Antiparasitics, TB, Leprosy, Derm (Week 6) Flashcards
Treatment for visceral leishmaniasis
Liposomal amphotericin B
Sodium stibogluconate (pentavalent antimony)
Miltefosine
Paromomycin is alternative
Malaria prophylaxis
Chloroquine (where there are sensitive strains)
Mefloquine (Lariam)
Doxycycline
Atovaquone proguanil (Malarone)
Malaria treatment
Uncomplicated: atovaquone proguanil, artemether/lumafantrine (Coartem), artesunate (only available through CDC)
Also…? Quinine sulfate plus doxycycline or clindamycin (toxicity: cinchonism = flushing, tinnitus, confusion, cardiac conduction problems)
Severe malaria: quinidine gluconate IV, artesunate, plasma exchange in severe malaria, monitor vol status to avoid pulmonary edema due to capillary leak syndrome
Treatment for lice, scabies (ectoparasites)
Topical: permethrin, malathion
Systemic: ivermectin
Fever
Increased core temperature in response to infection, usually 1-4 C
Triggered by cytokine release (IL-1, IL-6, TNF-alpha, INF-beta, INF-gamma) and ultimately results in PGE2 production
Markers of inflammation
Erythrocyte sedimentation rate (ESR)
C-reactive protein
Ferritin
Quantitative IL-6
Causes of fever other than infection
Malignancy (“B symptoms”)
Collagen vascular diseases (auto-immune)
Drugs (malignant hyperthermia of anesthetics, neuroleptic malignant syndrome)
“Central fever” (head trauma with CNS blood, stroke)
Antipyretics
Acetaminophen (Tylenol), NSAIDs (block/reduce cytokine-activated increase in core temperature)
Cooling blankets, ice packs (external cooling measures)
What could be some causes of fever of unknown origin (FUO)?
Infection
Malignancy
Collagen vascular (auto-immune)
Other: PE, DVT, hematoma, drugs, Familial Mediterranean fever, factitious fever
Septicemia
Bacteremia (bacteria in blood) with clinical manifestations (fever, chills)
Systemic inflammatory response syndrome (SIRS)
Any two or more of:
1) T>38 or <36
2) HR > 90 bpm
3) Respiratory rate >20 or PaCO2 <32
4) WBC > 12,000/ul, <4,000/ul or >10% bands
Septic shock
SIRS plus hypotension even with adequate fluid resuscitation
Severe sepsis
Septic shock + end-organ dysfunction (renal, pulmonary, CNS, liver, impaired glucose metabolism)
Can have consumptive coagulopathy to disseminated intravascular coagulation (DIC)
Is sepsis just a hyperactivation of the immune system?
No
LPS (gram negative endotoxin) and cytokine storm are present, but may be some immunosuppression (hypoimmunity) as well (loss of delayed type hypersensitivity, inability to clear infection, increased susceptibility to nosocomial infection, apoptosis of CD4 T-cells/B-cells/DCs)
Pathophysiology of sepsis
Decreased tissue perfusion, oxygen delivery (decreased SVR, vasodilation)
Myocardial depression (even though total cardiac output increased, not enough to compensate for decreased SVR)
Increased leukocyte-endothelial interaction
Metabolic acidosis (frequently lactic acidosis from tissue ischemia)
DIC
Treatment for sepsis
Empiric antimicrobial therapy
Hemodynamic support (volume expansion, vasopressors)
Ventilatory support
Early goal-directed therapy (CVP, oxygenation, urine output)–> less organ dysfunction, less sudden circulatory collapse
Infectious disease history taking
Travel history
Social history (work, hobbies, pets, sick contacts)
Foodborne disease
Medical history (immunocompromise (diabetes, cancer chemotherapy, chronic corticosteroids, HIV), past infections/exposures (TB, histo), immunizations)
Papulosquamous rash
Scaly papules or plaques
What does it mean that papulosquamous rashes are raised and scaly?
Raised: inflammatory infiltration and swelling of dermis and/or epidermis; proliferative thickening of epidermis called “acanthosis” or “epidermal hyperplasia”
Scaly: thickening of stratum corneum is “hyperkeratosis”; defective maturation of epidermis called “parakeratosis” and is abnormal retention of keratinocyte nuclei in stratum corneum
Differential for an annular plaque
Dermatophyte
Granuloma annulare
Discoid lupus
Sarcoidosis
Pityriasis rosea (herald patch)
Erythema annulare centrifigum
Urticaria
Psoriasis
Chronic relapsing inflammatory skin disease
Pathogenesis: immune based disease involving T cells (Th1 and Th17), neutrophils, and epidermal hyperproliferation/dysmaturation
Primary lesion: erythematous plaques that are sharply demarcated, silvery scale, typically symmetrical
Treatments: topical, systemic, biologics
On extensor surfaces (elbows, knees)
Auspitz sign
Pinpoint bleeding upon removal of scale
Thinning of epidermal plate above capillaries is what causes this
Different clinical presentations of psoriasis
Plaque-type psoriasis: most common; scaly plaques
Inverse psoriasis: common in axilla, groin, umbilicus; no scale because wet; prone to secondary infection
Guttate psoriasis: scattered scaly papules; can be associated with strep infection
Erythrodermic psoriasis: diffusely red scaly skin; fluid and electrolyte imbalances
Pustular psoriasis: sudden onset of erythematous macules and papules with sterile pustules; fevers, chills, arthralgias, leukocytosis (lots of neutrophils); often seen after discontinuation of systemic glucocorticoids
Psoriatic arthritis
Seronegative spondyloarthropathy
Symmetrical polyarthritis, oligoarticular, DIP, arthritis mutilans, axial/spondyloarthritis
Sausage fingers
Enthesitis (inflammation at site of tendon insertion into bone)
Exacerbating factors of psoriasis
Medications: lithium, beta-blockers, anti-malarials, indomethacin, quinidine, interferon
Withdrawal of systemic steroids
Infection/stress
Physical trauma to skin (Koebner phenomenon)
Diseases associated with psoriasis
Depression
Alcoholism
Diabetes
MI
Stroke
Treatment of psoriasis
Localized disease: topical: steroids, calcineurin inhibitors, vitamin D analogues (calcipotriene), retinoids (tazarotene), tar, anthralin, keratolytics (salicylic acid), emollients
Generalized disease: phototherapy, retinoids (acitretin), methotrexate, cyclosporine, tacrolimus, hydroxyurea, 6-thioguanine, anti-TNF, biologic therapy
Biologic therapies
Anti-TNFalpha therapies: adalimumab, golimumab, etanercept, infliximab
Anti CD-2 therapy: alefacept
Anti-IL 12/23 therapy: ustekinumab
Pityriasis rosea
Acute, self-limited (6-8 weeks) exanthematous skin disease (Christmas tree distribution)
Slighly inflammatory, oval, papulosquamous lesions (scaly papules and plaques) on the trunk and proximal areas of extremities
“Herald patch” is annular plaque that precedes eruption
Mistaken for tinea corporis
Presumed viral etiology (HHV6 or UUV7)
Treatment: none, topical steroids, UV, erythromycin
Pityriasis (tinea) versicolor
Dyschromic (hyper/hypopigmented) macules or papules with fine scale, often on trunk and proximal extremities
Pathophysiology: overgrowth of M. furfur (pityrosporum) with minimal inflammation and production of dicarboxylic acid moiety that interacts with melanin synthesis pathway
Treatment: topical selenium sulfide, topical ketoconazole, oral ketoconazole; may resolve over months
Eczema and dermatitis
Synonyms!
Descriptive, and not a diagnosis
Broad range of conditions that begin as spongiosis and may progress to lichenified stage
Types of dermatitis
Contact dermatitis
Seborrheic dermatitis
Stasis dermatitis
Atopic dermatitis
Nummular dermatitis
Nummular dermatitis
AKA nummular eczema, discoid eczema
Very itchy, coin-shaped scaly plaque sometimes with crusts or vesicles on extremities
Treatment: emollients and topical anti-inflammatories
Atopy
Hereditary tendency to develop allergies to food and inhalant substances and in general to develop over-reactive epithelial surfaces
Atopic dermatitis
Chronic, itchy eczema associated with personal or family history of atopy
Itching often precedes appearance of lesions and get into vicious itch-scratch cycle
Pathophysiology: skin is hypersensitive; langerhans cells directly stimulate T cells without presence of antigen; Th2 response
Usually starts after age 2 months, and most who will have it get it by age 5
Treatment: topical steroids, antibiotics or systemic medications depending on severity
Atopic dermatitis and family history
Affected families may have asthma, allergic rhinitis (hay fever) as well
If one parent atopic, more than half of their children will have allergic symptoms by age 2
Associated with defective skin barrier, in many cases in conjunction with mutations in FLG gene (codes filaggrin, key constituent of cornified cell envelove essential for skin barrier function)
Tendency to Th2 driven immunity
Exacerbations/triggers for atopic dermatitis
Food allergies
Skin infections
Irritating clothes or chemicals
Heat or cold (sweating causes itching)
Dry skin (overbathing)
Staph aureus
Itch-scratch (treat with antihistamines)
Stages of atopic dermatitis
Infantile (2mo - 2 years): head, diaper area, flexor and extensor surfaces; central face spared = headlight sign; ill-marginated scaly plaques, excoriations
Childhood (2 - 10 years): antecubital fossae, popliteal fossae, face, neck, upper chest
Adult: antecubital fossae, popliteal fossae, face, neck, upper chest
Associated findings with atopic dermatitis
Infra-orbital folds (Dennie-Morgan lines)
Hyperlinearity of palms
Lichen simplex chronicus
Labs to diagnose atopic dermatitis
Elevated IgE
Elevated eosinophils
How to treat atopic dermatitis flares
Topical steroids (stronger if worse disease or thicker skin)
Antibiotics if evidence of impetiginization (weey, crusted, doesn’t have to be cellulitis)
Systemic medications if severe (cyclosporine, azathioprine, mycophenolate mofetil, methotrexate, PUVA, nbUVB)
3 topical steroids to know
Low: desonide 0.05% (mild problems or face/axilla/groin)
Medium: triamcinolone 0.1% (workhorse for most dermatitis, but avoid on face or prolonged on groin/axilla)
High: fluocinonide 0.05% (for contact dermatitis, psoriasis, lichenified eczema, but avoid face/groin/axilla prolonged use)
Side effects of potent topical corticosteroids
Atrophy of skin
Telangiectasias
Striae
Acneiform eruption
Rosacea-like dermatitis
Exacerbation of periorificial dermatitis
Pruitus
Hypopigmentation
Cataracts/glaucoma (controversial)
Adrenal suppression
Cushingoid syndrome (moon facies, buffalo hump, truncal obesity, hypertension)
Exacerbation of some infections, dermatophytosis
Topical tacrolimus and pimecrolimus
Topical calcineurin inhibitors
Inhibit inflammation by preventing cytokine release
Weaker than steroids
Put patient on topical steroid first, then transition over
Don’t use in kids
What kind of skin condition gets superinfected?
Atopic dermatitis gets frequently superinfected (because decreased antimicrobial peptide production)
Psoriasis does not get superinfected (because increased antimicrobial peptide production)
Seborrheic dermatitis
Erythematous plaque with greasy scale
Prefers scalp, eyebrows, eyelids, nasolabial folds, ears but can also involve sternal area, axilla, umbilicus, groin, gluteal crease
Dandruff = mild seborrheic dermatitis
M. furfur/pityrosporum overgrowth plays a role
Associated with HIV, Parkinson’s
Can overlap with psoriasis (seboprosiasis)
Treatment: mild steroids, topical antifungals, selenium sulfide, zinc pyrithione
Contact dermatitis
Allergic contact dermatitis, or irritant contact dermatitis
Something from the outside get onto your skin
Blister beetles, poison oak, OTC antifungal, topical 5-FU, lip-licking
Can you use short course of oral steroids for skin disease?
No, never <10 days of oral steroids for skin disease!
Hints for differentiating papulosquamous diseases
Early childhood onset –> atopic dermatitis
Very itchy –> atopic dermatitis, other eczema, contact
Burning/stinging –> irritant contact dermatitis
“Outside job” shapes –> contact dermatitis
Psoriasis has better demarcated plaques than eczema
“Christmas tree” –> pitryiasis rosea
Seborrheic dermatitis –> typical locations and scale
What should you do if you’re not sure if it’s dermatitis or dermatophyte?
Treat dermatitis first (steroid) and schedule patient back
If steroid doesn’t help, then do KOH or culture fo dermatophyte (which you can then treat with antifungal)
Symptoms and findings with primary infection with tuberculosis
Symptoms: fever, fatigue, chest discomfort
CXR: hilar adenopathy, transient infiltrates, pleural effusion
PPD not positive until 1-3 months after primary infection!
With TB, will you always see acid fast bacilli (AFB; M. tuberculosis) on sputum sample?
No, sometimes won’t see the actual organism
But if you see caseating granuloma or multinucleated giant cell (Langerhans cell), can diagnose TB anyway!
Ghon complex
Seen in tuberculosis
Calcified pulmonary tubercle + hilar lymph node
Pathogenesis of active tuberculosis
Usually due to reactivation of primary infection (which was probably asymptomatic)
Cough, hemoptysis, fever, night sweats, weight loss
Slow onset
Focal or widespread pneumonia (upper lobes, apex of lower lobes in reactivation), pulmonary nodules, caseation/liquefaction/cavitation, bronchogenic spread
Pleural involvement (empyema, pneumothorax, bronchopleural fistula)
Disseminated disease (Miliary tuberculosis, Pott’s disease, scrofula)
Other sites affected by TB
Reactivation of extrapulmonary tubercles or dissemination from lung can cause:
Pott’s disease: vertebral bodies
Scrofula: lymph nodes
Kidneys, GI, pericarditis, CNS
How do you tell Pott’s disease from staph aureus infection?
TB goes to vertebral body itself and not discs
S. aureus arises in disc then travels to 2 adjacent vertebral bodies
What means you will be more contagious?
Infection in lungs, airways, larynx
AFB positive sputum (increased burden of organisms)
Cavitary disease (higher number of bacteria, easier to transmit)
Reading PPD test
Test positive at >5mm induration: HIV +, recent contact of TB, patients with fibrotic changes on chest radiograph, patients with organ transplant/immunocompromise
Test positive at >10mm induration: recent arrival from high-prevalence countries, IV drug users, medical pesonnel, mycobacteriology lab personel, patients with clinical conditions that place them at high risk (silicosis, diabetes, renal failure, cancer, gastrectomy), children <4 or those exposed to adults in high-risk categories
Test positive at >15mm induration: no known risk factors for TB
How would you get a false positive or false negative on PPD?
False positive: had BCG vaccine within 5 years; non-tuberculous mycobacterial infection
False negative (anergy): other recent overwhelming infection, recent live virus vaccination, under 6 months old, HIV, immunosuppression
Booster phenomenon
Some people with latent infection may have negative PPD when tested years after primary infection, but that initial skin test will stimulate (boost) ability to react to tuberculin so SECOND skin test is then positive
This does NOT indicate new infection, just that first PPD was false negative!
Two step testing
Use this for initial skin testing of adults who will be retested periodically (health care workers)
If first test positive then person is infected (duh)
If first test negative, perform second test 1-3 weeks later –> if second test positive, consider person infected but if second test negative consider person uninfected
Anti-TB drugs
INH-SPIRE (or RIPE)
Isoniazid (INH)
Streptomycin (injected)
Pyrazinamide
Rifampin
Ethambutol
Second-line (just for MDR strains): paramino salacylic acid (PAS), ethionamide, cycloserine, capreomycin
New drug: rifapentine
How to treat TB
Use multiple drugs (INH-SPIRE)
As bacteria decrease, can decrease number of drugs
NEVER add single drug to failing regimen
Failure usually due to non-adherence
Patient isolation until non-infectious on treatment (respiratory AFB smear-negative)
Initial phase with RIPE drugs daily for 2 months; continuation phase with Isoniazid and rifampin daily for 4 months (longer in compromised hosts/disseminated disease)
Multidrug resistant TB
Multidrug resistant (MDR): resistant to isoniazid and rifampin
Extensive drug resistant (XDR): MDR also resistant to at least 3 of 6 second line drugs
TB drug toxicities
Isoniazid: hepatotoxicity, neuropathy
Rifampin: hepatotoxicity, orange discoloration or urine, contact lenses (all secretions), drug interactions
Ethambutol: optic neuritis
Non-tuberculous mycobacteria
M avium intracellulare (MAI, MAC): infections look like TB, but arise in AIDS patients at end stage disease
M. abscessus (local disease or dissemination in immunosuppression)
M. chelonae (other pulmonary disease)
M. fortuitum (other pulmonary disease)
M. kansasii (environmental, pulmonary disease similar to TB)
M. marinum (in fish tanks, local infection of soft tissue, lymphatics)
M. leprae
M. bovis (ingestion of contaminated milk, causes GI tuberculosis or pulmonary similar to TB if inhaled)
Mycobacterium avium complex (Mycobacterium avium-intracellulare)
Similar clinical presentation to TB, but usually in AIDS patients at end stage disease
Causes chronic lung disease (bronchiectasis), cavitary nodular disease
Disseminated disease in AIDS/immunosuppression (fever, night sweats, severe weight loss, diarrhea, bone marrow infiltration)
ESKAPE bacteria
Bacteria that have become very antibiotic resistant
Enterococcus (VRE)
Staphylococcus aureus (MRSA)
Klebsiella
Acinetobacter
Pseudomonas
ESBL (E. coli, Enterobacter; resistant to all oral agents)
Note: gram - are the biggest problem–we have no drugs for ESBL and very few drugs for others!
What drug do we use to treat very drug resistant gram - bacteria?
Colistin
Lots of toxicities (nephrotoxicity) so stopped using in 1960’s but had to start using it again once bacteria started becoming so resistant
Reasons why we’re not making good, new antibiotics
1) Science: difficult to do
2) Economics: not good investment ($-50 million)
3) Regulatory: R&D too risky/expensive
The non-inferiority problem of RCTs for antibiotics
In order to prove efficacy in RCT by non-inferiority, need previous RCTs of older drugs
However, older drugs are SO old that they didn’t have RCTs back then so there never were and never will be RCTs for older antibiotics!
Why is the bacterial capsule anti-phagocytic?
1) Some capsules are rich in sialic acid, which has an affinity for serum protein H, which is a complement regulatory protein that leads to degradation of opsonin C3b (by factor I and formation of C3 convertase)
2) Some capsules cover C3b that does bind to bacterial surface (so prevent C3b from binding its receptor on phagocytes)
Why are splenectomized patients at risk for bacteremia by encapsulated organisms?
Because spleen removes opsonized bacteria (and senescent RBCs and antibody-coated cells) from the blood stream
If no spleen, will still have encapsulated (though opsonized?) bacteria in the blood stream
Tuberculoid vs. lepromatous leprosy
Tuberculoid leprosy: person has good strong immune response; granuloma forms and limits spread of microorganism; localized damage to superficial nerves and skin; thickened (palpable) nerves; hypopigmented/hairless lesions; elevated, sharply defined plaques, decreased sensitivity to sharp/dull and hot/cold; multi-nucleated giant cells; acid fast stain is negative
Lepromatous leprosy: person has weak immune response; host cannot contain microorganism; inflammatory damage at cooler skin, nerves, testes, sensory loss at face/extremities; get secondary infections/burns; lose eyebrows, saddle-nose deformity, leonine facies, infertility; disseminated nodules; foamy macrophages and few lymphocytes; many bacilli on acid fast stain
Why do you lose hair in leprosy?
Nerve innervating hair follicle is infected with mycobacterium leprae and causes hair to fall off
How is leprosy transmitted?
Human to human via nasal discharge
From armadillos!
Acne
Caused by propionibacterium acnes, which is normal bacterial commensal
Important childhood exanthems
Rubeola
Scarlet fever
Rubella (German measles)
Erythema infectiosum (fifth disease)
Roseola
Hand-Foot and Mouth Disease
Varicella
What causes the inflammatory response that produces the exanthem?
Not yet known!
Possibly:
1) Direct invasion of blood vessel walls by virus
2) Immune complex deposition
3) Cell-mediated immune responses
Measles (Rubeola)
Downward progression from face, and resolves in that order too
Becomes confluent on face
Koplik’s spots on buccal mucosa
Subacute sclerosing panencephalitis causes personality changes (very rare)
Scarlet fever
Group A strep (beta-hemolytic)
White strawberry tongue then red strawberry tongue
Enanthem (inside) of palatal petechiae, bright red oropharynx
Sandpaper-like fine papules
Pastia’s lines (flexular accentuation with petechiae)
Desquamation
Rubella (German Measles)
Enanthem during prodrome (Forschheimer’s spots)
Downward spread from face
Erythema infectiosum (fifth disease)
Slapped cheeks
Lacy, reticulated pattern of erythema on trunk and extremities
No enanthem
In adults can cause arthritis
In pregnant women can cause hydrops fetalis
Roseola infantum (HHV6)
Enanthem of erythema of soft palate and oropharynx
Febrile seizures
Hand foot and mouth disease
Coxsackie A16 virus
Enanthem of small vesicles and erosions on gingivae, lingual and buccal mucosae–painful!
Gray-white vesicles on hands, feet, butt
Varicella (chicken pox)
Enanthem of mucosal vesicles and erosions
Exanthem occurs in crops (macules to papules to vesicles to pustules to crusts)
Begins on trunk
Verrucae (warts)
HPV
Verrucae vulgaris (3D warts)
Verruca plana (flat warts)
Verruca plantaris (on soles of feet)
How do arthropods (insects) cause disease?
1) Direct, nonallergic local tissue damage (stings, bites, tissue invasion)
2) Allergic reactions (papular urticaria) to secretions, skins, scales
3) Producing systemic toxicity
4) Transmitting disease (malaria, other parasites)
Clinical presentation of scabies
Primary lesion (burrows) about half a centimeter long, pinkish
Involves interdigital spaces, flexular aspect of wrists, axillae, waist, ankles, feet, butt, belt area
Nodules, pustules, papules, crusted plaques
Erythematous scaly plaque in diaper distribution
Intense pruitus accentuated at night and exacerbated by hot bath or shower
Can get secondary bacterial infections with group A strep pyogenes and S. aureus
Scabies
Sarcoptes scabei, variety hominis
Female mite burrows in epidermis, takes blood meal and lays eggs which hatch and propagate infestation
Transmission from CLOSE skin to skin contact
If scabies mites are only found in a few places, what causes systemic immune response (papules everywhere)?
Poop (scabela) from scabies mite causes immune response
Crusted scabies
AKA Norwegian scabies
In immunocompromised (HIV, elderly, transplant)
Lesions are hyperkeratotic, crusted, cover large areas
Marked scaline
Sometimes no pruitis
Tons of mites and eggs in these lesions!
Treatment for scabies
Wash bed linens, clothing in hot water
Permethrin (Elimite) 5% cream
Sulfur in petrolatum 10% concentration
Ivermectin
Permethrin kills adults but not eggs so must treat now and one week later to kill eggs that have hatched after 1 week
All family members and close contacts must receive treatment too
Myiasis
Infestation of skin by larvae of botfly (Dermatobia hominis), or just any larvae in open wound
Cutaneous larva migrans
Caused by Ancylostoma braziliense or caninum (cat and dog hookworms)
Infection caused by walking/laying on ground contaminated with feces
Skin lesions are serpiginous and very itchy
Treat with topical tiabendazole
Tungiasis
Female flea in skin is full of eggs and train of poop coming out of skin
Treat by anesthetizing and gauging it out
Pediculosis capitis (head lice)
Live on hairs of head and feed on scalp
Female lays 300 eggs in 30 day life cycle
Causes itchy scalp and see eggs (nits) in the hair
Treat with permethrin cream rinse 1%, lindane shampoo 1%, or if resistant: malathion, ivermectin
Pediculosis corporis (body lice)
Pruitus and excoriations
Body lice are vectors (via their poop!) for trench fever (bartonella quintana) and epidemic typhus (rickettsia prowazekii)
Pediculosis pubis (crab lice)
STD, but occasional transmission via fomites
Infestation of pubic hair, mustache, axillae, eyelashes, eyebrows (coarse hairs)
Maculae coeruleae (gray to bluish macules 1cm in size)
Papular urticaria
Very general term, but refers to bug bites
Erythematous papule, very pruitic, excoriated
Can be seen in linear groups of 3 (breakfast, lunch, dinner)
Bedbugs
Cimex lectularius
Bites in lines of 3 (breakfast, lunch and dinner)
Treat with topical steroids
Allergic reactions to insect stings
Bee, hornet, wasp have melittin (protein) antigen in venom that causes degranulation of basophils and mast cells releasing histamine, Phospholipase A, hyaluronidase
Normal reaction: itch and pain for hours
Severe local reaction: itch and pain + swelling
Toxic reaction: >10 stings, headache, fever, GI symptoms
Anaphylactic reaction: urticaria, bronchospasm, hypotension (will carry epinephrine pen)
Brown recluse spider
Loxosceles reclusa
Characteristic violin-case pattern on cephalothorax
Venom contains sphingomyelinase D
Bite is not very painful
Erythema with central ischemia then surrounding edema, necrosis, can lead to fever, DIC, shock
Treatment: prednisone, dapsone, surgical excision
Black widow spider
Latrodectus mactans
Red hourglass on underside of abdomen
Venom contains alpha latrotoxin (neurotoxin that depolarizes neurons and stimulates uncontrolled exocytosis of NTs)
Abdominal rigidity, muscle cramps
Treatment: antivenom, IV calcium gluconate, muscle relaxants
