ML

CH 5 – Infection

Infection: Core Concepts

Definition and Scope

  • 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.

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

Chain of Infection (6 Links)

  • 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.

Phases of Acute Infection

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}

Complications

  • Septicemia = pathogen + toxins in blood.

  • Bacteremia = bacteria in blood (subset of septicemia).

  • Septic shock = systemic vasodilation & organ hypoperfusion.

  • Chronic infection = persistent low-grade disease.

Manifestations of Infection

  • Local: heat, pain, edema, redness, incapacitation, lymphadenitis, purulent exudate.

  • Systemic: fever, weakness, headache, malaise, anorexia, nausea.

Laboratory & Diagnostic Tests

  • 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.

General Treatment Principles

  • Antimicrobial drugs

    • Antibacterials, antifungals, antivirals (specific to pathogen class).

  • Symptom reduction

    • Adequate fluids, rest, analgesics/antipyretics.

Applied Clinical Concepts

Shingles (Herpes Zoster)

  • 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.

Influenza

  • 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.

Viral Hepatitis (HAV, HBV, HCV, HDV, HEV)

  • 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

    1. Prodrome: fatigue, anorexia, low-grade fever.

    2. Icterus: jaundice, hepatomegaly, clay-colored stools, dark urine.

    3. 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).

Tuberculosis (TB)

  • 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.

Urinary Tract Infection (UTI)

  • 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.

Acute Pyelonephritis

  • 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.

Bacterial Meningitis

  • 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.

Tinea (Dermatophytosis)

  • 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.

Malaria

  • 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.