Infection
A state of cellular, tissue, and organ destruction caused by invasion of microorganisms.
Requires penetration of the three host lines of defense (physical barriers, innate immunity, adaptive immunity).
Modern challenges
Multiple drug-resistant (MDR) microbes.
Global travel/globalization → rapid spread of harmful pathogens.
General Attributes
Disease-producing microbes that harm the host by:
Directly destroying host cells.
Interfering with host metabolic functions.
Releasing toxins that damage surrounding tissue.
Obligate vs. Facultative
Obligate: require a host for replication (e.g., viruses).
Facultative: can live both inside or outside a host (e.g., many bacteria).
Major Taxonomic Groups
Bacteria
Viruses
Rickettsiae, Mycoplasmas, Chlamydiae (intermediate forms)
Fungi
Protozoa
Helminths
Infectious Agent
Bacteria, fungi, viruses, rickettsiae, protozoa.
Reservoirs (habitats for growth)
People, equipment, water.
Control: sanitizing environment.
Portal of Exit
Excretions, secretions, skin, droplets.
Control: covering secretions, trash disposal, airflow control.
Means of Transmission
Direct contact, ingestion, fomites, airborne.
Control: handwashing, isolation, sterilization, universal precautions.
Portal of Entry
Mucous membranes, GI/GU tracts, respiratory tract, broken skin.
Control: covering potential entry points, hand hygiene.
Susceptible Host
High-risk states: immunosuppression, diabetes, surgery, burns, elderly.
Control: treat underlying disease, recognize high-risk patients, sterilization.
Phase | Pathophysiology | Typical Clinical Manifestations |
---|---|---|
Exposure | Pathogen contacts host | None |
Incubation | Microbe replicates, host defenses begin | None |
Prodrome | Early activation of immune response | Fatigue, low-grade fever, weakness, nausea ("subclinical illness") |
Clinical Illness | Peak pathogen load; host fights | Local: pain, heat, redness, swelling, pus, loss of function. Systemic: fever, malaise, weakness, anorexia, headache, nausea |
Convalescence | Immune containment and repair | Gradual resolution OR transition to chronic infection |
Possible Complications | If defenses fail | \text{Septicemia} \rightarrow \text{Septic shock} \rightarrow \text{Death} |
Septicemia = pathogen + toxins in blood.
Bacteremia = bacteria in blood (subset of septicemia).
Septic shock = systemic vasodilation & organ hypoperfusion.
Chronic infection = persistent low-grade disease.
Local: heat, pain, edema, redness, incapacitation, lymphadenitis, purulent exudate.
Systemic: fever, weakness, headache, malaise, anorexia, nausea.
WBC count
Leukocytosis (>11{,}000\,\text{/µL}) suggests infection.
Leukopenia (<4{,}000\,\text{/µL}) may appear in overwhelming infection or viral suppression.
Serum antibody titers (IgM/IgG).
Cultures of blood, urine, sputum, CSF, etc.
Sensitivity testing to guide antimicrobials.
Antimicrobial drugs
Antibacterials, antifungals, antivirals (specific to pathogen class).
Symptom reduction
Adequate fluids, rest, analgesics/antipyretics.
Etiology
Reactivation of latent varicella-zoster virus (VZV) residing in dorsal root ganglia.
Pathogenesis
Virus travels along sensory nerve to skin → dermatomal eruption.
Clinical Picture
Pain, grouped vesicular rash, erythema restricted to a dermatome.
Significance: Illustrates latency & reactivation.
Pathophysiology
Viral infection of airway epithelial cells via respiratory droplets.
Causes epithelial necrosis.
Reassortment → gradual genetic drift during replication.
Manifestations
Cough, sore throat, nasal congestion/drainage, shortness of breath, chills, fever, body aches, weakness, malaise.
Diagnosis
History/physical, rapid viral assay (rapid flu swab).
Treatment & Prevention
Handwashing, vaccination, masks.
Supportive care: hydration, nutrition, analgesics.
Antivirals (e.g., oseltamivir) ideally within <48\,\text{h} of symptoms.
Pathophysiology
Acute/chronic inflammation of liver via fecal-oral (A,E) or blood/body fluid (B,C,D) routes.
Leads to varying hepatic necrosis.
Incubations
HAV/HEV: 1!\text{–}2\,\text{mo}; HBV/HCV/HDV: 2!\text{–}3\,\text{mo}.
Carrier & Chronicity
Present in HBV, HCV, HDV.
Clinical Course
Prodrome: fatigue, anorexia, low-grade fever.
Icterus: jaundice, hepatomegaly, clay-colored stools, dark urine.
Recovery: symptom resolution; hepatomegaly may persist.
Diagnostics
Viral antibodies (Anti-HAV, Anti-HCV, Anti-HDV, Anti-HEV) or HBsAg.
Labs: urine/serum bilirubin, clotting time.
Treatment & Prevention
Vaccines (A,B). Hand hygiene. Avoid contaminated food/blood.
Support: fluids, rest, low-fat diet, analgesics.
Antivirals (e.g., Tamiflu cited, though primarily for influenza).
Global Impact: Most prevalent & deadly infectious disease worldwide.
Agent: Mycobacterium tuberculosis (acid-fast, frequently drug-resistant).
Transmission: Inhaled airborne droplets; humans are sole reservoir.
Pathogenesis
Primary exposure → Ghon complex (granuloma + lymph node involvement).
Latent TB may persist for years.
Reactivation (secondary TB) → progressive or disseminated disease.
Clinical Manifestations
90\% asymptomatic.
Symptomatic: malaise, weight loss, fatigue, anorexia, low-grade fever, night sweats, chronic productive cough with hemoptysis, site-specific lesions.
Diagnosis
Tuberculin skin test, chest X-ray, sputum culture, nucleic acid amplification.
Treatment
Transmission control: isolation, negative pressure rooms, N95 masks.
Multi-drug regimen: isoniazid, rifampin, pyrazinamide, ethambutol/streptomycin.
Directly Observed Therapy (DOT) improves adherence.
Pathophysiology
Ascending bacterial infection (E. coli most common) → epithelial necrosis.
Manifestations
Dysuria, urgency, frequency, hematuria, small volumes, cloudy/purulent urine.
Diagnosis
History/physical, urinalysis, urine culture, leukocyte esterase dipstick.
Treatment
Full course of antibiotics, ↑ fluids, abstain from intercourse & caffeine until resolved.
Pathophysiology
Bacterial infection of kidneys (often E. coli).
Risk factors: renal calculi, urine stasis, frequent intercourse, STIs, hormonal changes.
Can progress to chronic scarring (narrowed calyces, parenchymal atrophy).
Manifestations
Fever, costovertebral angle pain, nausea/vomiting, dysuria, urgency, lower abdominal pain, hematuria.
Diagnosis
Symptoms + urinalysis, urine culture, imaging.
Treatment
IV fluids, antibiotics, analgesics; surgery if structural cause.
Etiology
Neisseria meningitidis (common), Streptococcus pneumoniae, Haemophilus influenzae (in non-immunized).
Pathogenesis
Respiratory droplets → bloodstream → CNS; exudate blocks circulation, ↑ intracranial pressure.
Manifestations
Rapid (<24\,\text{h}) severe headache, photophobia, nuchal rigidity, altered consciousness, seizures, fever, leukocytosis.
Physical Signs
Kernig and Brudzinski signs positive.
Diagnostics
Blood cultures, CSF analysis: cloudy, neutrophils↑, glucose↓, positive Gram stain.
Treatment
Vaccination programs, prompt IV antibiotics, corticosteroids, fluids, proph. antibiotics for contacts.
Pathophysiology
Fungal dermatophytes spread by direct contact → keratinized tissue thickening.
Clinical Types
Corporis (body ringworm): annular red patch.
Versicolor: hypopigmented patches.
Capitis: scalp hair loss/breakage.
Pedis (athlete’s foot): toe web maceration.
Cruris (jock itch): groin erythema/pruritus.
Unguium (onychomycosis): nail thickening/discoloration.
Diagnostics
H&P, microscopy (KOH prep), fungal culture, Wood light.
Treatment & Prevention
Proper hygiene, avoid infected contacts.
Topical/oral antifungals.
Pathophysiology
Protozoan Plasmodium spp. transmitted by Anopheles mosquitoes.
Incubation ≈ 1\,\text{mo} post-exposure.
Eradicated in U.S.; >1\,000,000 deaths/yr globally (mostly sub-Saharan African children).
Manifestations
Cyclic headache, chills, high fever, profuse sweating, cough, fatigue, malaise, myalgia/arthralgia.
Diagnostics
Travel history, physical, labs: hemoglobin ↓, platelets ↓, LFTs ↑, LDH ↑, lymphocytes altered, peripheral smear showing parasitized RBCs.
Treatment & Prevention
Mosquito avoidance: bed nets, long sleeves, repellents with DEET.
Antimalarial pharmacology:
Quinolines, antifolates, artemisinins, antimicrobials.
Antipyretics for fever control.
These bullet-point notes capture every major and minor element from the transcript, explain mechanisms, list clinical data, give all preventive and therapeutic measures, and interrelate phases, diagnostics, and complications across infectious diseases.