Infectious and Skin Diseases Flashcards by Mary Kate Heard

Clinical Presentation of Immune Response:

Clinically, histologically, impt mediator, etc

Clinically: redness, swelling, pain
Histologically: edema
Pyogenic: pus production
Granuloma: macrophages surrounded by T cells
Tumor necrosis factor (TNF): important mediator

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When does the immune response end?

when phagocytes clear all antigen
Lack of T-cell stimulation results in apoptosis

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Acute vs. Chronic Inflammation

Acute Inflammation

Dilaton of small blood vessels
Increased microvasculature permeability
Migration and activation of immune cells

More WBCs

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Acute vs. Chronic Inflammation

Chronic Inflammation

Infiltration by macrophages, lymphocytes, plasma cells
Increased tissue destruciton
Attempts at healing

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Meningitis - Infectious Disease

What are the 3 layers of the Meninges?

Meninges protects CNS

Dura mater (tough mother)
Arachnoid (and subarachnoid)
Pia mater (tender mother)

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Meningitis - Infectious Disease

Dura mater

Outermost covering
Dense CT

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Meningitis - Infectious Disease

Arachnoid

Middle layer
Subarachnoid space is fluid filled with many projections
Large blood vessels

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Meningitis - Infectious Disease

Pia mater

Innermost covering (immediately next to the nerve tissue)
Loose CT and small blood vessels

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Meningitis - Infectious Disease

Meningitis

What is it? General Presentation?

Bacterial or viral infection
Acute onser fever
Headache
Stiff neck
Photophobia (light sensitiviy)
Confusion

Usually inflammation of subarachnoid space

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Meningitis - Infectious Disease

How does Meningitis cause Neuronal Injury?

Inflammation in subarachnoid space
substantial infiltration bvy neutrophils
May breach blood-brain barrier and cause localized inflammation in neural tissue
Damage to blood vessels can cause hemorrhage into the brain

Most damage is due to increases pressure

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Meningitis - Infectious Disease

Meningitis Pathogenesis

Coloization of nasopharynx
Evade Opsonization in the bloodstream
CSF access through endothelium of Blood-brain barrier

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Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against colonization or mucosal invasion (stage 1)

Secretory IgA (IgA protease secretion)
Ciliary Activity (Ciliostasis)
Mucosal Epithelium (Adhesive pili)

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Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against intravascular survival (stage 2)

Complement (Evasion of alternative pathway by polysaccharide capsule)

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Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against Crossing of blood brain barrier (stage 3)

Cerebral endothelium (adhesive pili)

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Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against Survival within CSF (stage 4)

Poor opsonic activity (Bacterial replication)

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Meningitis - Infectious Disease

Pathogen Strategy: Immunoglobulin A (IgA)

Where does it come from? What is it? What does it do?

Produce dby plasma cells associated with mucosa
First line of defense
Opsonization
Primarily acs through exclusion, bindng, and crosslinking
Extensive glycosylation to prevent degredation by proteases

Not an inflammatory Ig

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Meningitis - Infectious Disease

Pathogen Strategy: Ciliostasis

Prevent movementof bacteria out of bronchial tubes
Attachment of bacteria to cilia impedes movements
Toxins - may damage axoneme or deplete ATP

Meningitis - Infectious Disease

Pathogen Strategy: Adhesive Pili

Pili bind non-ciliated mucosal cells allowing them to cross the epithelium and basement membrane

Infection occurs most easily in simple epithelia (Nasopharynx, intestines)

Meningitis - Infectious Disease

Pathogen Strategy: Bacterial Toxins: Exotoxins

Secreted by living bacteria
Highly antigenic (antitoxin neutralizes)
Highly Toxic (fatal in microgram quantities)
Usually do not induce fever
Usually bind to specific receptors

Meningitis - Infectious Disease

Pathogen Strategy: Bacterial Toxins: Endotoxins

Secreted when bacteria cells are killed
Weakly immunogenic
Toxic at 10-100s micrograms
Induce fever
no specific receptors

Part of cell wall then released

Parasitic Diseases

How do parasitic diseases cause damage?

Can be caused by single celled and multicellular organisms

Damage can be caused by consumption by parasite (parasite is consuming something the host organism needs)
Damage may actually result from immune response to parasite

Parasitic Diseases: Trichinosis

Trichinosis

What causes it? What does it do?

Obtained by ingestion of undercooked meat, usually pork
Infects skeletal muscle

Parasitic Diseases: Trichinosis

Symptoms of Trichinosis

Fever
Myalgia (muscle pain)
Periorbital edema

Parasitic Diseases: Trichinosis

Life Cycle of Trichinella spiralis

Adult in intestines produce larva
Larva infiltrate blood
Exit blood vessels in skeletal muscle
Adults die and muscle fiber calcifies

# Parasitic Diseases: Trichinosis Enteric Phase of Trichinosis

Strong immune response to larvae: T helper cells produce cytokines, Eosinophil and Mast cell activation Increases intestinal mobility: T helper cytokines, mast cell granules, expel larvae from gut in animal models Inflammatory response to larvae elsewhere can cause widespread destruction

# Parasitic Diseases: Trichinosis Muscle Phase of Trichinosis

Muscle cell is co-opted as a nurse Disruption of myofibrils Enlarged/central nuclei Collagen capsule formation

# Parasitic Diseases: Trichinosis Clinical Presentation of the Enteric Stage

Typical of enteric disease Diarrhea and nausea Vomiting, pain, low grade fever (immune response)

# Parasitic Diseases: Trichinosis Clinical Presentation of Muscle Stage

Typical of infection/muscle damage Myalgia and paralysis Fever, headache, skin rash Edema and conjuctivitis

# Integumentary Disorders What are the two types of disorders of the skin?

Growths: Cyst, Malformation, Begnin/malignant neoplasm Dermatitis (rashes): non-neoplastic

# Integumentary Disorders: Psoriasis Psoriasis

Inflammatory skin disease Scaling skin condition Reddness, swelling, edema

# Integumentary Disorders: Psoriasis Pathology of Psoriasis

Thickened epidermis (elngated rete ridges) Neutrophil infiltration Excessive epidermal proliferation (shortned cell cycle, 2X peoliferative population) Accmulation of nucleated cells in the stratum corneum (parakeratosis) Endothelial cell proliferation

# Integumentary Disorders: Psoriasis Pathogenesis of Psoriasis

Immunologic abnormalities: * T helper lymphocytes (MHCs) * cytokine overexpression (TNF, IFNy, IL-2) * Presence of unique dendritic cells * Genetic link to HLA-C * Sensitized T cells accumulate in epidermis (IFNy) * Can be induced by localized trauma

# Integumentary Disorders: Psoriasis What is the relationship between Angiogenesis and Psoriasis

Angiogenic facors can be found in psoriatic lesions TNFa TGFb IL8 VEGF

# Integumentary Disorders: Psoriasis VEGF

Released from keratinocutes Stimulate epidermal hyperplasia, vascular growth, leukocyte infiltration Regulates psoriatic keratinocyte activity

# Integumentary Disorders: Verrucae Verrucae (warts) | What causes it? What does it do?

Squamoproliferative Caused by HPV Generally regress (self limited) Virus transmitted by contact Viral typing can confirm if problematic infection (poor prognosis -> cancer)

# Integumentary Disorders: Verruca Verruca Pathology

Epidermal hyperplasia is uneven Cytoplasmic vacuolization (halos) Increased keratohyalin granules Eosinophilic keratin aggregates in cells

# Integumentary Disorders: Verruca Verruca Development

HPV viral proteisn in keratinocytes E6 of HPV may interfere with maturation

# Integumentary Disorders: Pemphigus Blisters | What are they

Acantholysis Dissolution of intercellular bridges ## Footnote Which ones determine where blister forms

# Integumentary Disorders: Pemphigus What are the three types of blisters?

Subcorneal: Suprabasal: Subepidermal:

# Integumentary Disorders: Pemphigus Pemphigus

Autoimmune formation of blisters Autoantibodies attack the intracellular junctions: inepidermis or mucosa

# Integumentary Disorders: Pemphigus Types of pemphigus

Foliaceus: subcornal lesion Vulgaris: suprabasal lesion Bullous Pemphigoid: subepidermial, nonacantholytic lesion ## Footnote Eosinophils, lymphocytes, and sometimes neutrophils seen in lesion