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major defenses against Tinea

*2-macroglobulin keratinase inhibitor, unsaturated transferrin*, epidermal desquamation, lymphocytes, macrophages, epidermal Langerhans cells, dermal dendritic cells, neutrophils and mast cells.
*CMI is the major defense against dematophytic infections and fungal infections in general*


Tinea office/lab tests

-Wood's lamp.
-KOH prep of hair, skin, or nail scrapings.(Cellufluor white aids in staining). Culture hair skin, or nail scrapings on Dermatophyte Test Medium or Sabouraud-glucose agar containing chloramphenicol and cycloheximide.
(when too deep to use Wood's lamp)


Tinea ddx: Infectious Etiology.

coalesced HSV lesions,
lyme borreliosis (erythema migrans),
secondary syphilitic lesions,
tuberculoid leprosy,
HPV coalesced papules (verruga vulgaris).


Tinea ddx: Papulosquamous diseases.

Pityriasis rosea (cause unknown thought to be a virus),
eczema (cause unknown but many patients are atopic),
psoriasis (cause unknown),
lichen planus (cause unknown but may be drug related),
urticaria (multiple causes), erythema multiforme (viral infections, e.g. HSV, and many drugs),
drug-induced eruptions, SLE, sarcoidosis, etc.


Tinea ointment/powder tx

Ointments at night, and powders by day include Whitfield's (salicylic acid and benzoic acid), sulfur, tolnaftate (Tinactin)R, DesenexR (undecylenic acid or zinc undecylenate), haloprogin, clotrimazole (Mycelex)R, griseofulvin, imidazole derivatives, naftin.


T. cruris ddx

1. Candidal intertrigo (Uniformly red, with no central clearing; satellite lesions)
2. Erythrasma (Uniformly brown and scaly, with no active edge; *fluoresces a brilliant coral red*)
3. Mechanical intertrigo (Sharp edge, no central clearing or scale)
4. Psoriasis (Silvery scale and sharp margination; pitted nails; knee, elbow, and scalp lesions)
5. Seborrheic dermatitis (Greasy scales; scalp (dandruff) and sternal involvement)


important anaerobes of mouth/oropharynx:

Treponema denticola, T. vincentii.
Porphyromonas sp:
Prevotella sp:
Fusobacterium nucleatum
Aggregatibacter (formerly Haemophilus, Actinobacillus)
Actinomyces israelii.
Lactobacillus sp
Bifidobacterium sp
Peptostreptococcus sp


NF of gastrointestinal tract:

*Bacteroides sp., especially Bacteroides fragilis*
*Bifidobacterium sp.*
Lactobacillus sp.
Clostridium perfringens, type A
*Clostridium difficile*
Enterococcus (E. faecalis, E. faecium)
Peptostreptococcus sp


NF of the adult female vagina:

Gardnerella vaginalis
Mobiluncus sp.
Bacteroides sp.
Lactobacillus sp
Clostridium perfringens, type A
Peptostreptococcus sp


NF of skin and cornea:

Propionibacterium acnes and other diphtheroids.
Streptococci (*Aerotolerant anaerobic*, G+ cocci in chains)
Enterococcus (*Aerotolerant anaerobic*, G+cocci in chains) Peptostreptococcus sp (*Obligate anaerobic*, G+ cocci in chains)


C. perfringens toxin:
Perfringolysin (Theta [θ/H] toxin):

In low concentrations causes:
-Priming and degranulation of PMNs.
-PMNs to increase production of adherence molecules (FYI e.g.,
integrins [CD11/CD18] FYI).
-Endothelial cells to produce platelet activating factor (PAF, a proinflammatory autocoid), which mediates adherence of PMNs to endothelial cells and alters vascular integrity (makes vessels leaky), relaxes tension of vascular walls.

In high concentrations, causes the complete lysis of RBCs, PMNs.


more trichinosis dx

-Bentonite flocculation test (CDC) - utilizes Ag bound to bentonite clay to determine Ab levels.
-Indirect fluorescent antibody test (IFA), latex agglutination test, ELISA/EIA to detect T. spiralis-specific antibodies during the 1st week of infection.

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