Infections and Diseases of Skin and CNS
Skin Structure, Microbiota, and Protective Barriers
Skin anatomy: epidermis (outermost), dermis (thick supportive layer), and hypodermis (subcutaneous tissue).
Keratin in the epidermal layer forms a protective, water-repellent barrier and undergoes shedding; this layer helps resist damage, including UV exposure. When there is trauma, this barrier can be disrupted, separating epidermal components and leading to bleeding and damage to nerves, blood vessels, and lymphatics.
Sweat glands in the epidermis can harbor bacteria; glands contribute to the microenvironment and potential infections (e.g., folliculitis).
Chemical changes affect microbiota: pH lowering can make the surface inhospitable to many microorganisms; high lipid concentrations can influence microbial communities. Environmental factors and hygiene also reshape the dermal microbiota.
Key protective molecules in skin secretions:
Lysozyme enzymes found in sweat, tears, and saliva help with antimicrobial defense.
Immunoglobulin A (IgA) provides mucosal-like immune protection on the skin.
Normal skin microbiota commonly discussed:
Staphylococcus aureus (gram-positive cocci, grape-like clusters, non-motile, non-spore-forming, can tolerate high salt, extreme pH, and high temperature).
Streptococcus pyogenes (group A Streptococcus; beta-hemolytic, often throat/thoracic colonization, can be pathogenic).
Propionibacterium (Cutibacterium) acnes (acne-associated bacterium).
Health vs disease context:
Both Staphylococcus aureus and Streptococcus pyogenes can be part of normal flora but may become pathogenic with population growth or barrier disruption.
Focus of many lectures includes Staphylococcus aureus and Streptococcus pyogenes as primary pathogens.
Key Differentiating Tests and Toxins (Staphylococcus vs Streptococcus)
Catalase test: distinguishes Staphylococcus (catalase-positive) from Streptococcus (catalase-negative).
Reaction: 2\,\mathrm{H2O2} \rightarrow 2\,\mathrm{H2O} + \mathrm{O2}
Coagulase test: Staphylococcus aureus is coagulase-positive; this helps differentiate S. aureus from other Staphylococci.
Virulence factors and toxins:
Staphylococcus aureus:
Coagulase (clots plasma)
Hyaluronidase (digests hyaluronic acid; disrupts connective tissue)
Exfoliative toxins A and B (exfoliatins) leading to epidermal damage in certain syndromes (e.g., SSSS).
Catalase activity helps pathogen differentiation in diagnostics.
Streptococcus pyogenes (Group A Streptococcus):
Hyaluronidase and streptokinase as virulence factors that aid tissue invasion and spread.
Staphylococcus aureus and MRSA (Methicillin-Resistant S. aureus)
Staphylococcus aureus: gram-positive cocci in clusters; grape-like appearance; non-motile; resistant to some environmental stresses; not spore-forming.
MRSA vs MSSA:
MRSA: resistant to methicillin and many other antibiotics; often requires vancomycin or other gram-positive targeting antibiotics.
MSSA: methicillin-sensitive; treated with other beta-lactams.
Common clinical presentation:
Skin infections: redness, tenderness, localized lesions with or without pus; fever may be present.
Direct or indirect transmission: contact with infected individuals or contaminated surfaces; hospital and community settings.
Diagnostic and management notes:
Culture and sensitivity testing to guide antibiotic choice.
Vancomycin commonly used for MRSA coverage; other MRSA-active agents include linezolid, daptomycin, and certain cephalosporins depending on resistance.
Impetigo (Staphylococcal and Streptococcal) and Exfoliative Toxins
Impetigo: very superficial skin infection (epidermal involvement) with crusting; often seen as golden crusts around lesions; commonly in children.
Etiology:
Can be caused by Staphylococcus aureus, Streptococcus pyogenes, or a mix of both.
Exfoliative toxins (S. aureus):
Exfoliative toxins A and B cause superficial skin changes and blistering by promoting epidermal detachment.
Staphylococcal Scalded Skin Syndrome (SSSS)
Also called Staphylococcal Scalded Skin Syndrome (four S’s: Staphylococcus Scalded Skin Syndrome).
Pathogenesis: exfoliative toxins A and B from Staphylococcus aureus cause widespread epidermal splitting and desquamation, especially in young children.
Clinical description: skin appears wrinkled, like crumpled tissue paper; widespread blistering and shedding of the epidermis; high risk in infants and young children, with relatively lower mortality in children than in adults.
Mortality: higher in adults; overall lower in pediatric populations but severe in adults.
Cellulitis and Deep Skin Infections
Cellulitis: deeper infection than impetigo; marked pain, swelling, warmth, and redness; can be accompanied by fever and systemic symptoms.
Classic risk factors: immunocompromised individuals, diabetes, vascular insufficiency, and skin barrier disruption (shaving injuries, wounds).
Common sites: legs (thighs often cited), but can occur anywhere; tends to spread quickly and may form a red line indicating spread.
Complications: can lead to secondary infections or systemic infection if not treated.
Clostridium perfringens and Gas Gangrene (Clostridial Myonecrosis)
Bacterium: Clostridium perfringens, an anaerobic, spore-forming gram-positive rod.
Pathogenesis: produces a toxin-rich infection that leads to gas gangrene and necrosis of muscle tissue; gas production creates gas bubbles in tissue detectable by imaging.
Toxins:
Alpha toxin (phospholipase C) promotes red blood cell lysis, edema, tissue destruction, and collagenase activity.
Other toxins contribute to tissue damage.
Treatments and management:
Surgical debridement and removal of necrotic tissue; incision and drainage when necessary.
Antibiotics: penicillin G; adjunctive clindamycin (
to suppress toxin production).Hyperbaric oxygen therapy can help in some cases by increasing tissue oxygen tension to suppress anaerobes.
Wound care includes cleaning and ensuring adequate oxygenation.
Other Skin Lesions: Morphology and Terminology
Bullae: large fluid-filled blisters.
Cyst: semisolid, small lesion.
Macule: flat pigmented area with color change; not raised.
Maculopapular: flat or slightly raised with color change; measles/rubella-type presentations.
Papule: small, raised bump (wart-like).
Plaque: large, elevated, flat-topped lesion; e.g., psoriasis.
Purpura: non-blanching large patches or bruises due to bleeding under the skin.
Petechiae: tiny non-blanching red dots due to capillary bleeding.
Pustules: small, pus-filled raised lesions (acne, smallpox-type lesions).
Vesicles: fluid-filled, clear fluid-filled lesions.
Scales: flaky skin.
Fungal and Parasitic Infections of the Skin
Ringworm family (tinea): name depends on location:
Tinea capitis (scalp)
Tinea barbae (beard area)
Tinea corporis (body)
Tinea cruris (groin, “jock itch”)
Tinea pedis (foot)
Tinea unguium / onychomycosis (nail)
Tinea versicolor (Malassezia furfur): pigment changes on the skin; superficial fungal infection.
Antifungals: azole drugs (e.g., fluconazole); labeled as “Zol” by the lecturer; good coverage for superficial and some systemic fungal infections.
Warts and molluscum contagiosum:
Human papillomavirus (HPV): warts; plantar warts can be painful; common warts may appear on fingers and other exposed areas.
Molluscum contagiosum: small, waxy, dome-shaped papules with a central case; can occur on face, arms, legs, and genitals; more common in immunocompromised; sometimes needs removal.
Leishmaniasis: Leishmania spp. (donovani most common in several regions) causing cutaneous or mucocutaneous disease; vector is the sandfly; treatment with antiparasitic medications such as amphotericin B and/or miltefosine; granulomatous lesions with possible mucocutaneous involvement; endemic to the Mediterranean, parts of Asia, South America, and deserts; transmission requires a sandfly bite.
Loa loa (loiasis): a filarial parasite transmitted by biting flies; can migrate through subcutaneous tissues and the eye; diagnosis and treatment involve antiparasitic therapy.
Elephantiasis (lymphatic filariasis): caused by filarial parasites; lymphatic obstruction leading to massive swelling, typically of the legs and genitalia; long-term morbidity.
Rainworms (tinea terminology) and naming by location, not by organism:
Tinea capitis, tinea corporis, tinea cruris, tinea pedis, tinea unguium (onychodystrophy).
Tinea versicolor caused by Malassezia species; pigments (hypo- or hyperpigmented patches).
Dermatology notes: direct contact, shared items (gloves, slippers, barber tools), bed linens and hotel transfers contribute to spread.
Vaccination and public health notes:
Vaccines exist for many fungal and viral skin infections (e.g., measles, rubella, varicella, HPV) and bacterial pathogens (e.g., Haemophilus influenzae type b, pneumococcus). Adherence to vaccination guidelines reduces disease burden.
Varicella Zoster Virus (VZV): Chickenpox and Shingles
Chickenpox (varicella): vesicular lesions all over the face and body; incubation period 10-20\text{ days}; disease lasts 4-7\text{ days}; new lesions stop growing around day 5; risk of secondary bacterial infection if lesions break.
Varicella vaccine available; disease is generally mild but can be life-threatening in immunocompromised individuals.
Shingles (herpes zoster): reactivation of latent VZV in dorsal root ganglia; unilateral dermatomal vesicular rash; can lead to postherpetic neuralgia; vaccine recommended around age 50.
Relationship: you cannot have shingles without a prior chickenpox infection; reactivation occurs later in life due to latent virus.
Other notes: herpes viruses are a broad family; multiple HHV types exist (HHV-1, HHV-2, HHV-3, HHV-6, HHV-8, etc.).
Measles and Rubella: Maculopapular Rash Diseases
Measles (rubeola):
Transmission: droplet spread; high contagion; conjunctivitis, fever, Koplik spots inside the mouth; a characteristic maculopapular rash that starts on the face and progresses downward.
The incidence rose recently due to gaps in vaccination; herd immunity historically around 90-95\%.
Severe complication risk includes subacute sclerosing panencephalitis (SSPE), a rare but deadly neurodegenerative disease with high mortality (
rare but possible; rate extremely low but significant when it occurs).
Rubella (German measles):
Generally milder rash; important due to congenital rubella syndrome when pregnant mothers are infected (deafness, cardiac anomalies, ocular defects, mental/physical retardation).
Transmission: droplets; rash is pink maculopapular and trunk-first, then to extremities; congenital issues require vaccination to prevent.
A mnemonic aid: differentiate measles vs rubella visually and clinically; both are transmitted by droplets.
Fifth disease (erythema infectiosum) and Roseola (sixth disease):
Fifth disease: Parvovirus B19; “slapped cheek” appearance; fever and mild symptoms; generally mild.
Roseola infantum: caused by human herpesvirus 6 (HHV-6) / sometimes HHV-7; high fever for ~3 days, followed by a rash; 70% of cases may have no rash; often resolves without complication.
Measles vs rubella visual cues and vaccine implications summarized; note about droplet vs contact transmission for these viruses; vaccines reduce disease burden.
Human Papillomavirus (HPV) and Molluscum Contagiosum
HPV: causes warts; many types exist (the lecturer mentioned types 6, 9, and 11 as associated with warts; clinically, 6 and 11 are well-known for genital warts; others can be oncogenic in some strains, e.g., 16, 18). Vaccination recommended for preteens.
Plantar warts (verrucae plantares): deep and painful; may be painless in other locations; removal via medical procedures.
Molluscum contagiosum: small, waxy, dome-shaped papules with a central umbilication; can affect face, arms, legs, and genitals; more common in immunocompromised individuals; often self-limited but may require removal if bothersome; incidence variable by region (noted higher in Pacific Islands).
Parasitic and Vector-Borne Infections of the Skin
Leishmaniasis: Leishmania donovani (and others) cause cutaneous and mucocutaneous disease; transmitted by female sandflies; geographic distribution includes the Mediterranean, Southeast Asia, parts of South America; localized cavitating ulcers can become mucocutaneous disease; treatment includes antiparasitics (e.g., amphotericin B, miltefosine).
Tinea infections (ringworm) are caused by dermatophytes; geographic distribution and locations depend on site; treatment with antifungal agents.
Tinea versicolor (Malassezia furfur): pigmented patches on skin; treat with antifungal creams or oral antifungals as needed.
Loa loa (loiasis): a filarial parasite transmitted by deer flies; migrates through the body and can be seen in the eye; treatment with antiparasitics.
Elephantiasis (lymphatic filariasis): swelling due to lymphatic obstruction by filarial parasites; chronic condition leading to deformities.
Rabies: zoonotic viral infection from animal bites; vaccines exist for post-exposure prophylaxis; prevention is key.
Polio, Tetanus, and Botulism
Polio (poliovirus): causes neuromuscular paralysis by infecting the anterior horn cells of the spinal cord; primarily acquired via fecal-oral route; prevention via vaccination (Salk IPV injectable; Sabin OPV oral in the past; OPV is largely discontinued in favor of IPV in many places due to safety concerns).
Tetanus (Clostridium tetani): causes painful muscle spasms due to tetanus neurotoxin blocking inhibitory neurotransmission in the spinal cord; back arching can occur; vaccination (tetanus toxoid) every ~10 years; wound hygiene and prompt treatment essential; tetanus immune globulin (if exposure risk is high) may be used in some settings.
Botulism (Clostridium botulinum): botulinum toxin blocks acetylcholine release at neuromuscular junctions, causing flaccid paralysis; common causes include improperly canned foods; toxin used medically for cosmetic purposes (Botox).
Types of botulism: foodborne, infant, wound; treatment includes antitoxin; no routine routine vaccine exists; toxoid vaccines may be considered for certain high-risk scenarios.
Central Nervous System (CNS) Infections: Meningitis and Beyond
CNS overview: brain and spinal cord protected by meninges (dura, arachnoid, pia) and wrapped by the meninges; cerebrospinal fluid (CSF) cushions and nourishes the CNS; CSF is typically clear.
Lumbar puncture (CSF sampling): usually performed at the L3–L4 or L4–L5 interspaces to avoid spinal cord injury (the spinal cord ends around L1–L2 in adults; variability exists). Opening pressure can indicate infection.
Bacterial meningitis is an urgent medical condition; viral meningitis generally has a better prognosis.
First-line bacterial meningitis treatment (empiric): \text{ceftriaxone} (a third-generation cephalosporin) due to broad spectrum coverage.
Blood-brain barrier (BBB): selective barrier that protects the CNS; many molecules cannot cross; some drugs (e.g., certain antibiotics) can cross the BBB due to lipophilicity or specific transport mechanisms; Benadryl crosses BBB (causing drowsiness in first-generation antihistamines) whereas second-generation antihistamines (e.g., cetirizine) do not cross as readily.
Gut-brain axis: emerging evidence linking gut microbiome to CNS function; embryology links between gut and neural development; Hirschsprung’s disease as an example of neural-immune-gut interactions.
Meningitis pathogens and features:
Neisseria meningitidis: gram-negative diplococci; cause of meningitis in young adults; can cause meningococcemia with vascular damage and petechial/purpuric rashes; high mortality risk; transmission via nasopharyngeal route; treat with broad-spectrum antibiotics and supportive care.
Streptococcus pneumoniae: gram-positive diplococci; common cause of community-acquired pneumonia and meningitis; may present without vascular collapse; vaccine available.
Haemophilus influenzae type b (Hib): gram-negative coccobacillus; causes meningitis and epiglottitis; vaccination has dramatically reduced Hib disease burden.
Listeria monocytogenes: gram-positive rod; meningitis risk in neonates, elderly, and immunocompromised hosts; vaccination not routinely given for adults; covered by certain antibiotics; clinical emphasis varies by patient group.
Cryptococcus neoformans: fungal meningitis; associated with bird droppings and immunocompromised status (e.g., HIV/AIDS); treated with antifungals (e.g., amphotericin B, fluconazole).
Coccidioides immitis (Coccidioidomycosis): causes Valley fever; endemic to the southwestern United States (e.g., Arizona, parts of California); spores inhaled from dust; can disseminate to meninges causing meningitis; treatment may include fluconazole and amphotericin B.
Viral meningitis: often caused by enteroviruses or herpes simplex viruses; typically self-limited; better prognosis than bacterial meningitis.
Specific notes on imaging, diagnosis, and therapy: CSF analysis (cell count, glucose, protein), Gram stain, and culture guide therapy; subacute cases may require rapid empiric therapy due to high risk.
Polio and Vaccine Notes
Poliovirus causes paralytic disease by destroying anterior horn cells in the spinal cord; route: fecal-oral; prevention via vaccination (inactivated polio vaccine, IPV, now standard; oral polio vaccine (OPV) largely discontinued in many regions due to risks of vaccine-derived poliovirus).
Global goals have led to near-eradication; remaining pockets in certain regions (e.g., India, Pakistan, some areas) require continued surveillance and vaccination.
Final Practical Takeaways for Exams
Remember the key distinctions:
Staphylococcus aureus versus Streptococcus pyogenes: catalase test for Staph; coagulase positivity; exfoliative toxins in S. aureus versus hyaluronidase/streptokinase in S. pyogenes.
MRSA versus MSSA: antibiotic resistance patterns and treatment implications.
Impetigo is superficial; cellulitis is deeper and more aggressive.
SSSS is exfoliative-toxin-mediated desquamation, primarily in children.
Gas gangrene is an anaerobic, endospore-forming infection with gas production and alpha toxin; requires rapid surgical and medical management.
DERMATOLOGY vocabulary (bullae, vesicles, pustules, plaques, macules, papules, etc.) and clinical recognition of typical lesion morphology.
Varicella-zoster virus has two faces: varicella (chickenpox) and herpes zoster (shingles); vaccinate to reduce disease burden; shingles vaccine reduces risk of reactivation.
Measles, rubella, roseola, fifth disease: recognize hallmark signs (Koplik spots for measles; congenital rubella syndrome risks; slapped-cheek appearance; roseola fever pattern).
HPV and molluscum contagiosum: warts vs molluscum; importance of vaccination and hygiene.
Leishmaniasis, loiasis, elephantiasis: vector-borne and filarial diseases with varying geographic distributions and treatments.
CNS infections emphasize the blood-brain barrier, lumbar puncture landmarks (L3-L4), and empiric use of ceftriaxone for bacterial meningitis.
Vaccination prevents many CNS and skin infections; public health measures dramatically reduce disease burden.
Key LaTeX-formatted facts to memorize:
2\,\mathrm{H2O2} \rightarrow 2\,\mathrm{H2O} + \mathrm{O2} (catalase test reaction).
Incubation and disease durations: 10-20\text{ days} (varicella incubation), 4-7\text{ days} (clinical course), 5\text{ days} (new lesions stop growing).
MRSA treatment: \text{vancomycin} as a common agent; note resistance patterns.
Meningitis pathogens summarized: Neisseria meningitidis (gram-negative diplococci); Streptococcus pneumoniae (gram-positive diplococci); Haemophilus influenzae type b (gram-negative coccobacillus).
Valley fever geography and vectors: Coccidioides immitis in southwestern regions; spores inhaled; treatment includes fluconazole and/or amphotericin\,B.
Ethical and practical implications:
Importance of vaccination to prevent severe diseases (measles, rubella, varicella, Hib, pneumococcus, HPV, polio).
Hygiene and infection control in healthcare and community settings to prevent MRSA and other skin infections.
Safe handling of wounds and prompt treatment to prevent necrotizing infections.
Awareness of zoonotic and vector-borne diseases in travel or endemic regions.
Real-world relevance:
Understanding skin barrier function and microbiota helps explain susceptibility to infections and the impact of lifestyle and hygiene.
The BBB concept guides antibiotic choices for CNS infections and explains why some drugs cause CNS side effects.
Public health vaccination programs dramatically reduce incidence of many of these diseases and prevent outbreaks in communities.
Quick Reference: Pathogens at a Glance
Staphylococcus aureus (incl. MRSA): catalase-positive, coagulase-positive; exfoliative toxins A/B; impetigo, boils, cellulitis, SSSS.
Streptococcus pyogenes (Group A): beta-hemolytic; hyaluronidase, streptokinase; scarlet fever, rheumatic fever, necrotizing fasciitis.
Clostridium perfringens: anaerobic; alpha toxin; gas gangrene; endospores.
Varicella-zoster virus: varicella (chickenpox); reactivation as shingles; vaccination reduces burden.
Measles (rubeola): conjunctivitis, Koplik spots; vaccine-driven herd immunity; SSPE is a rare complication.
Rubella (German measles): congenital rubella syndrome risk; vaccination.
Parvovirus B19: fifth disease; slapped-cheek rash.
HHV-6 (roseola): high fever; rash may be absent; common in children.
HPV: warts; genital warts linked to HPV types 6, 11 (and oncogenic types for cancer risk).
Molluscum contagiosum: poxvirus; waxy, umbilicated papules.
Leishmania donovani: cutaneous/mucocutaneous leishmaniasis; sandfly vector; antiparasitics.
Loa loa: eye migration; filarial nematode; DEC treatment considered.
Tetanus toxin: blocks inhibitory neurotransmission; propulsion toward spastic paralysis; vaccination.
Botulinum toxin: inhibits acetylcholine release; flaccid paralysis; botox applications; antitoxin treatment available.
Polio: anterior horn neuron destruction; fecal-oral transmission; vaccine-driven eradication efforts.
Bacterial meningitis culprits: Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b.
Fungal meningitis: Cryptococcus neoformans; Coccidioides immitis (valley fever).