Histoplasmosis Aetiology: Caused by Histoplasma capsulatum var. duboisii (distinct from the classi Histoplasma capsulatum var. capsulatum causing pulmonary histoplasmosis), dimorphic fungus found in soil, particularly enriched by bird/bat droppings. Pathogenesis: Inhalation of microconidia, which convert to the yeast form at bod temperature; in African histoplasmosis, the organism characteristically produce larger yeast forms and shows a predilection for skin, subcutaneous tissue, and bon rather than the lungs (unlike the classic pulmonary form). Clinical features: cutaneous and subcutaneous nodules/ulcers, lymphadenopathy, and osteolytic bone lesions; disseminated disease can occur in immunocompromised patients. Laboratory diagnosis: histopathology of biopsy specimens showing large yeast form with narrow-based budding; fungal culture (dimorphism demonstrated by mould form at room temperature and yeast form at 37°C); serology in some settings. Treatment: Itraconazole for mild-moderate disease; Amphotericin B fo severe/disseminated disease, often followed by itraconazole maintenance therapy. Prognosis: generally good with treatment for localised disease; disseminated diseas in immunocompromised patients carries higher morbidity/mortality.
General characteristics of Enterobacteriaceae (with 5 examples)
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General characteristics of Enterobacteriaceae (with 5 examples) General characteristics: 1. Gram-negative bacilli. 2. Facultative anaerobes. 3 Oxidase-negative (this distinguishes them from Pseudomonas and Vibrio, which ar oxidase-positive). 4. Ferment glucose (with or without gas production). 5. Reduc nitrates to nitrites. 6. Grow readily on ordinary/MacConkey media. 7. Motil (peritrichous flagella) or non-motile depending on genus. 8. Many possess O (somatic) H (flagellar), and K (capsular) antigens used for serotyping. Examples: Escherichia coli, Klebsiella pneumoniae, Salmonella species, Shigell species, Proteus mirabilis (also acceptable: Enterobacter, Yersinia species).
Essay on Staphylococcus aureus infection Morphology: Gram-positive cocci arranged in irregular clusters (“grape-like”); non
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Essay on Staphylococcus aureus infection Morphology: Gram-positive cocci arranged in irregular clusters (“grape-like”); non motile, non-sporing, facultative anaerobe; catalase-positive (distinguishing Staphylococci from Streptococci) and coagulase-positive (distinguishing S. aureus from coagulase-negative staphylococci like S. epidermidis). Mode of transmission: direct contact with infected/colonised skin or mucosa contaminated fomites, and respiratory droplets; anterior nares are the principa reservoir/carriage site in humans. Virulence factors: 1. Coagulase — converts fibrinogen to fibrin, walling off infection and protecting the organism. 2. Protein A — binds the Fc portion of IgG, preventing opsonisation and phagocytosis. 3. Alpha-toxin (haemolysin) — pore-forming toxin causing cell lysis. 4. Panton-Valentine leukocidin (PVL) — destroys leukocytes associated with necrotising skin/soft tissue and pulmonary infections (CA-MRSA). 5 Toxic Shock Syndrome Toxin-1 (TSST-1) — a superantigen causing toxic shoc syndrome. 6. Exfoliative toxins — cause staphylococcal scalded skin syndrome. 7 Enterotoxins — heat-stable, cause staphylococcal food poisoning (preformed toxin ingestion). 8. Capsule/biofilm — enhances immune evasion, especially on prostheti devices. Laboratory diagnosis: Gram stain (Gram-positive cocci in clusters), culture on blood agar (golden/beta-haemolytic colonies) and mannitol salt agar (mannitol fermentation yellow colour change), catalase test (positive), coagulase test (positive, distinguishing from coagulase-negative staphylococci), and cefoxitin disc/PCR for methicillin resistance (MRSA). Clinical presentation/diseases associated: skin and soft tissue infections (boils abscesses, cellulitis, impetigo), bacteraemia/endocarditis, osteomyelitis and septi arthritis, pneumonia (including post-influenza and ventilator-associated), toxic shoc syndrome, staphylococcal scalded skin syndrome, and food poisoning (rapid-onse vomiting from preformed enterotoxin). Treatment: Beta-lactamase-resistant penicillins (e.g., flucloxacillin, cloxacillin) fo methicillin-sensitive strains; vancomycin, linezolid, or daptomycin for MRSA; drainag of abscesses is essential adjunct therapy. Prevention and control: hand hygiene, contact precautions for MRSA colonised/infected patients, decolonisation protocols (nasal mupirocin, chlorhexidin body wash) for high-risk carriers, and wound care. Complications: metastatic abscess formation, endocarditis, septic emboli, and sepsis
Bacterial Meningitis Aetiology: Common causative organisms vary by age group: - Neonates: Group B
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Bacterial Meningitis Aetiology: Common causative organisms vary by age group: - Neonates: Group B Streptococcus, E. coli, Listeria monocytogenes. - Infants/children: Streptococcu pneumoniae, Neisseria meningitidis, Haemophilus influenzae type b. - Adults Streptococcus pneumoniae, Neisseria meningitidis. - Elderly/immunocompromised Streptococcus pneumoniae, Listeria monocytogenes. Pathogenesis: Organisms typically colonise the nasopharynx, invade the bloodstream (bacteraemia), cross the blood-brain barrier (facilitated by capsular virulence factor and specific adhesins), and multiply in the subarachnoid space where host immun defences are relatively deficient, triggering an intense inflammatory respons (cytokine release, neutrophil influx) that causes cerebral oedema, raised intracrania pressure, and vasculitis, leading to neuronal injury. Clinical presentation: fever, severe headache, neck stiffness (meningismus) photophobia, altered consciousness, and in children — irritability, poor feeding bulging fontanelle. Kernig’s and Brudzinski’s signs may be positive. Petechial/purpuri rash suggests meningococcaemia. Laboratory diagnosis: Lumbar puncture for cerebrospinal fluid (CSF) analysis — typically shows raised opening pressure, elevated white cell count (neutrophi predominant), elevated protein, and reduced glucose (low CSF:blood glucose ratio) in bacterial meningitis; Gram stain and culture of CSF for organism identification; blood cultures; PCR/latex agglutination for rapid antigen detection. Treatment: Empirical broad-spectrum antibiotics started immediately without waiting for results (e.g., ceftriaxone ± vancomycin, with ampicillin added if Listeria i suspected in neonates/elderly), adjusted once culture and sensitivity results ar available; adjunctive dexamethasone (reduces neurological complications, particularl in pneumococcal meningitis) given with or just before the first antibiotic dose. Prognosis: variable; mortality and neurological sequelae (hearing loss, cognitiv impairment, seizures) are significant, particularly with pneumococcal meningitis and delayed treatment. Complications: hearing loss, seizures, hydrocephalus, cerebral abscess, subdura effusion, and death. Three causative agents and age groups primarily affected: 1. Streptococcu pneumoniae — affects all age groups but especially young children and the elderly. 2 Neisseria meningitidis — affects infants, adolescents, and young adults (outbreak common in close-contact settings such as dormitories/military barracks — the African “meningitis belt” is notable). 3. Group B Streptococcus — affects neonates (within th first month of life).
(Duplicate of Question 17’s causative agents/age groups — see
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(Duplicate of Question 17’s causative agents/age groups — see above.) 19/34. Diphtheria (i) Aetiological agent: Corynebacterium diphtheriae, a Gram-positive, club-shaped (pleomorphic) bacillus, arranged in “Chinese letter” or “V/L” patterns; toxin production requires the bacterium to be lysogenised by a bacteriophage carrying the tox gene. (ii) Pathogenesis: The organism colonises the pharyngeal/tonsillar mucosa (non invasive) and produces diphtheria exotoxin (an AB toxin), which inhibits host protein synthesis by ADP-ribosylating elongation factor-2 (EF-2), causing local tissue necrosis The resulting necrotic epithelium, fibrin, inflammatory cells, and bacteria form characteristic tough, greyish pseudomembrane that can obstruct the airway Absorbed toxin can also cause distant systemic effects, notably on the myocardium and peripheral nerves. (iii) Clinical presentations: sore throat, low-grade fever, and a grey-whit pseudomembrane over the tonsils/pharynx that bleeds when scraped; may extend t cause airway obstruction (“bull neck” from cervical lymphadenopathy and oedema) systemic toxin effects include myocarditis (arrhythmias, heart failure) and cranial/peripheral neuropathies (palatal palsy, later generalised paralysis) occurring days to weeks after onset. (iv) Diagnosis: clinical recognition of the pseudomembrane; throat swab culture on selective media (Löffler’s serum slope or tellurite agar), Albert’s/methylene blue stain showing metachromatic granules; toxigenicity testing (Elek test) to confirm toxin production. (v) Treatment: prompt administration of diphtheria antitoxin (neutralise circulating, unbound toxin — must be given early, based on clinical suspicion, withou waiting for laboratory confirmation) plus antibiotics (penicillin or erythromycin) t eradicate the organism and halt further toxin production; airway management i critical in obstructive cases. (vi) Prevention and control: routine immunisation with diphtheria toxoid (part of th Pentavalent/DPT vaccine series), isolation of cases, contact tracing with prophylacti antibiotics and vaccination of contacts.
Essay on Streptococcus pyogenes infection Morphology: Gram-positive cocci in chains; catalase-negative (distinguishing from
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Essay on Streptococcus pyogenes infection Morphology: Gram-positive cocci in chains; catalase-negative (distinguishing from Staphylococci); Group A beta-haemolytic Streptococcus (Lancefield group A). Mode of transmission: respiratory droplets (pharyngitis), direct contact with skin lesions (impetigo, cellulitis). Virulence factors: 1. M protein — major virulence factor; anti-phagocytic and mediates adherence; basis of serotyping and target of protective (but type-specific immunity. 2. Streptolysin O and S — haemolysins causing beta-haemolysis Streptolysin O is antigenic (basis of the ASO titre test). 3. Pyrogenic (erythrogenic exotoxins — superantigens responsible for the rash of scarlet fever and streptococca toxic shock syndrome. 4. Streptokinase — activates plasminogen, aiding tissu spread. 5. Hyaluronidase — “spreading factor,” breaks down connective tissue. 6 DNase (streptodornase) — degrades DNA in pus, aiding spread. 7. Capsule (hyaluronic acid) — anti-phagocytic. Laboratory features: beta-haemolysis on blood agar, bacitracin-sensitiv (distinguishing from other beta-haemolytic streptococci), Gram-positive cocci in chains, positive rapid antigen detection test or throat culture; elevated Anti Streptolysin O (ASO) titre indicates recent infection (used in diagnosing post streptococcal sequelae). Diseases associated: - Suppurative: pharyngitis/tonsillitis, scarlet fever, impetigo cellulitis, erysipelas, necrotising fasciitis, streptococcal toxic shock syndrome puerperal sepsis. - Non-suppurative (immune-mediated, delayed): acute rheumati fever, acute post-streptococcal glomerulonephritis. Treatment: Penicillin remains first-line (no significant resistance reported) erythromycin/clindamycin for penicillin-allergic patients; clindamycin is added fo severe invasive disease (necrotising fasciitis, toxic shock) due to its ability to suppres toxin production. Complications: rheumatic fever (and resultant rheumatic heart disease), acut glomerulonephritis, necrotising fasciitis, and streptococcal toxic shock syndrome. 21/36. Non-suppurative complications of Streptococcus pyogenes These are immune-mediated sequelae occurring 1–3 weeks after a streptococca infection, not due to direct bacterial invasion but to cross-reactive immune responses.
Acute Rheumatic Fever: follows streptococcal pharyngitis (not skin infection)
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Acute Rheumatic Fever: follows streptococcal pharyngitis (not skin infection) thought to result from molecular mimicry, where antibodies against M protein cross-react with cardiac, joint, and neural tissue antigens. Presents with the Jone criteria features — migratory polyarthritis, carditis (potentially leading to rheumati heart disease/valvular damage, especially mitral valve), subcutaneous nodules erythema marginatum, and Sydenham’s chorea. Prevention/treatment involve prompt antibiotic treatment of streptococcal pharyngitis and secondary prophylaxi (long-term penicillin) to prevent recurrent attacks in those with established rheumatic fever.
Germ tube test — presumptive identification of Candida albicans (positive germ
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Germ tube test — presumptive identification of Candida albicans (positive germ tube formation in serum within 2–3 hours distinguishes C. albicans from most non- albicans species).
Enterohaemorrhagic E. coli (EHEC) Aetiology: A pathotype of E. coli, most notably serotype O157:H7, which produce
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Enterohaemorrhagic E. coli (EHEC) Aetiology: A pathotype of E. coli, most notably serotype O157:H7, which produce Shiga-like (Verotoxin) toxins. Mode of transmission: ingestion of contaminated/undercooked beef, unpasteurised milk/juice, contaminated vegetables, or via person-to-person faecal-oral spread; low infectious dose facilitates outbreaks. Clinical presentation: initial watery diarrhoea progressing to bloody diarrhoe (haemorrhagic colitis) with severe abdominal cramps, typically without high fever; subset (especially children) progress to haemolytic uraemic syndrome (HUS) — th triad of microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidne injury — occurring roughly 5–10 days after diarrhoea onset. Diagnosis: stool culture on sorbitol-MacConkey agar (O157:H7 is sorbitol non fermenting, unlike most other E. coli), Shiga toxin detection by immunoassay or PCR. Complications: haemolytic uraemic syndrome, acute kidney injury, thromboti thrombocytopenic purpura-like presentation, and (rarely) death. Treatment: primarily supportive (fluid/electrolyte management); antibiotics are generally avoided, as they may increase toxin release from lysing bacteria and precipitate or worsen HUS; management of HUS may require dialysis and careful fluid management.
Streptococcus pneumoniae (laboratory diagnosis) Morphology: Gram-positive diplococci (“lancet-shaped”), encapsulated, alpha
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Streptococcus pneumoniae (laboratory diagnosis) Morphology: Gram-positive diplococci (“lancet-shaped”), encapsulated, alpha haemolytic on blood agar. Laboratory diagnosis: 1. Gram stain: Gram-positive lancet-shaped diplococci in sputum/CSF. 2. Culture: alpha-haemolytic (green discolouration) colonies on blood agar. 3. Optochin sensitivity test: S. pneumoniae is optochin-sensitiv (distinguishing it from other alpha-haemolytic streptococci like Streptococcus viridans which are optochin-resistant). 4. Bile solubility test: S. pneumoniae colonies ar lysed by bile (bile-soluble), unlike viridans streptococci. 5. Quellung reaction capsular swelling test using type-specific antisera, used for serotyping. 6. Latex agglutination/urinary antigen test: rapid detection of pneumococcal antigen particularly useful in pneumonia and meningitis. 7. Blood/CSF culture in invasiv disease (bacteraemia, meningitis).
Serovars of Chlamydia trachomatis and diseases caused
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Serovars of Chlamydia trachomatis and diseases caused Serovar group Disease A, B, Ba, C Trachoma (chronic conjunctivitis leading to blindness) D–K Genital tract infections (urethritis, cervicitis, pelvic inflammatory disease), neonatal conjunctivitis (inclusion conjunctivitis) and neonatal pneumonia L1, L2, L3 Lymphogranuloma venereum (LGV) 27/28. Serovars of Chlamydia trachomatis — repeated (see Question 26). 27b. Developmental cycle of Chlamydiae Chlamydia trachomatis is an obligate intracellular bacterium with a unique biphasi developmental cycle: 1. Elementary body (EB) — the small, metabolically inactive infectious extracellular form; attaches to and is endocytosed by susceptible hos epithelial cells. 2. Within the host cell (in a membrane-bound vacuole/inclusion), th EB reorganises into a reticulate body (RB) — the larger, metabolically active, non infectious intracellular form. 3. The RB replicates by binary fission within th inclusion. 4. RBs then reorganise back into infectious EBs. 5. The host cell ruptures (o the inclusion is released by exocytosis), releasing new EBs to infect adjacent cells completing the cycle (typically over 48–72 hours).
Satellite phenomenon (See Viruses/Bacteria Question 23/32 above — the satellite phenomenon describe
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Satellite phenomenon (See Viruses/Bacteria Question 23/32 above — the satellite phenomenon describe enhanced growth of Haemophilus influenzae colonies near Staphylococcus aureus on blood agar, due to S. aureus providing Factor V (NAD) and lysing red cells to releas Factor X, both required by H. influenzae for growth.)
Essay on tuberculosis (aetiology, pathogenesis, clinical
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Essay on tuberculosis (aetiology, pathogenesis, clinical presentation, laboratory diagnosis, treatment) Aetiology: Mycobacterium tuberculosis — an acid-fast, slow-growing, obligate aerobi bacillus with a lipid-rich (mycolic acid) cell wall responsible for its acid-fastness and resistance to standard staining and many disinfectants. Pathogenesis: Transmitted via inhalation of airborne droplet nuclei. Bacilli ar engulfed by alveolar macrophages but resist intracellular killing (inhibiting phagolysosome fusion), multiplying within macrophages. This triggers a cell-mediated (Type IV hypersensitivity) immune response with formation of granulomas (tubercles — organised collections of macrophages, epithelioid cells, Langhans giant cells, and lymphocytes, often with central caseous necrosis — which wall off but do not alway eliminate the organism, allowing latent TB infection. Reactivation may occur later i immunity wanes (e.g., HIV co-infection, malnutrition, immunosuppression), causing post-primary (reactivation) TB, typically in the lung apices where oxygen tension i highest. Clinical presentation: chronic cough (>2 weeks), haemoptysis, low-grade feve (often with evening/night sweats), weight loss, and fatigue; extrapulmonary TB can affect lymph nodes (most common extrapulmonary site), pleura, bone/spine (Pott’ disease), meninges, and other organs. Laboratory diagnosis: 1. Sputum smear microscopy for acid-fast bacilli (Ziehl Neelsen stain). 2. GeneXpert MTB/RIF — rapid molecular test detecting M tuberculosis DNA and rifampicin resistance simultaneously. 3. Culture (gold standard — on Löwenstein-Jensen medium (solid, slow, 6–8 weeks) or liquid culture (e.g., MGIT faster). 4. Chest X-ray — upper lobe infiltrates, cavitation, or miliary pattern. 5 Tuberculin skin test (Mantoux) or Interferon-Gamma Release Assays (IGRAs) — fo detecting latent infection (not active disease). 6. Histopathology of biopsy specimens in extrapulmonary disease, showing caseating granulomas. Treatment: Standard first-line regimen (DOTS strategy) — an intensive phase o Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol (RIPE) for 2 months, followed b a continuation phase of Rifampicin and Isoniazid for 4 months (total 6 months for drug susceptible TB); drug-resistant TB requires longer, individualised second-line regimen (see MDR-TB management under General Section Question 26). Prevention: BCG vaccination (protects mainly against severe childhood forms), earl case detection and treatment, contact tracing, isoniazid preventive therapy for high risk contacts/latent infection, and infection control measures (ventilation, N9 respirators, airborne isolation) in healthcare settings.
Candidiasis Aetiology: Candida albicans (most common), and other non-albicans species (C
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Candidiasis Aetiology: Candida albicans (most common), and other non-albicans species (C glabrata, C. tropicalis, C. krusei) — dimorphic yeasts that are part of normal human flora (skin, gut, genital tract) but become pathogenic under altered host conditions. Pathogenesis: Overgrowth typically results from disruption of normal flora (e.g broad-spectrum antibiotic use), altered local environment (moisture, pH changes), o impaired host immunity (diabetes, HIV/AIDS, corticosteroid use, neutropenia) allowing the yeast form to transition to the more invasive pseudohyphal/hyphal form which adheres to and invades epithelial surfaces. Clinical syndromes: - Oropharyngeal candidiasis (oral thrush) — white plaques on an erythematous base. - Oesophageal candidiasis — odynophagia, dysphagia (common AIDS-defining illness). - Vulvovaginal candidiasis — thick, curd-like (“cottage cheese” discharge with pruritus. - Cutaneous candidiasis — intertrigo in moist skin folds. Invasive/disseminated candidiasis — candidaemia, endocarditis, in severel immunocompromised or critically ill patients (e.g., with central venous catheters). Treatment options: topical antifungals (nystatin, clotrimazole) for mucocutaneou disease; oral fluconazole for oropharyngeal/oesophageal/vaginal candidiasis echinocandins (e.g., caspofungin) or Amphotericin B for invasive/systemic candidiasis particularly with azole-resistant species.
Laboratory diagnosis of vaginal candidiasis
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Laboratory diagnosis of vaginal candidiasis
Clinical specimen: high vaginal swab.
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Clinical specimen: high vaginal swab.
Wet mount microscopy (with 10% KOH) — demonstrates budding yeast cells and
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Wet mount microscopy (with 10% KOH) — demonstrates budding yeast cells and pseudohyphae.
Gram stain — Gram-positive budding yeast cells and pseudohyphae.
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Gram stain — Gram-positive budding yeast cells and pseudohyphae.
Culture on Sabouraud Dextrose Agar — creamy white colonies.
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Culture on Sabouraud Dextrose Agar — creamy white colonies.
Vaginal pH testing — typically normal (<4.5) in candidiasis, which helps
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Vaginal pH testing — typically normal (<4.5) in candidiasis, which helps differentiate it from bacterial vaginosis and trichomoniasis (both usually pH >4.5).
Life cycle of Strongyloides stercoralis Strongyloides stercoralis has a unique life cycle combining both free-living and
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Life cycle of Strongyloides stercoralis Strongyloides stercoralis has a unique life cycle combining both free-living and parasitic cycles, and the capacity for autoinfection.
Infective filariform larvae in contaminated soil penetrate intact human skin
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Infective filariform larvae in contaminated soil penetrate intact human skin (commonly the feet).
Larvae migrate via the bloodstream to the lungs, penetrate alveoli, ascend the
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Larvae migrate via the bloodstream to the lungs, penetrate alveoli, ascend the tracheobronchial tree, and are swallowed.
In the small intestine, larvae mature into adult parthenogenetic females that
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In the small intestine, larvae mature into adult parthenogenetic females that burrow into the mucosa and lay eggs (no free-living adult male is needed in the parasitic human cycle).
Eggs hatch into rhabditiform larvae within the intestinal mucosa, which are
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Eggs hatch into rhabditiform larvae within the intestinal mucosa, which are passed in the stool.
In the environment, rhabditiform larvae either:
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In the environment, rhabditiform larvae either: Moult twice to become infective filariform larvae (direct/homogonic cycle), or Develop into free-living adult males and females that reproduce sexually, producing further generations of larvae (indirect/heterogonic, free-living cycle) before eventually producing infective filariform larvae.
Autoinfection: some rhabditiform larvae can moult to the infective filariform stage
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Autoinfection: some rhabditiform larvae can moult to the infective filariform stage within the intestine or on the perianal skin itself, re-penetrating the intestinal mucosa or perianal skin without leaving the host — allowing the infection to persist for decades and, in immunosuppressed patients, to cause a life-threatening hyperinfection syndrome with widespread larval dissemination.
Enteric fever — WHO and CDC classification of Salmonella
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Enteric fever — WHO and CDC classification of Salmonella Enteric fever (typhoid and paratyphoid fever) is caused by Salmonella enteric serovar Typhi and Salmonella enterica serovar Paratyphi (A, B, C) — Gram-negativ bacilli transmitted via the faecal-oral route (contaminated food/water), which invad the intestinal mucosa, disseminate via the lymphatics and bloodstream (bacteraemia) and localise in the reticuloendothelial system (liver, spleen, bone marrow, Peyer’ patches of the ileum), producing a systemic febrile illness with stepwise fever, relativ bradycardia, abdominal pain, constipation or diarrhoea, hepatosplenomegaly, and “rose spots”; complications include intestinal perforation and haemorrhage. Classification of Salmonella (WHO/CDC — Kauffmann-White scheme, based on somatic O, flagellar H, and (for S. Typhi) Vi capsular antigens): - Genus Salmonell contains two species: Salmonella enterica (with six subspecies) and Salmonella bongori. - Salmonella enterica subspecies enterica contains the vast majority o medically important serovars, further divided into over 2,500 serovars (serotypes based on antigenic structure, broadly grouped functionally into: 1. Typhoida serovars — S. Typhi, S. Paratyphi A, B, C — adapted to humans, cause systemi enteric fever. 2. Non-typhoidal serovars — e.g., S. Typhimurium, S. Enteritidis — broad host range (zoonotic), typically cause self-limiting gastroenteritis but can caus invasive disease in immunocompromised hosts (notably in HIV-infected individuals and young children in sub-Saharan Africa).
Non-gonococcal urethritis (a) Aetiology: Urethritis not caused by Neisseria gonorrhoeae; the most common
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Non-gonococcal urethritis (a) Aetiology: Urethritis not caused by Neisseria gonorrhoeae; the most common cause is Chlamydia trachomatis (serovars D–K); other causes include Mycoplasm genitalium, Ureaplasma urealyticum, Trichomonas vaginalis, and Herpes simple virus. (b) Pathogenesis: These organisms adhere to and infect the columnar/transitiona epithelium of the urethra, triggering a local inflammatory response with mucopurulen or clear discharge; Chlamydia, being obligate intracellular, causes a more indolent often less purulent inflammatory response than gonococcal infection, and infection i frequently asymptomatic, particularly in women, allowing silent progression to pelvi inflammatory disease. (c) Clinical diseases: urethral discharge (typically thinner/less purulent than gonococcal discharge), dysuria, urethral itching/discomfort; can be asymptomatic complications include epididymitis in men, and pelvic inflammatory disease, ectopi pregnancy, and infertility in women due to ascending infection; reactive arthritis (a part of a triad with conjunctivitis and urethritis) can occur. (d) Treatment: Azithromycin (single dose) or Doxycycline (7-day course) as first-lin for chlamydial urethritis; partner treatment and screening/treatment for other STIs i essential; syndromic management often includes coverage for gonorrhoea as wel given frequent co-infection.
General characteristics of Trematodes (Flukes), classes, and
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General characteristics of Trematodes (Flukes), classes, and examples General characteristics: - Flatworms (Platyhelminthes), typically flat, leaf-shaped bodies (except schistosomes, which are cylindrical). - Possess oral and ventral sucker for attachment. - Most are hermaphroditic (except Schistosomes, which have separat sexes). - Have complex life cycles requiring one or more intermediate hosts, almos always including a freshwater snail as the first intermediate host. - Lack a body cavit (acoelomate) and a complete digestive system (blind-ending gut, no anus). Classes/groups and examples (by organ system affected): 1. Blood fluke (Schistosomes) — Schistosoma haematobium (urinary schistosomiasis), Schistosom mansoni (intestinal schistosomiasis), Schistosoma japonicum. 2. Liver flukes — Fasciola hepatica, Clonorchis sinensis. 3. Lung flukes — Paragonimus westermani. 4 Intestinal flukes — Fasciolopsis buski. 2–3. Classification and general life cycle of Trematodes; drug treatment General life cycle pattern (using the schistosome/blood fluke pattern as an illustrative example, with variations noted for other flukes): 1. Adult flukes (in th definitive host, usually humans) produce eggs, which are passed in urine, faeces, o sputum depending on species. 2. Eggs reach fresh water and hatch to release free swimming miracidia. 3. Miracidia penetrate a specific freshwater snail (firs intermediate host) and develop through sporocyst stages, multiplying asexually. 4 Free-swimming cercariae are released from the snail into water. 5. For blood fluke (Schistosomes): cercariae directly penetrate intact human skin on contact with infested water, shed their tails, become schistosomulae, migrate via th bloodstream/lymphatics to the lungs then liver, mature into adult worms, and migrat to their final site (venous plexus of bladder for S. haematobium, mesenteric veins for S mansoni) where paired adults produce eggs. 6. For other flukes (liver, lung intestinal): cercariae encyst as metacercariae on aquatic vegetation or in a second intermediate host (e.g., fish, crustaceans), and humans become infected by ingesting the metacercariae (raw/undercooked fish, crustaceans, or contaminated aquati vegetation); metacercariae excyst in the gut and migrate to their target organ (liver lung, or remain in the intestine) to mature into adults. Drug treatment: - Praziquantel is the drug of choice for most trematode infections including all schistosome species, Clonorchis sinensis, Paragonimus westermani, and Fasciolopsis buski. - Triclabendazole is preferred specifically for Fasciola hepatic (liver fluke), as praziquantel is less effective against this species. 4/29. Medical significance of Arthropods Direct effects: 1. Bites/stings causing local tissue damage, pain, and allergic/anaphylactic reactions (e.g., bee stings, spider bites). 2. Entomophobi (psychological distress). 3. Myiasis — infestation of tissue by fly larvae. 4. Dermatiti from contact with arthropod secretions/allergens. Indirect effects (as vectors of disease): 1. Mechanical transmission — passiv carriage of pathogens on body parts (e.g., houseflies transmitting enteric pathogens)
Biological transmission — the pathogen undergoes development or multiplication
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Biological transmission — the pathogen undergoes development or multiplication within the arthropod before transmission (e.g., malaria in the mosquito). Examples of pathogens transmitted by arthropods, with respective vector: Pathogen type Example Arthropod vector Viral Dengue virus Aedes aegypti mosquito Viral Yellow fever virus Aedes aegypti mosquito Viral Chikungunya virus Aedes mosquito Parasitic Plasmodium falciparum Anopheles mosquito (malaria) Parasitic Wuchereria bancrofti Culex mosquito (filariasis) Parasitic Trypanosoma brucei (African Tsetse fly (Glossina species) trypanosomiasis) Bacterial Yersinia pestis (plague) Rat flea (Xenopsylla cheopis) Bacterial Borrelia recurrentis (relapsing Body louse fever) Bacterial Rickettsia species (typhus) Body louse / ticks
Direct and indirect effects of Arthropods of medical importance
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Direct and indirect effects of Arthropods of medical importance Direct effects: 1. Bites/stings causing local irritation, pain, or systemic allergi reactions (including anaphylaxis). 2. Injection of toxins/venom (e.g., scorpion sting spider bite). 3. Invasion of tissues (myiasis by fly larvae; tungiasis by sand fleas). 4 Blood loss from heavy infestation (e.g., severe lice or tick infestation). 5. Allergi dermatitis/hypersensitivity reactions to arthropod parts or excreta (e.g., dust mit allergy). Indirect effects: 1. Mechanical vectors — passive transport of pathogens on bod surfaces or in the gut without multiplication (e.g., houseflies and cockroache spreading enteric bacteria/protozoan cysts). 2. Biological vectors — pathogen undergoes essential development and/or multiplication within the arthropod befor being transmitted to a new host (e.g., malaria parasite development in Anophele mosquito, filarial larvae development in mosquitoes).
HPV — Risk factors, clinical manifestations, and prevention
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HPV — Risk factors, clinical manifestations, and prevention (See Viruses Section, Question 26, for full detail.) 7/25/26. Onchocerciasis (River Blindness) Aetiology: Onchocerca volvulus, a filarial nematode, transmitted by the bite o infected blackflies (Simulium species), which breed in fast-flowing rivers (hence “rive blindness”). Epidemiology: Endemic in riverine communities in sub-Saharan Africa (including Nigeria), with smaller foci in Yemen and Latin America; a major cause of preventabl blindness in endemic communities. Pathogenesis: Infective larvae are deposited on the skin during a blackfly bite migrate through subcutaneous tissue, and mature into adult worms that reside in fibrous subcutaneous nodules (onchocercomata). Adult female worms release larg numbers of microfilariae, which migrate through the skin, connective tissue, and eyes. Disease results primarily from the host’s intense inflammatory response t dying/dead microfilariae (both spontaneous death and post-treatment), which cause chronic inflammation and fibrosis. Clinical findings/manifestations: - Pruritic dermatitis (severe itching), skin depigmentation (“leopard skin”), and thickened, wrinkled skin (“lizard skin”). Subcutaneous nodules (onchocercomata), typically over bony prominences. - Ocula involvement — punctate/sclerosing keratitis, iridocyclitis, chorioretinitis — leading t progressive visual impairment and blindness (“river blindness”). - Lymphadenopath (“hanging groin” in advanced disease). Laboratory diagnosis: skin snip microscopy demonstrating emerging microfilaria (gold standard); slit-lamp examination of the cornea/anterior chamber fo microfilariae; nodulectomy with histological examination of adult worms; serology/PCR in reference settings; the Mazzotti reaction (skin itching after a test dose o diethylcarbamazine) is historically used but rarely performed now due to risk of sever reactions. Treatment: Ivermectin — the drug of choice, kills microfilariae (not adult worms) given as periodic single doses (typically annually) since it does not achieve full cure doxycycline (targets the Wolbachia endosymbiotic bacteria required by the worm fo fertility/survival, providing a macrofilaricidal effect) may be used as an adjunct in som regimens. Prevention/control: Mass drug administration (community-directed treatment with ivermectin, CDTI) in endemic areas; vector control (larviciding of blackfly breeding sites in fast-flowing rivers); health education.
Dengue Fever Aetiology: Dengue virus (DENV, serotypes 1–4), a single-stranded RNA virus of th
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Dengue Fever Aetiology: Dengue virus (DENV, serotypes 1–4), a single-stranded RNA virus of th family Flaviviridae, transmitted by Aedes aegypti (and Aedes albopictus) mosquitoes. Clinical manifestations: - Classic dengue fever: sudden high fever, sever headache (retro-orbital pain), myalgia and arthralgia (“breakbone fever”) maculopapular rash, and mild bleeding manifestations (petechiae, gum bleeding). Severe dengue (dengue haemorrhagic fever/dengue shock syndrome): occur typically with secondary infection by a different serotype (antibody-dependen enhancement); characterised by plasma leakage (haemoconcentration, pleura effusion, ascites), significant thrombocytopenia, and haemorrhagic manifestations potentially progressing to hypovolaemic shock. Investigations/laboratory diagnosis: full blood count (leucopenia thrombocytopenia, rising haematocrit indicating haemoconcentration); NS1 antigen test (positive in the first few days of illness); IgM/IgG serology (IgM appears after da 5, IgG indicates past exposure or, if rising in paired samples, recent infection); RT-PCR for viral RNA (early acute phase, also identifies serotype). Treatment: No specific antiviral therapy; management is supportive — careful fluid management (avoiding both under- and over-hydration, guided by haematocrit and clinical status), antipyretics (paracetamol; NSAIDs and aspirin should be avoided due to bleeding risk), and close monitoring for warning signs of severe dengu (abdominal pain, persistent vomiting, mucosal bleeding, lethargy, rapid drop in platele count with rising haematocrit). Prevention: vector control (elimination of mosquito breeding sites/stagnant water insecticide use, larviciding), personal protection (repellents, protective clothing, bed nets), and a licensed dengue vaccine (recommended only for those with prio confirmed dengue infection due to risk of enhanced disease in dengue-naïve vaccinees per WHO guidance). 9/10/14/15/16/30c. Severe Malaria Definition: Severe malaria is defined as Plasmodium infection (typically P. falciparum with one or more life-threatening complications, in the presence of asexua parasitaemia and no other identifiable cause for the symptoms. Five species of Plasmodium causing malaria in humans: 1. Plasmodium falciparum — most severe/lethal form. 2. Plasmodium vivax 3. Plasmodium ovale 4 Plasmodium malariae 5. Plasmodium knowlesi (zoonotic, primarily in Southeast Asia) WHO clinical criteria for severe malaria (major criteria — any one, in the presence of P. falciparum parasitaemia, defines severe malaria): 1. Impaired consciousness/coma (cerebral malaria). 2. Prostration (generalised weakness, inabilit to sit/stand/walk unassisted). 3. Multiple convulsions (more than two episodes in 24 hours). 4. Acidosis (base deficit or elevated plasma lactate). 5. Hypoglycaemia (<2. mmol/L). 6. Severe malarial anaemia (haemoglobin ≤5 g/dL or haematocrit ≤15% in high-transmission areas, or ≤7 g/dL in low-transmission areas, with parasitaemia). 7 Renal impairment/acute kidney injury (creatinine >265 μmol/L or urea >20 mmol/L)
Jaundice (bilirubin >50 μmol/L) with parasitaemia. 9. Pulmonary oedema/Acut
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Jaundice (bilirubin >50 μmol/L) with parasitaemia. 9. Pulmonary oedema/Acut Respiratory Distress Syndrome. 10. Significant bleeding/disseminated intravascula coagulation. 11. Shock (compensated or decompensated). 12. Hyperparasitaemi (>10% parasitised red cells, or per local threshold). Aetiology and pathogenesis: Severe malaria results predominantly from P falciparum due to its ability to cause high parasite burdens and cytoadherence — infected red blood cells express P. falciparum erythrocyte membrane protein (PfEMP1) on their surface, causing them to adhere to vascular endothelium (sequestration) in the brain, placenta, and other organs, obstructing microcirculation causing local hypoxia, and triggering an intense inflammatory cytokine response; thi underlies complications such as cerebral malaria, severe anaemia (from haemolysi and dyserythropoiesis), and multi-organ dysfunction. Laboratory diagnosis: 1. Thick blood film — for detecting and quantifying parasitaemia (most sensitive). 2. Thin blood film — for species identification and assessing parasite morphology/stage. 3. Rapid diagnostic test — detecting P falciparum histidine-rich protein-2 (HRP-2) or lactate dehydrogenase (pLDH) antigens
Supportive investigations: full blood count, blood glucose, renal function, live
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Supportive investigations: full blood count, blood glucose, renal function, live function, lactate, and blood gas analysis to assess for and grad severity/complications. Treatment: - Severe malaria: intravenous (or intramuscular where IV access i unavailable) Artesunate is the WHO-recommended first-line treatment, followed by complete course of oral artemisinin-based combination therapy (ACT) once the patien can tolerate oral medication; intravenous quinine is an alternative where artesunate i unavailable. - Supportive care: correction of hypoglycaemia, management of seizures careful fluid management, blood transfusion for severe anaemia, and rena replacement therapy for acute kidney injury where indicated. Prevention: use of insecticide-treated bed nets, indoor residual spraying, intermitten preventive treatment in pregnancy (IPTp) and infancy, prompt diagnosis and treatmen of uncomplicated cases to prevent progression, and the RTS,S/AS01 and R21/Matrix-M malaria vaccines now recommended by WHO for children in endemic areas. 11/17. Essay on Malaria (aetiology, lifecycle, clinical manifestations, pathogenesis, laboratory diagnosis, treatment, prevention) Aetiology: Plasmodium species (see the five species above), transmitted by the bite o an infected female Anopheles mosquito. Life cycle: 1. In the mosquito (sexual cycle/sporogony): an infected femal Anopheles mosquito takes a blood meal from an infected human, ingesting gametocytes; these develop into gametes, fertilise to form a zygote, which develop into a motile ookinete, penetrates the mosquito midgut wall, and forms an oocyst; th oocyst matures and ruptures to release sporozoites, which migrate to the mosquito’ salivary glands. 2. Transmission to human: an infected mosquito injects sporozoite into a human during a subsequent blood meal. 3. Pre-erythrocytic (liver) stage sporozoites travel via the bloodstream to the liver, invade hepatocytes, and multipl asexually (exoerythrocytic schizogony) to form thousands of merozoites per infected liver cell over 1–2 weeks (asymptomatic phase); P. vivax and P. ovale can form dorman liver-stage hypnozoites, responsible for relapses months to years later. 4 Erythrocytic stage: released merozoites invade red blood cells, undergo asexua replication (trophozoite → schizont → merozoites), and rupture the red cell to releas more merozoites, which invade further red cells — this cyclical process is responsibl for the clinical symptoms and the classical periodic fever pattern. 5. Some merozoite differentiate into sexual forms (gametocytes), which are ingested by another feeding mosquito, continuing the cycle. Pathogenesis: Red cell rupture causes haemolysis, release of parasite antigens/toxin (e.g., glycosylphosphatidylinositol) triggering cytokine release (fever, malaise), and (in P. falciparum) cytoadherence/sequestration of infected red cells in th microvasculature (see severe malaria pathogenesis above), causing organ-specifi complications. Clinical manifestations: classic paroxysm — cold stage (rigors), hot stage (high fever), and sweating stage (defervescence) — occurring cyclically corresponding t synchronised red cell rupture (every 48 hours for P. vivax/P. ovale — “tertian,” every 7 hours for P. malariae — “quartan,” though P. falciparum often has les regular/continuous fever); accompanied by headache, myalgia, malaise nausea/vomiting, and splenomegaly; progression to severe malaria as detailed above in high-risk/non-immune individuals, particularly young children and pregnant women in endemic areas. Laboratory diagnosis: thick and thin blood films (Giemsa stain) — the gold standard for detection, species identification, and parasitaemia quantification; rapid diagnosti tests (antigen-based); PCR for low-level parasitaemia/species confirmation in research or complex settings. Treatment: - Uncomplicated malaria: Artemisinin-based Combination Therap (ACT), e.g., artemether-lumefantrine, or artesunate-amodiaquine. - Severe malaria intravenous artesunate (see above). - P. vivax/P. ovale: addition of primaquine (afte G6PD testing, due to haemolysis risk) to eradicate liver hypnozoites and preven relapse. Prevention: vector control (insecticide-treated nets, indoor residual spraying, larva source management), chemoprophylaxis for travellers and intermittent preventiv therapy for pregnant women and infants in endemic areas, prompt diagnosis and treatment, and malaria vaccination (RTS,S/AS01, R21/Matrix-M).
Life cycle of Dracunculus medinensis (Guinea worm)
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Life cycle of Dracunculus medinensis (Guinea worm)
Humans become infected by drinking water contaminated with copepods (water
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Humans become infected by drinking water contaminated with copepods (water fleas) harbouring infective third-stage larvae.
In the human stomach/duodenum, gastric acid digests the copepod, releasing
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In the human stomach/duodenum, gastric acid digests the copepod, releasing larvae, which penetrate the intestinal wall and migrate to the retroperitoneal space where they mature and mate.
After mating, the male dies; the fertilised female migrates through subcutaneous
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After mating, the male dies; the fertilised female migrates through subcutaneous tissue (over approximately 10–14 months) toward the skin surface, typically of the lower limb.
The gravid female induces a painful blister/ulcer at the skin surface; on contact with
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The gravid female induces a painful blister/ulcer at the skin surface; on contact with water, the worm protrudes and releases thousands of first-stage larvae into the water.
Larvae are ingested by freshwater copepods, within which they develop (through
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Larvae are ingested by freshwater copepods, within which they develop (through two moults) into infective third-stage larvae over about 2 weeks, completing the cycle when the copepod-contaminated water is again ingested by a human (or, in some settings, an animal reservoir such as dogs).
Life cycle of Nematodes and drug treatment General life cycle pattern of nematodes (illustrated with soil-transmitted
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Life cycle of Nematodes and drug treatment General life cycle pattern of nematodes (illustrated with soil-transmitted helminths, e.g., Ascaris lumbricoides): 1. Adult worms reside in the human intestine females lay eggs which are passed in the faeces. 2. Eggs embryonate in soil unde suitable conditions of warmth and moisture, becoming infective (containing an infective larva). 3. Humans are infected by ingesting embryonated eggs (faecal-ora route, contaminated food/water/soil) — as in Ascaris and Trichuris — or, fo hookworms and Strongyloides, by skin penetration of infective larvae from soil. 4 Ingested/penetrating larvae undergo tissue migration (e.g., through the lungs, in Ascaris and hookworm — the “pulmonary migration” phase) before returning to th intestine to mature into adults, completing the cycle. (Filarial nematodes, by contrast require an arthropod intermediate host/vector — see the Wuchereria bancrofti and Onchocerca volvulus life cycles.) Drug treatment: - Albendazole and Mebendazole — broad-spectrum, effectiv against most soil-transmitted helminths (Ascaris, hookworm, Trichuris, Enterobius). Ivermectin — drug of choice for Strongyloides stercoralis and Onchocerca volvulus. Diethylcarbamazine (DEC) — used for lymphatic filariasis (Wuchereria bancrofti). Pyrantel pamoate — alternative for Ascaris, hookworm, and Enterobius.
Histopathology: Periodic Acid-Schiff (PAS) stain on nail clippings, useful when
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Histopathology: Periodic Acid-Schiff (PAS) stain on nail clippings, useful when culture is negative but clinical suspicion remains high.
Wood’s lamp examination: of limited use for nail infections but may show
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Wood’s lamp examination: of limited use for nail infections but may show fluorescence in some dermatophyte scalp infections.
Cestodes (Tapeworms) — classification and life cycle of one
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Cestodes (Tapeworms) — classification and life cycle of one example Classification of medically important Cestodes: 1. Taenia saginata — bee tapeworm. 2. Taenia solium — pork tapeworm (medically important also for causing cysticercosis). 3. Diphyllobothrium latum — fish tapeworm. 4. Hymenolepis nana — dwarf tapeworm (notable for direct human-to-human transmission without an intermediate host). 5. Echinococcus granulosus — causes hydatid disease (cysti echinococcosis). Life cycle of Taenia solium (as an example): 1. Humans (definitive host) harbou the adult tapeworm in the small intestine; gravid proglottids (segments) containing eggs are passed in the faeces. 2. Pigs (intermediate host) ingest eggs from faecall contaminated soil/food; eggs hatch into oncospheres, which penetrate the intestina wall, disseminate via the bloodstream, and develop into cysticerci (larval cysts) in th pig’s muscle tissue. 3. Humans acquire the adult tapeworm infection (taeniasis) b eating raw or undercooked pork containing cysticerci; the larva evaginates in the smal intestine, attaches via its scolex, and matures into an adult tapeworm over about months. 4. Human cysticercosis occurs when humans instead ingest T. solium egg directly (via faecal-oral contamination, or autoinfection from a person with intestina taeniasis) — oncospheres are released, penetrate the gut wall, and disseminate to form cysticerci in human tissues, notably muscle, subcutaneous tissue, and the centra nervous system (neurocysticercosis, a major cause of acquired epilepsy in endemi areas).
Classification of Protozoa of medical importance (with diseases)
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Classification of Protozoa of medical importance (with diseases) Group Example Disease Sarcodina (Amoebae) Entamoeba histolytica Amoebiasis (amoebic dysentery, liver abscess) Mastigophora (Flagellates) Giardia lamblia Giardiasis Trichomonas vaginalis Trichomoniasis Trypanosoma brucei African trypanosomiasis (sleeping sickness) Leishmania species Leishmaniasis Sporozoa (Apicomplexa) Plasmodium species Malaria Toxoplasma gondii Toxoplasmosis Cryptosporidium parvum Cryptosporidiosis Ciliophora (Ciliates) Balantidium coli Balantidiasis
Protozoa — classification, species, diseases (2024 mock)
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Protozoa — classification, species, diseases (2024 mock) (See Question 19 above for classification.) Species and diseases (summary): - Entamoeba histolytica — amoebiasis. - Giardi lamblia — giardiasis. - Trichomonas vaginalis — trichomoniasis. - Plasmodium falciparum/vivax/ovale/malariae/knowlesi — malaria. - Toxoplasma gondii — toxoplasmosis. - Trypanosoma brucei gambiense/rhodesiense — African sleeping sickness. - Leishmania donovani — visceral leishmaniasis (kala-azar). Cryptosporidium parvum — cryptosporidiosis. - Balantidium coli — balantidiasis. 21/24. Protozoa causing diarrhoeal illness; Entamoeba histolytica Protozoa associated with diarrhoeal illness: 1. Entamoeba histolytica 2. Giardi lamblia 3. Cryptosporidium parvum 4. Cyclospora cayetanensis Entamoeba histolytica discussion: Morphology: Exists in two forms — the motile, invasive trophozoite (contain ingested red blood cells when pathogenic — “haematophagous trophozoite”) and th infective, environmentally resistant cyst (quadrinucleate when mature). Life cycle: Infection is acquired by ingestion of mature (quadrinucleate) cysts in faecally contaminated food or water. Cysts excyst in the small intestine, releasing trophozoites that divide and colonise the large intestine. Trophozoites may eithe encyst (passed in stool as cysts, completing the transmission cycle) or invade th colonic mucosa, causing amoebic colitis, and can disseminate haematogenousl (typically via the portal vein) to the liver, causing amoebic liver abscess. Clinical presentation: - Intestinal amoebiasis: ranges from asymptomatic cys passage, to mild diarrhoea, to amoebic dysentery (bloody, mucoid stools with lowe abdominal cramps, tenesmus, and often minimal fever). - Extraintestina amoebiasis: amoebic liver abscess (right upper quadrant pain, fever, hepatomegaly “anchovy paste” appearance of aspirated abscess contents); rarely, pleuropulmonar or brain abscess. Laboratory diagnosis: stool microscopy for cysts/trophozoites (haematophagou trophozoites confirm invasive disease); stool antigen detection (ELISA) — mor sensitive and specific than microscopy, and distinguishes E. histolytica from th morphologically identical non-pathogenic E. dispar; serology (useful for extraintestina disease); imaging (ultrasound/CT) for liver abscess; PCR where available. Treatment: Metronidazole (or tinidazole) for invasive disease (tissue amoebicide) followed by a luminal agent (e.g., paromomycin or diloxanide furoate) to eradicat residual intraluminal cysts and prevent relapse/transmission. Prevention: safe water supply, proper sanitation and sewage disposal, food hygiene and hand hygiene.
Opportunistic protozoa associated with immunosuppression
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Opportunistic protozoa associated with immunosuppression
Cryptosporidium parvum
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Cryptosporidium parvum
Toxoplasma gondii
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Toxoplasma gondii
Cystoisospora (Isospora) belli
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Cystoisospora (Isospora) belli
Cyclospora cayetanensis (Also acceptable: microsporidia species.)
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Cyclospora cayetanensis (Also acceptable: microsporidia species.) Clinical manifestation, diagnosis, and treatment of one — Cryptosporidium parvum: - Clinical manifestation: in immunocompetent individuals, causes self limiting watery diarrhoea; in immunocompromised patients (particularly advanced HIV/AIDS), causes severe, chronic, profuse watery diarrhoea with significan fluid/electrolyte loss and wasting; can involve the biliary tract (cholangitis) in sever cases. - Diagnosis: modified Ziehl-Neelsen (acid-fast) stain of stool showing acid-fas oocysts; stool antigen ELISA; PCR. - Treatment: Nitazoxanide in immunocompeten patients; the most important intervention in HIV-infected patients is immun reconstitution via antiretroviral therapy, as specific antiparasitic treatment is often ineffective without immune recovery; supportive rehydration is essential.
Guinea Worm Infestation (Dracunculiasis) Epidemiology: Historically widespread in Africa and Asia; now nearing eradication
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Guinea Worm Infestation (Dracunculiasis) Epidemiology: Historically widespread in Africa and Asia; now nearing eradication with remaining transmission largely confined to a few countries (e.g., Chad, South Sudan, Mali, Ethiopia); Nigeria was certified free of Guinea worm transmission. Aetiology: Dracunculus medinensis, a large nematode (“fiery serpent”). Pathogenesis: (See Question 12 life cycle above.) Disease is caused by the emerging gravid female worm, which induces an intensely painful, burning blister (often on th lower limb) as it prepares to discharge larvae on contact with water; secondar bacterial infection of the ulcer/worm tract is a common complication. Lifecycle management/prevention: 1. Filtration of drinking water through a fine mesh cloth filter to remove copepods. 2. Provision of safe drinking water source (boreholes, treated water). 3. Health education on avoiding entry into water source when a worm is emerging (to prevent contaminating the water with larvae). 4. Vecto (copepod) control using larvicides (e.g., temephos) in water sources. 5. Cas containment and management — controlled extraction of the worm by slow winding around a stick, with wound care. 6. Surveillance and case reporting as part of globa eradication efforts. 24 (repeat). Enterobius vermicularis (Pinworm) Life cycle: Humans (only natural host) ingest infective eggs (via hand-to-mouth transfer, contaminated fomites, or inhalation of airborne eggs); eggs hatch in the smal intestine, larvae mature into adults in the caecum/colon; gravid female worms migrat at night to the perianal region to lay eggs, causing intense pruritus; eggs becom infective within hours, facilitating rapid autoinfection and person-to-person transmission (highly contagious, common in children/institutional settings). Clinical manifestation: perianal pruritus (particularly nocturnal), restles sleep/irritability in children; occasionally vulvovaginitis in girls from aberran migration; usually otherwise asymptomatic. Diagnosis: Cellophane (Scotch) tape test — adhesive tape applied to the periana skin in the early morning (before washing/defecation) and examined microscopicall for eggs; stool microscopy is often negative as eggs are deposited perianally, no typically in stool. Treatment: Albendazole or Mebendazole (single dose, repeated after 2 weeks to cove autoinfection); treatment of the whole household is often recommended given ease o transmission. Complications: perianal excoriation/secondary bacterial infection from scratching vulvovaginitis, and rarely appendicitis (from worm migration into the appendix).
Trichomonas vaginalis Morphology: A pear-shaped, flagellated protozoan (four anterior flagella plus
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Trichomonas vaginalis Morphology: A pear-shaped, flagellated protozoan (four anterior flagella plus recurrent flagellum forming an undulating membrane), exists only as a trophozoite (n cyst stage), motile with a characteristic jerky/twitching movement on wet mount. Life cycle: Direct person-to-person transmission (predominantly sexual), trophozoite colonise the vaginal/urethral mucosa, dividing by binary fission; there is no cyst stag or environmental intermediate stage — transmission requires direct mucosal contact. Clinical manifestation: In women — frothy, yellow-green, malodorous vagina discharge, vulvovaginal irritation/pruritus, dysuria, and characteristic “strawberr cervix” (punctate cervical haemorrhages) on speculum examination; many infection are asymptomatic. In men — usually asymptomatic, occasionally mild urethritis. Laboratory diagnosis: wet mount microscopy of vaginal/urethral discharge showing motile, flagellated trophozoites (rapid but only moderately sensitive); culture (mor sensitive, historically the gold standard); nucleic acid amplification tests (NAAT) — most sensitive and now preferred where available; vaginal pH typically elevated (>4.5). Treatment: Metronidazole or tinidazole (oral, single dose or short course) treatment of sexual partner(s) is essential to prevent reinfection, even if asymptomatic Prevention: safer sexual practices (condom use), partner notification and treatment and screening in high-risk populations.
Toxoplasma gondii Morphology/life cycle: An obligate intracellular protozoan parasite with a comple
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Toxoplasma gondii Morphology/life cycle: An obligate intracellular protozoan parasite with a comple life cycle. The definitive host is the cat family (Felidae), in which the sexual cycl occurs in the intestinal epithelium, producing oocysts shed in cat faeces. Humans and other warm-blooded animals serve as intermediate hosts, acquiring infection via: 1 Ingestion of oocysts from cat faeces-contaminated soil, water, or unwashed produce. 2 Ingestion of tissue cysts (bradyzoites) in raw or undercooked meat (particularly pork lamb). 3. Transplacental (vertical) transmission from an acutely infected mother to th fetus. 4. Rarely, blood transfusion or organ transplantation. Within the intermediate host, the parasite disseminates and forms tissue cyst (bradyzoites), particularly in muscle and brain, which can persist lifelong and reactivate under immunosuppression. Clinical significance: - Immunocompetent hosts: usually asymptomatic or mild, self limiting mononucleosis-like illness (lymphadenopathy, fever). - Congenita toxoplasmosis: transplacental infection, especially with primary maternal infection during pregnancy, can cause the classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications, along with other complications such as microcephaly and developmental delay; risk of transmission increases with gestational age, but severit is greater with earlier infection. - Reactivation in immunocompromised patient (e.g., advanced HIV/AIDS): causes toxoplasmic encephalitis — focal neurologica deficits, seizures, altered mental status — a leading cause of intracerebral mas lesions in AIDS patients. - Ocular toxoplasmosis — chorioretinitis, causing visua impairment. Diagnosis: serology (IgM/IgG antibodies; IgG avidity testing helps date the infection in pregnancy), PCR (particularly of amniotic fluid for congenital infection, o CSF/blood in immunocompromised patients), and imaging (CT/MRI showing ring enhancing lesions in cerebral toxoplasmosis). Treatment: Pyrimethamine plus sulfadiazine (with folinic acid to reduce bon marrow toxicity) is the standard regimen for active disease (congenital, ocular, o cerebral toxoplasmosis); spiramycin is used to reduce vertical transmission risk when maternal infection is diagnosed in pregnancy without confirmed fetal infection. Prevention: avoiding consumption of raw/undercooked meat, thorough washing o fruits/vegetables, avoiding contact with cat litter (or using gloves and handwashing especially during pregnancy, and good hand hygiene. 30a. Cysticercosis (See also Question 18 above.) Cysticercosis is the tissue infection caused by the larva (cysticercus) stage of Taenia solium, acquired by ingestion of T. solium eggs (via faecal oral contamination or autoinfection). Larvae disseminate to and encyst in muscle subcutaneous tissue, eyes, and critically the central nervous system, causing neurocysticercosis — the most common cause of acquired epilepsy in endemi regions, also presenting with headache, raised intracranial pressure, and foca neurological deficits depending on cyst location and stage (viable, degenerating, o calcified). Diagnosis relies on neuroimaging (CT/MRI showing cystic lesions, often with a visible scolex) and serology; treatment involves antiparasitic therapy (albendazole ± praziquantel) combined with corticosteroids (to control inflammation from dying cysts and antiepileptic drugs as needed, with surgery reserved for specific complication (e.g., obstructive hydrocephalus, ocular cysts). 30b. Urinary Schistosomiasis Caused by Schistosoma haematobium, transmitted via cercariae penetrating skin during contact with infested freshwater containing the intermediate host snail (Bulinu species). Adult worms reside in the venous plexus of the bladder, and eggs deposited in the bladder wall trigger a granulomatous inflammatory response, causing haematuri (classically terminal haematuria), dysuria, and urinary frequency; chronic infection leads to bladder wall fibrosis/calcification, hydronephrosis, and is a recognised ris factor for squamous cell carcinoma of the bladder. Diagnosis is by urine microscopy fo terminal-spined eggs (best detected in urine collected around midday) and/o cystoscopy with biopsy in chronic cases. Treatment is with praziquantel. 30c. Severe malaria (See Question 9/10/14/15/16 above for full detail.)
Subcutaneous mycosis Definition: Fungal infections involving the dermis, subcutaneous tissue, and
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Subcutaneous mycosis Definition: Fungal infections involving the dermis, subcutaneous tissue, and sometimes underlying bone, typically acquired by traumatic inoculation of funga elements from soil or plant material through the skin. Examples and features: 1. Mycetoma (see Bacteria Section, Question 7, fo actinomycetoma; eumycetoma is the fungal form, caused by organisms such a Madurella mycetomatis) — chronic swelling with sinus tracts discharging grains. 2 Sporotrichosis (Sporothrix schenckii) — classically causes nodular/ulcerative lesion along lymphatic channels (“lymphocutaneous” pattern) following inoculation via thorn prick (“rose gardener’s disease”). 3. Chromoblastomycosis — caused b dematiaceous (pigmented) fungi, presents as slowly progressive, verrucous (wart-like skin plaques/nodules, typically on the lower limbs. General features: slow, chronic, localised progression; diagnosis by direc microscopy, histopathology, and culture of biopsy material; treatment depends on th specific agent but often involves prolonged antifungal therapy (itraconazole i commonly used) and, in some cases, surgical excision. 2–3. Classification of mycotic infections (with examples of agents) Fungal infections are classified by the depth of tissue involvement:
Superficial mycoses — infections confined to the outermost layers of skin, hair,
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Superficial mycoses — infections confined to the outermost layers of skin, hair, and nails, with minimal to no host inflammatory response. Examples: Malassezia furfur (pityriasis versicolor), Trichophyton/Microsporum species causing tinea (dermatophytosis, sometimes classified separately as “cutaneous”).
Cutaneous mycoses (Dermatophytoses) — infections of keratinised tissue (skin,
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Cutaneous mycoses (Dermatophytoses) — infections of keratinised tissue (skin, hair, nails) caused by dermatophytes, provoking a host inflammatory response. Examples: Trichophyton rubrum, Microsporum canis, Epidermophyton floccosum.
Subcutaneous mycoses — infections of the dermis, subcutaneous tissue, and
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Subcutaneous mycoses — infections of the dermis, subcutaneous tissue, and sometimes bone, following traumatic inoculation. Examples: Sporothrix schenckii (sporotrichosis), Madurella mycetomatis (eumycetoma).
Systemic (deep) mycoses — infections of internal organs, usually acquired by
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Systemic (deep) mycoses — infections of internal organs, usually acquired by inhalation, which can disseminate widely, especially in immunocompromised hosts. Examples: Histoplasma capsulatum (histoplasmosis), Cryptococcus neoformans (cryptococcosis), Coccidioides immitis (coccidioidomycosis).
Opportunistic mycoses — infections caused by normally low-virulence fungi that
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Opportunistic mycoses — infections caused by normally low-virulence fungi that cause disease specifically in immunocompromised hosts. Examples: Candida albicans (candidiasis), Aspergillus fumigatus (aspergillosis), Pneumocystis jirovecii (pneumocystis pneumonia), Mucorales (mucormycosis).
Superficial vs cutaneous mycosis — clinical manifestations
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Superficial vs cutaneous mycosis — clinical manifestations Feature Superficial mycosis Cutaneous mycosis (dermatophytosis) Depth of involvement Outermost keratin layer Full thickness of keratinised (stratum corneum), hair shaft skin, hair, and nails surface Host inflammatory response Minimal to none Present — erythema, scaling, itching Typical presentation Hypo/hyperpigmented, scaly Well-demarcated, macules (e.g., pityriasis erythematous, scaly, often versicolor) with minimal annular (“ring-like”) lesions symptoms with central clearing and active advancing border; itching common Example organism Malassezia furfur Trichophyton, Microsporum, Epidermophyton species Example disease Pityriasis (Tinea) versicolor Tinea corporis, tinea pedis, tinea capitis, tinea cruris, onychomycosis
Sporotrichosis Aetiology: Sporothrix schenckii, a dimorphic fungus found in soil, decaying
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Sporotrichosis Aetiology: Sporothrix schenckii, a dimorphic fungus found in soil, decaying vegetation, and on thorny plants (roses, hay). Pathogenesis: Traumatic inoculation into the skin (classically via a thorn prick — “rose gardener’s disease”); the fungus grows as a mould in the environment and converts to a yeast form at body temperature; spreads along lymphatic channels from the primary inoculation site, producing sequential nodules. Clinical features: A primary painless nodule/ulcer develops at the inoculation sit (typically on a limb), followed by the appearance of similar nodules along the draining lymphatic chain (lymphocutaneous sporotrichosis) — the classic and most common presentation; disseminated disease (osteoarticular, pulmonary, or meningeal) is rar and occurs mainly in immunocompromised individuals. Laboratory diagnosis: culture of pus/tissue on Sabouraud dextrose agar (definitiv diagnosis — shows mould-to-yeast dimorphism); histopathology may show yeast form (often difficult to detect due to low numbers, hence culture is preferred); serology in some settings. Preventive measures: use of protective clothing/gloves when handling soil, plants hay, or thorny vegetation (e.g., gardening, farming). Treatment: Itraconazole is the treatment of choice for mos cutaneous/lymphocutaneous disease; saturated solution of potassium iodide is an older, low-cost alternative; Amphotericin B is reserved for severe/disseminated disease.
Short notes Antisepsis: The application of an antimicrobial (antiseptic) agent to living tissue (skin
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Short notes Antisepsis: The application of an antimicrobial (antiseptic) agent to living tissue (skin or mucous membranes) to reduce the number of microorganisms and preven infection, without necessarily achieving sterility (e.g., use of chlorhexidine or alcohol based skin preparation before a surgical procedure or injection). Heat sterilization: Use of heat to destroy all microbial life, including spores. Tw main types: - Moist heat (autoclaving): uses steam under pressure (typically 121°C at 15 psi for 15–20 minutes); more effective than dry heat as moisture enhances hea penetration and protein denaturation; used for surgical instruments, culture media. Dry heat: uses hot air ovens (typically 160–180°C for 1–2 hours); works by oxidation used for items that would be damaged by moisture (e.g., glassware, oils, powders). Yeast: Unicellular fungi that reproduce asexually, typically by budding (or occasionall fission); round to oval in shape; example — Candida albicans, Saccharomyce cerevisiae. Moulds: Multicellular, filamentous fungi composed of branching tubular structure called hyphae, which collectively form a mycelium; reproduce by formation of spores example — Aspergillus species, dermatophytes.
Agents of opportunistic mycotic infection
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Agents of opportunistic mycotic infection
Candida albicans (and other Candida species)
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Candida albicans (and other Candida species)
Aspergillus fumigatus
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Aspergillus fumigatus
Cryptococcus neoformans
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Cryptococcus neoformans
Pneumocystis jirovecii
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Pneumocystis jirovecii
Mucorales (e.g., Rhizopus species — causing mucormycosis)
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Mucorales (e.g., Rhizopus species — causing mucormycosis) 8/12. Laboratory diagnosis and management of systemic/invasive fungal infection Laboratory diagnosis: 1. Direct microscopy — wet mount with 10% KOH preparation of clinical specimens (sputum, CSF, tissue) to visualise fungal element (hyphae, yeast forms, spherules). 2. India ink stain — for Cryptococcus neoforman in CSF, demonstrating the characteristic capsule. 3. Culture — Sabouraud Dextros Agar (with antibiotics ± cycloheximide depending on the suspected organism) incubated at both 25°C and 37°C to demonstrate dimorphism where relevant; ma take days to weeks depending on the organism. 4. Histopathology — special stain (Periodic Acid-Schiff [PAS], Gomori Methenamine Silver [GMS]) on tissue biopsy t visualise fungal elements and assess tissue invasion. 5. Antigen detection — Cryptococcal antigen (CrAg) test (serum/CSF), Aspergillus galactomannan antigen (1,3)-β-D-glucan (a pan-fungal marker). 6. Molecular methods — PCR for specifi fungal DNA, increasingly used for rapid diagnosis. 7. Serology — antibody detection useful for some systemic mycoses (e.g., histoplasmosis) but limited value in immunocompromised patients who may not mount a detectable antibody response. Management: - Amphotericin B (conventional or liposomal formulation) — broad spectrum, remains the drug of choice for many severe/life-threatening systemi mycoses (cryptococcal meningitis, mucormycosis, severe histoplasmosis). - Azole (fluconazole, itraconazole, voriconazole, posaconazole) — used for step down/maintenance therapy or as primary therapy in less severe disease; voriconazol is first-line for invasive aspergillosis. - Echinocandins (caspofungin, micafungin) — primarily used for invasive candidiasis. - Management of the underlying immunosuppression (e.g., antiretroviral therapy in HIV) is essential for durabl control/cure. - Surgical debridement is critical in mucormycosis and some cases o aspergillosis.
Aetiology and lab diagnosis of pyogenic meningitis
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Aetiology and lab diagnosis of pyogenic meningitis (Note: pyogenic — i.e., bacterial — meningitis; see also Bacteria Section, Question 1 for full detail.) Aetiology: Bacterial causes vary with age — Group B Streptococcus, E. coli, Listeri monocytogenes (neonates); Streptococcus pneumoniae, Neisseria meningitidis Haemophilus influenzae type b (children/adults); Listeria monocytogenes als important in the elderly and immunocompromised. Laboratory diagnosis: Lumbar puncture with CSF analysis showing turbid/cloud fluid, elevated opening pressure, high neutrophil-predominant white cell count elevated protein, and low glucose (reduced CSF:plasma glucose ratio); Gram stain o CSF for rapid organism identification; CSF culture (definitive); blood cultures; late agglutination or PCR for rapid antigen/organism detection where available.
Opportunistic mycotic infections Pathogenesis: Occur in hosts with impaired immune defences (HIV/AIDS, neutropeni
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Opportunistic mycotic infections Pathogenesis: Occur in hosts with impaired immune defences (HIV/AIDS, neutropeni from chemotherapy, organ transplantation/immunosuppressive therapy, diabetes prolonged broad-spectrum antibiotic use, indwelling catheters), allowing normally low virulence or environmental fungi to invade and cause disease, often disseminating widely due to inadequate host containment. Clinical syndromes: - Candidiasis — mucocutaneous (oral thrush, oesophagitis) t invasive candidaemia. - Aspergillosis — invasive pulmonary aspergillosis, allergi bronchopulmonary aspergillosis, aspergilloma. - Cryptococcosis — meningiti (classically in advanced HIV/AIDS), pulmonary disease. - Pneumocystis pneumonia — an AIDS-defining illness, presenting with progressive dyspnoea, dry cough, and fever. - Mucormycosis — rapidly progressive, angio-invasive infection, classicall rhino-orbito-cerebral in uncontrolled diabetics (especially with ketoacidosis). Diagnosis: (as detailed in Question 8/12 above) — microscopy, culture, histopathology antigen tests (CrAg, galactomannan, beta-D-glucan), and imaging (e.g., CT ches showing the “halo sign” in invasive aspergillosis). Management: appropriate systemic antifungal therapy targeted to the organism (se Question 8/12), combined with reversal/control of the underlying immunosuppression wherever possible, as antifungal therapy alone is often insufficient without immun recovery.
Laboratory diagnosis of invasive fungal infection (See Question 8/12 above for comprehensive detail — direct microscopy, culture
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Laboratory diagnosis of invasive fungal infection (See Question 8/12 above for comprehensive detail — direct microscopy, culture histopathology with special stains, antigen detection tests, molecular/PCR methods and serology.)
Dermatophytes — definition and classification of clinical types
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Dermatophytes — definition and classification of clinical types Definition: Dermatophytes are a group of closely related fungi (genera Trichophyton Microsporum, and Epidermophyton) that have the ability to invade and utilise keratin in skin, hair, and nails, causing superficial infections collectively known a dermatophytoses or “tinea” infections. Classification of clinical types (by anatomical site): 1. Tinea capitis — scalp/hair
Tinea corporis — body (glabrous skin) — “ringworm.” 3. Tinea cruris — groin
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Tinea corporis — body (glabrous skin) — “ringworm.” 3. Tinea cruris — groin (“jock itch”). 4. Tinea pedis — feet (“athlete’s foot”). 5. Tinea unguium (onychomycosis) — nails. 6. Tinea barbae — beard area. 7. Tinea manuum — hands.
Laboratory diagnosis of fungal infection of the toes
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Laboratory diagnosis of fungal infection of the toes (onychomycosis/tinea pedis)
Specimen collection: nail clippings/scrapings from the affected nail (subungual
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Specimen collection: nail clippings/scrapings from the affected nail (subungual debris) or skin scrapings from the web spaces/soles.
Direct microscopy: 10–20% KOH preparation to dissolve keratin and visualise
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Direct microscopy: 10–20% KOH preparation to dissolve keratin and visualise fungal hyphae or spores under the microscope.
Culture: Sabouraud Dextrose Agar (with cycloheximide/chloramphenicol to inhibit
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Culture: Sabouraud Dextrose Agar (with cycloheximide/chloramphenicol to inhibit contaminants), incubated at 25–28°C for up to 2–4 weeks, with identification based on colony morphology and microscopic features (macroconidia/microconidia).
Cutaneous mycosis Aetiology: Dermatophyte fungi — genera Trichophyton, Microsporum
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Cutaneous mycosis Aetiology: Dermatophyte fungi — genera Trichophyton, Microsporum Epidermophyton — which are keratinophilic (keratin-digesting) and classified by thei natural habitat/source: anthropophilic (human-to-human transmission), zoophili (animal-to-human), and geophilic (soil-to-human). Pathogenesis: Fungal spores/hyphae from an infected host, animal, or soil contact th skin, and (aided by warmth, moisture, and minor trauma) invade the stratum corneum hair, or nails, digesting keratin via secreted keratinases; the host inflammator response to fungal antigens and metabolic products produces the characteristi erythema, scaling, and pruritus, with the growing colony spreading centrifugally producing the classic annular lesion with central clearing. Clinical syndrome: well-demarcated, erythematous, scaly, annular (ring-shaped plaques with a raised, active advancing border and relatively clear centre; pruritus i common; specific patterns depend on the site involved (see Question 13 classification — tinea corporis, cruris, pedis, capitis, unguium). Diagnosis: KOH microscopy of skin/hair/nail scrapings showing septate hyphae culture on Sabouraud Dextrose Agar for species identification; Wood’s lamp examination (some Microsporum species fluoresce green under UV light, useful in tinea capitis). Treatment: Topical antifungals (e.g., clotrimazole, terbinafine cream) for localised skin infections; oral antifungals (terbinafine, itraconazole, griseofulvin) for extensiv disease, tinea capitis, or onychomycosis, given the difficulty of topical agent penetrating hair follicles/nails adequately.