Pod: Skin Infections

Front 1

How does normal skin keep organisms from invading the body?

Back 1

1. low pH: 5~6 (priopionibacterium spp near sebaceous areas)
2. cooler temperature
3. dryness, lipids
4. high salt concentration
5. desquamation

Front 2

Why do axilla, groin, and web of toes contain much higher organism load than back of forearms?

Back 2

moisture

Front 3

What are some normal flora of dry skin?

Back 3

1. staphylococcus epidermidis
2. anaerobic GNC
3. corynebacterium spp
4. propionibacterium spp in sebaceous areas(contribute to low pH of dry skin)

Front 4

What are some normal flora in axilla, groin, and web of toes?

Back 4

1. falcutative anaerobic GNR
2. strict anaerobic GNR

Front 5

How does moiture help organism penetrate intact skin?

Back 5

allow skin maceration and breakdown of stratum corneum

Front 6

What are some factors that aid in skin invasion?

Back 6

1. moisture
2. trauma
3. compromise to blood supply (peripheral vascular disease): tissue necrosis

Front 7

What is the most common factor that predispose for skin invasion?

Back 7

Trauma
1. mild: torn hangnail
2. major: gunshot, wound, burns, catheters, nosocomial.

Front 8

The following are associated with infection of which layer of the skin or tissue:
1. impertigo
2. erysipelas
3. cellulitis
4. folliculitis
5. fasciitis
6. gangreen

Back 8

1. epidermis
2. dermal lymphatics
3. subcutaneous tissue
4. hair follicles
5. superficial fascia
6. tissue death: myonecrosis

Front 9

What are abscesses(content)? Give 3 examples of skin abcesses.

Back 9

Abscess:walled off infected site containing necrotic WBC(neutrophils) and bacteria. Capsule is made of fibrin.
1. folliculitis: superficial
2. furuncles: enlarged follicular abscess
2. carbuncles: cluster of furuncles. deep subcutaneous spread

Front 10

What is the most severe form of gangreen?

Back 10

myonecrosis: invasion of organisms into healthy muscle tussue.

Front 11

Organisms can enter from outside via cuts, wounds, etc. How does organisms enter from inside?

Back 11

1. direct extension
2. hematogenously (via blood)

Front 12

What are some clinical manifestations involved in skin infection caused by organisms that enter from inside?

Back 12

1. abscess
2. necrosis
3. exanthem(rash): common with viruses. ex. measles, rubella, chicken pox, RMSF.

Front 13

The skin manifestion of bacterial infection is caused by____.

Back 13

bacterial toxins

Front 14

What are some characteristics of Staphylococcus aureus?
1. Gram stain
2. catalase + or -
3. coagulase + or -
4. intra or extracellular
5. aerobe ot anaerobe
6. does it form spores

Back 14

1. GPC in clusters
2. catalase +
3. coagulase +
4. extracellualr
5. facultative anaerobe
6. non-spore forming

Front 15

What test can be used to distinguish staph from strep?

Back 15

catalase test:
+: staph
-: strep

Front 16

What's the function of catalase?

Back 16

convert H2O2 to water and oxygen.

Front 17

Staphylococcus aureus is resistant to:
A. drying
B. heating
C. high salt
D. all the above

Back 17

D.

Front 18

Where is staph aureus usually found?

Back 18

1. nose: primary
2. skin
3. vagina: mostly post-menopausal women
4. feces, perineum

Front 19

How does staph aureus colonize? (molecules that aid in binding)

Back 19

1. clumping factor(bound coagulase): bind to fibrinogen at 3 different locations
2. produce slime (biofilm) to adnere to tissue and devices
3. able to stimulate uptake in nonprofessional phagocytic cells via receptor mediated endocytosis.

Front 20

T/F: Patients who are carriers of staph aureus and are on hemodialysis or paritoneal dialysis are more likely to develop infection.

Back 20

T.

Front 21

How does staph aureus spread?

Back 21

1. nose to hand contact
2. respiratory droplet
3. contaminated fomites

Front 22

What are some molecules in staph aureus that can trigger body's immune response?

Back 22

1. peptidoglycans, teichoic acid: alternative complement pathway, aggregate PMNs
2. protein A: alternative complement pathway, aggregate PMNs

Front 23

How does staph aureus survive body's immune response?

Back 23

1. capsule: avoid phagosytosis: not absolutely required for virulence
2. protein A: bind to Fc region of IgG. can still activate alternative complement pathway
3. catalase: reduce effects of PMN oxidative burst
4. coagulase: form fibrin clots that impedes PMNs
5. hemolysin: lyse RBC to free iron for organism's metabolism
6. Panton-Valentine Leukocidin: kill PMNs by forming pores in their membranes.

Front 24

What are some factors that impedes PMN's function in combating against Staph aureus?

Back 24

1. catalase:reduce oxidative burst of PMNs
2. coagulase: wall off PMNs by forming fibrin capsules.
3. Panton-Valentine Leukocidin: form pores in membranes of PMNs.

Front 25

What are some factors that impedes antibodies' function in combating against Staph aureus?

Back 25

Protein A: binds Fc of IgG

Front 26

What are some enzymes produced by staph aureus that aid in spreading?

Back 26

1. hyaluronidase: spread along tissue planes
2. staphylokinase: release organisms caught in fibrin clots
3. lipase/phospholipase: impair granulocyte formation

Front 27

What are the 2 toxins produced by staph aureus that cause tissue damage?

Back 27

1. exfoliative toxin(serine protease): cause scalded skin syndrome.
2. cytotoxin α, Panton-Valentine Leukocidin: pore forming toxins. Form abscesses, desctruct tissues.

Front 28

What are the 2 superantigens produced by staph aureus that cause systemic problems such as shock and symtoms of food poisoning?

Back 28

1. toxic shock toxin (superantigen): activate T cells and cause shock and death.
2. enterotoxin(superantigen):release inflammatory mediators from mast cells. cause intestinal peristalsis, food poisoning.

Front 29

What is agr?

Back 29

Accessory gene regulation: main regulation of virulence factors of staph aureus.

Front 30

Is staph aureus virulent if agr is absent?

Back 30

No.

Front 31

What is the major immune reponse that battle against staph aureus infection?

Back 31

PMNs.
People who are deficient in PMNs will suffer from severe staph aureus infection.

Front 32

What are the clinical manifestations of staph aureus infecitons?

Back 32

1. folliculitis, furuncles, carbuncles(systemic)
2.impertigo
3. post surgical wound infection: edema, pain, pus.
3. cellulitis(periorbital), lymphangitis, abscess
4. staphylococcal scalded skin syndrome(SSSS): exfolitin toxin.
5. Toxic shock syndrom (TSS): found in persons lacking antibodies to TSST. Menstrual TSS related to tampons usage.
6. infection following sytemic spread: bacteremia, endicarditis, septic arthritis, pneumonia.
7. food poisoning: enterotoxin.

Front 33

The leading cause of endocarditis in IV drug users is ______.

Back 33

staph aureus

Front 34

What is the leading cause of septic arthritis?

Back 34

staph aureus

Front 35

What are some specific findings indicative of toxic shock toxin produced by staph aureus?

Back 35

1. sunburn rash: erythematous, deep red.
2. diarrhea, vomiting, hypotension.

Front 36

Why is staphylococcal food poisoning so easily developed after ingest contaminated food?

Back 36

Enterotoxin produced are resistant to heat, gastric acid, and jejunal enzymes.

Front 37

Is there a vaccine for staph aureus? What is the target?

Back 37

Yes, although not very effective. It targets the capsule, showed benefit in dialysis patients.

Front 38

How does Staph epidermidis compansate for its absent coagulase?

Back 38

produce thick exopolysaccharide slime: adhere to devices, protect from PMNs and antibodies.

Front 39

Why do only 10% people infected with Staph aureus develop TSS?

Back 39

90% people do have antibodies against TSST.

Front 40

T/F: Staph aureus infection is mostly likely associated with foreign bodies and treatment involves removal of the foreign materials.

Back 40

F. Staph epidermitis is.

Front 41

What is the common cause of UTI in young sexually active women?

Back 41

Staph saprophyticus

Front 42

How to diagnose staph infections?

Back 42

1. Gram stain:GPC in clusters
2. culture: β-hemolytic, MAC selective agar

Front 43

Can staph aureus be distinguished from staph epidermidis on gram stain? If not, what test can be used to distinguish them?

Back 43

No.
Coagulase test.

Front 44

What tests other than gram stain and culture of staph should be performed in an outbreak situation?

Back 44

genetic typing: pulse-field electrophoresis/ PCR.

Front 45

How to treat staph aureus infection?

Back 45

1. drain abscess
2. vancomycin, linezolid, daptomycin, trimethoprim/sulfa

Front 46

What is the resistance of staph aureus against penicillin? Which gene is involved?

Back 46

1. MecA gene: altered PBP that has poor affinity for β-lactams.
2. MRSA carried with MecA gene(hospital acquired).

Front 47

Why is CA-MRSA more virulent?

Back 47

acquired Pantom-Valentine Leukocidin gene: take out PMNs.

Front 48

How do you prevent staph aureus infections?

Back 48

1. eliminate carrier: in some states
2. handwashing.

Front 49

Where are bacteroides fragilis found in the body? What is its morphology?

Back 49

intestinal flora, female genital tract.
anaerobic GNB

Front 50

Where are fusobacterium sp found in the body? What is its morphology?

Back 50

oral cavity, intestines, female genital tract.
anaerobic GNB

Front 51

Where are prevotella sp found in the body? What is its morphology?

Back 51

oral cavity, intestines, female genital tract.
anaerobic GNB

Front 52

Where are peptostreptococcus sp found in the body? What is its morphology?

Back 52

oral cavity, intestines, female genital tract.
anaerobic GPC

Front 53

Where are clostridium sp found in the body? What is its morphology?

Back 53

GI tract.
anaerobic GPR

Front 54

What are some significant pathogens of skin and soft tissue that are anaerobic?

Back 54

Staph aureus
Bacteroides fragilis
Fusobacterium sp
Prevotella sp
peptostreptococcus sp
clostridium sp

Front 55

Aspiration of oral anaerobe may result in ______.

Back 55

pneumonia or lung abscess.

Front 56

How does anaerobic organism cause intraabdominal infections such as peritonitis?

Back 56

Inoculation of fecal flora into sterile site like the -peritoneum.

Front 57

What are some ways that anaerobes infect skin and soft tissue?

Back 57

1. aspiration of oral anaerobes and cause pneumonia or lung abscess.
2. innoculation of fecal flora into sterile sites like the peritoneum and cause peritonitis.

Front 58

Can anaerobes be recovered in urine, CNS, and acute respiratory infections?

Back 58

No.

Front 59

Which of the following are found in the intestine?
A. bacteroides fragilis
B. fusobacterium sp
C. prevotella sp
D. peptostreptococcus sp
E. clostridium sp

Back 59

A.B.C.D.E.

Front 60

Which of the following are found in the oral cavity?
A. bacteroides fragilis
B. fusobacterium sp
C. prevotella sp
D. peptostreptococcus sp
E. clostridium sp

Back 60

B.C.D.

Front 61

Which of the following are found in the ffemale genitial tract?
A. bacteroides fragilis
B. fusobacterium sp
C. prevotella sp
D. peptostreptococcus sp
E. clostridium sp

Back 61

A.B.C.D.

Front 62

What is the significance of finding Clostridium septicum in the blood?

Back 62

malignancy (ie colon cancer)

Front 63

What are some clues of anaerobic infection?

Back 63

1. foul odor to discharge: volitile short-chain fatty acides and amines.
2. no growth in culture
3. mixed morphology in stain
4. tissue necrosis, abscess or gangreen.
5. infection secondary to human or insect bite.

Front 64

What kind of organism will you suspect when you find foul odor to discharge?

Back 64

anaerobes

Front 65

What kind of organism will you suspect when you see mixed morphologies on gram stain?

Back 65

anaerobes

Front 66

What kind of organism will you suspect when the patient is bitten by an animal or another human?

Back 66

anaerobes

Front 67

What kind of organism will you suspect when you see tissue necrosis, abscess, or gangrene on skin and soft tissue?

Back 67

anaerobes

Front 68

How to culture anaerobes?

Back 68

1. avoid collection of normal mucosal anaerobes.
2. avoid swabs
3. transport ASAP n anaerobic device to avoid oxygen

Front 69

How do you treat infection caused by anaerobes?

Back 69

1. drain abscesses, debridment of necrotic tissue.
2. use penicillin to suscepticble species.
3. use ampicillin/sulbactam, imipenem, metronidazole to organisms that produce β-lactamase.

Front 70

Which of the following organism produce β-lactamase?
A. Bacteroides fragilis.
B. Fusobacterium sp.
C. Prevotella sp.
D. Peptostreptococcus sp.
E. Clostridium sp.

Back 70

A.

Front 71

Which of the following organism do you suspect when bowl flora may be the source of infection?
A. Bacteroides fragilis.
B. Fusobacterium sp.
C. Prevotella sp.
D. Peptostreptococcus sp.
E. Clostridium sp.

Back 71

A.

Front 72

Describe the pathogenesis of bacteroides fragilis.

Back 72

1. introduction of bowl flora to sterile sites by perforation, trauma, surgery.
2. proliferation of aerobes that reduces O2 content
3. proliferation of anaerobes: adhesins, antiphagocytic capsule, short-chain fatty acids (antiphagocytic), desctructive enzymes.
4. form abscesses

Front 73

What are the virulences factors of bacteroides fragilis?

Back 73

1. adhesin: adhere to peritoneal surface.
2. capsule: antiphagocytic
3. short-chain fatty acids: antiphagocytic
4. destructive enzymes: tissue destruction, abscesses.

Front 74

What is the gram stain for clostridium perfringens?

Back 74

GPB, "boxcar appearance"

Front 75

Does clostridium perfringens produce spores?

Back 75

Yes. Spores are found in soil.

Front 76

What is the byproduct of clostridium perfringens anaerobic fermentation?

Back 76

Gas

Front 77

Describe the pathogenesis of clostridium perfringens.

Back 77

1. organism introduced into wounds.
2. spores germinate, replicate(every 8-10min), produce toxins, allow invasion.
3. hypotension, systemic signs.

Front 78

What is the major toxin that clostridium perfringens produce?

Back 78

α-toxin (lecithinase):
-attack all kinds of cells.
-split lecithin
-damage RBC, WBC, platlets, endothelial cells.
-cause hemolysis, platlet destruction, capillary damage, tissue necrosis, shock.

Front 79

What organism has a "boxcar appearance" on a gram stain?

Back 79

clostridium perfringens

Front 80

Why is α-toxin produced by clostridium porefringens so deadly?

Back 80

It splits lecithin which exists in all our cell membranes.

Front 81

What organism is often part of polymicrobial flora in infections such as wound infections, perirectal abscess, diabetic foot, and decubitus ulcers?

Back 81

clostridium perfringens

Front 82

What are some clinical manifestations of clostridium perfringens?

Back 82

1. crepitant cellulits: accompanied by gas in tissue.
2. fasciitis, suppurative myositis
3. myonecrosis(gas gangrene).
4. food poisoning.

Front 83

What is the name of this syptom?
Muscle necrosis and systemic toxicity.
Sudden onset and unrelenting pain.
Skin progress to magenta or bronze discoloration, hemorrhagic bullae.
Crepitus may be present.
No pus, but thin serosanguinous discharge.

Back 83

myonecrosis caused by α-toxin produced in clostridium perfringens.

Front 84

How to diagnose clostridium perfringens?

Back 84

1. clinical findings, tissue findings
2. gram stain: Boxcar, no neutrophils
3. double zone hemolysis on blood agar. Partial outer zone: α-toxin. complete inner zone: theta toxin.

Front 85

What is this organism?
Cause muscle necrosis and serious systemic hemolysis.
When plated in blood agar, show double zone hemolysis.

Back 85

colstridium perfringens

Front 86

Why is infection of clostridium perfringens so deadly?

Back 86

1. fast growing (8-10 min cycle)
2. toxins: α-toxin (lecithinase), lyse RBC, WBC, platlets, endothelial cells.

Front 87

How to treat for clostridium perfringen infection?

Back 87

1. immediate removal of necotic tissue.
2. daily reoperation if needed
3. penicillin and clindamycin
4. hyperbaric oxygen

Front 88

What organism causes spasms in the muscles of the neck and jaw, involes muscles of the trunk more than those of the limbs?

Back 88

Clostridium tetani.

Front 89

Describe clostridium tetani:
1. gram stain
2. aerobic or anaerobic
3. spore forming or not

Back 89

1. GPB
2. strict anaerobe
3. spore forming: extremely stable in environment.

Front 90

What is the name of the toxin in clostridium tetani that cause muscle spasms?

Back 90

Tetanospasmin(A/B toxin).

Front 91

Why is the diagnose for tetus only clinical?

Back 91

Difficult to recover since it's a strict anaerobe.

Front 92

Describe the pathogenesis of clostridium tetani.

Back 92

1. spore introduced to tissue: laceration, puncture, umbilical stump contaminated.
2. germinate under anaerobic condition.
3. production of tetanospasmin.
4. muscular rigidity and spasm.

Front 93

Describe the mechanism of tetanospasmin to cause spasms.

Back 93

1. irreversible binding to CNS.
2. carried to neurons in brain stem and spinal cord: retrograde axonal transport.
3. diffuse to terminals of inbitory cells.
4. prevent glycine and GABA release from inhibitory cells.
5. no inhibition of motor neurons.

Front 94

How is tetanus different from botulism?
How is it similar to botulism?

Back 94

Tetanus: inhibition of inhitory neurotransmitter release.
Botulism: Ach blocked, no excitation, cause muscle paralysis.
Both need to regerate nerve endings in order to recover.

Front 95

What are the four forms of tetanus?

Back 95

1. generalized
2. localized
3. cephalic
4. neonatal

Front 96

Generalized tetanus starts with_____, then progress to generalized spasms.

Back 96

Trismus: masseter rigidity.

Front 97

T/F: During generalized spasms, there is no loss of consiousness,no pain, and can be triggered by sensory stimuli.

Back 97

F. Very painful.

Front 98

How long does the symptoms of tetanus last if you give them antitoxin?

Back 98

2 wks.

Front 99

Give 3 complication of tetanus.

Back 99

1. laryngeal spasm, airway obstruction.
2. long bone fracture.
3. hypertension/abnormal heart ryhthm.
4. pulmonary embolism.

Front 100

What causes neonatal tetanus?

Back 100

1. contaiminated umbilical stump.
2. unvaccinated mother.

Front 101

One of CDC's goals is to immunize women if child bearing age. Why?

Back 101

Maternal antibodies will protect infants since 50% death is caused by neonatal tetanus.

Front 102

Why do people >60yrs more likely to get tetanus?

Back 102

waning immunity. Need boosters.

Front 103

Do you need to vaccinate people who had tetanus?

Back 103

Yes. Toxin is too potent, similar to diptheria.

Front 104

How to treat tetanus?

Back 104

1. remove anaerobic conditions
2. immune globulins to remove toxin
3. antibiotics to remove germinating organisms.
4. sedation(benzodiazapines), supportive care: nutrition, airway support.

Front 105

What group of mycobacteria is found in swimming pools, aquariums, and natural bodies of water?

Back 105

mycobacterium marinum

Front 106

Mycobacterium marinum grow best at what temperature?

Back 106

32 degree C.

Front 107

What are some clinical findings of Mycobacterium marinum?

Back 107

small papules which gradually enlarge, may ulcerate, spread along lymphatics. Similar to Nocardia.

Front 108

What is the route of entry for Mycobacterium marinum?

Back 108

minor trauma in swimming pools, aquariums, and natural bodies of water.

Front 109

What are the rapid grower groups of mycobacteria?

Back 109

1. mycobacteria fortuitum
2. mycobacteria chelonae
3. mycobacteria abscessus

Front 110

How to treat mycobacteria marinum?

Back 110

long period of antobiotic therapy. >18 months

Front 111

How to treat mycobacteria groups known as the rapid growers?

Back 111

conventional antibiotics.

Front 112

What mycobacteria is introduced through medical devices like the catheter, prosthetic devices?

Back 112

Fast growers: M. abscessus, M. chelonae, and M. fortuitum.

Front 113

What is a typical skin finding for M. abscessus, M. furtuitum, and M. chelonae?

Back 113

draining skin lesions.

Front 114

Describe mycobacterium leprae:
1. gram stain
2. intra or extracellular
3. acid fast or not
4. aerobic or anaerobic

Back 114

1. GPR
2. obligate intracellualr
3. acid fast
4. aerobic

Front 115

Has M. leprae been cultured in vitro?

Back 115

No. Undergo reductive evolution.

Front 116

What is special about M. Leprae's cell wall?

Back 116

lipid rich: phenolic glycolipid-1, immunogen(antigen).

Front 117

Describe the growth of M. leprae.

Back 117

extremely slow.
grow best at low temp.

Front 118

What is the host range for M. leprae?

Back 118

human
armadillo
certain monkeys.

Front 119

What are the endemic areas of M. leprae?

Back 119

India
Brazil
Madagascar
Mozambique
Myanmar
Nepal

Front 120

How does M. leprae transmit?

Back 120

person-person: nasal discharge, breast milk, insect bites.
Organisms viable via dry secretion, need long and close contact.

Front 121

What is the main factor that facilitate the transmission of M. Leprae?

Back 121

Organisms are viable in dry secretions.

Front 122

What organism has a very long incubation period?

Back 122

M. Leprae: 6 months to 2 years, 2-4 years most common.

Front 123

Where is M. leprae found in the body?

Back 123

deep tissue, but bot growing there (too warm).

Front 124

What cells are the taget for M. Leprae?

Back 124

macrophages, schwann cells.

Front 125

What is unique of M. leprae among mycobacterium spp?

Back 125

ability to infect peripheral nerves.

Front 126

People with hypergammaglobulinemia may still have this kind of leprosy.

Back 126

lepromatous (multibacillary) leprosy. Because antibodies are not helpful in controlling this kind of leprosy.

Front 127

This patient present with diffuse granulomas, extensive (>6) bilateral and symetric pattern of "leonine" skin patches. Diffuse nerve involvement.
1. What would you observe in the stain of the lesion?
2. What is the cause of the nerve involvemnet?
3. Would this patient show a positive skin test to lepromin?
4. How to treat?

Back 127

1. multibacillary form of M. Leprae.
2. edema around the nerves, not direct nerve damage.
3. No.
4. dapsone, rifampicin, and clofazimine for 12 months.

Front 128

Would IFN-γ help lepromatous leprosy patients?

Back 128

Unfortunately no.

Front 129

What is the primary target in tuberculoid leprosy?

Back 129

skin and nerves

Front 130

Patient presents with large erythmatous plaques, hypoesthetic. Histology showed giant cells and lymocyte infiltration.
1. What bacteria may cause this type of skin lesion (be speific).
2. Why is the area hypoesthetic (numb)?
3. Will this patient have a positive skin test to lepromin?
4. How to treat?

Back 130

1. tuberbuloid (paucibacillary) form of M. leprae.
2. nerve damage due to activated macrophage.
3. Yes.
4. dapsone, rifampicin for 6 months.

Front 131

What are some differences between the two forms of M. leprae?

Back 131

1. Lepromatous form has more skin lesions.
2. no skin test in lepromatous form.
3. lepromatous is more infectious and has worse prognosis.
4. lepromatous form diffuse granulomas (non-activated macrophages) whereas tuberculoid form giant cells (macrophages activated).
5. Tuberculoid form has less bacterial load.

Front 132

What long term deformities are involved with leprosy?

Back 132

1. facial structures: due to organism and cellular reaction.
2. hands and feet:due to peripheral nerve damage."claw hands".

Front 133

Patient shows "claw hands" and some facial deformity. What should you use to treat him?

Back 133

Patient has chromic tuberculoid leprosy.
Use dapsone, rifampicin, clofazimine.

Front 134

How to diagnose leprosy?

Back 134

1. suspision: hypoesthetic lesion, nerve thickening, endemic areas.
2. skin biopsy: presence of organism, cutaneous nerves. Special fast stain.

Front 135

Is there a vaccine for M. leprae?

Back 135

No. Bur BCG might have some protection.

Front 136

A patient with leprosy was treated with appropriate medication and developed vasculitis.
1. What type of leprosy does the patient have?
2. What caused the finding?
3. How to treat it?

Back 136

1. lepromatous (MB)
2. reversal reaction lead to immune complex formation.
3. treat with steroids or thalidomide to slow down host response.

Front 137

Patient presents with pityriasis versicolor.
1. What type of organism caused this?
2. what layer of skin is involved?
3. Name the organism.
4. How to treat it?

Back 137

1. fungus: superficial mycoses
2. stratum corneum
3. Malassezia furfur
4. topical keritolytic agents, topical miconazole cream.

Front 138

What are some skin findings caused by superficial mycoses?

Back 138

1. pityriasis versicolor
2. tinea nigra

Front 139

What are some hair findings caused by superficial mycoses?

Back 139

1. black piedra
2. white piedra

Front 140

Describe malassezia furfur:
1. type of organism
2. location

Back 140

1. lipophilic yeast
2. sebaceous gland, lipid-rich areas

Front 141

A hospitalized patient recently received IV lipid transfusion and developed hypopigmented macule on the skin. What organism caused it?

Back 141

Malassezia furfur

Front 142

List three cutaneous mycoses.

Back 142

1. microsporum: hair and skin
2. trichophyton: hair, skin, and nails
3. epidermalphyton: skin and nails

Front 143

A kid has several itchy annular scalding patch with raised margin (like a skin test) on his feet.
1. What type of organism causes it?
2. What is the technical name for te skin finding?
3. What tests can you use to confirm the suspision?
4. How to treat it?

Back 143

1. cutaneous mycoses
2. tinea pedis
3. Woods lamp (fluoresce green), KOH skin scraping and look for hyphae, and chains of arthrospores.
4.topical keratolytic compounds, topical azoles ie miconazole, clotrimazole. If more severe, use oral azoles ie itraconazole(Sporonox), terbinafine (Lamisil)

Front 144

A skin scraping from a skin lesion showed hyphae and chains of arthrospores. What is this organsim?

Back 144

cutaneous mycoses (dermatophytes)

Front 145

A skin scraping from a skin lesion fluoresced green under Woods lamp. What is this organsim?

Back 145

microsporum

Front 146

Which one of the cutaneous mycoses is zoophilic unlike the rest of the family?

Back 146

microsporum canis

Front 147

T/F: All dermatophytes in the US are all anthrophilic.

Back 147

F. Except microsporum canis which is zoophilic(dogs and cats).

Front 148

What is the difference between anthrophilic and zoophilic mycoses?

Back 148

Anthrophilic organisms: noninflammatory infections, harder to treat.
Zoophilic organisms: strong inflammation, response well to therapy.

Front 149

Why do dermatophytes stay only in the cutaneous layer?

Back 149

They need keratinocytes to grow.

Front 150

Name one fungus that cuase skin infections similar to nocardia and is thermally dimorphic.

Back 150

Sporothrix schenkii: cigar shaped when at 37 degree. filamentous mold with "rosette" conidia at 30 degree.

Front 151

A rose gardener presents a painless skin lesion that looks like that of nocadia.
What organism is this?

Back 151

sporothrix schenkii

Front 152

A timber worker presents a painless skin lesion that looks like that of nocadia.
1. What organism is this?
2. What might he have contacted with?

Back 152

1. sporothrix schenkii.
2. sphagnum moss.

Front 153

An AIDs patients presents with lesions in his joints. What do you suspect he has?

Back 153

sporothrix schenkii: extracutaneous sporotrichosis.

Front 154

How to treat sporothrix schenkii?

Back 154

1. Itraconazole-drug of choice
2. oral saturated potassium iodide: cheap but very nasty taste!

Front 155

Varicella zoster virus is a memeber of ______.

Back 155

Herpesviridae

Front 156

What is the causative agent of chicken pox? of shingles?

Back 156

varicella
zoster

Front 157

How does chicken pox spread?

Back 157

respiratory or contact with skin vesicles.

Front 158

Describe the pathogenesis of varicella.

Back 158

1. respiratory transmission
2. viral replication in regional lymph nodes
3. seeds reticuloendothelial system
4. primary viremia
5. replicate in internal organs(liver, spleen)
6. secondary viremia: most contagious
7. dermis seeded:mononuclear cells
8. skin vesicles formed
9. disseminated into lungs, liver, CNS in immunocompromised.
10. become latent in DRG.

Front 159

When is the patient with chicken pox most infectious?

Back 159

during secondary viremia before rash appears.
2 days before rash and 5 days after.

Front 160

The skin vesicle in chicken pox is filled with____.

Back 160

cloudy fluid (infectious), not pus.

Front 161

What is the difference in skin lesion between chicken pox and small pox?

Back 161

Chicken pox: fluid filled
Small pox: pus filled

Front 162

What is the incubation period for varicella?

Back 162

2 wks

Front 163

Describe the rash manifested in chicken pox.

Back 163

maculopapules, vesicles, scabs. Appear on trunk and face, then spread centripitally.

Front 164

What is the most common secondary bacterial infection of chicken pox?

Back 164

S. Aureus or Group A strep.

Front 165

Why is it better to have chicken pox in young age than older?

Back 165

Adults have well developed CMI, so host response causes more damage.

Front 166

What happens when immunocompromised children have chicken pox?

Back 166

1. more numerous lesions, often hemorrhagic
2. takes longer to heal
3. encephalitis, pneumonitis

Front 167

When is the most deangerous time for a pragnant women to have chicken pox?

Back 167

5 days before and 2 days after delivery.

Front 168

When do congenital chicken pox occur? What is the outcome?

Back 168

During 1st trimester of pregnancy.
Low birth weight, skin scarring, limb hypoplasia, microcephaly, chorioretinitis.

Front 169

An old guy presents unilateral vesicular eruption with a dermatomal pattern on his thorax and lumbar region. He describe it as very painful.
1. What does the man have?
2. What is the causative agent?

Back 169

1. shingles
2. zosster

Front 170

Acute-phase pain associated with shingles is due to ____.

Back 170

viral replication and inflammation.

Front 171

How to diagnose VZV?

Back 171

1. History, physical exam
2. DFA

Front 172

How to treat chicken pox?

Back 172

1. topical soap for pruitis
2. acyclovir, famcyclovir, or valcyclovir

Front 173

How to treat shingles?

Back 173

1. control pain with analgesics
2. antivirals

Front 174

Is there a vaccine for varicella?

Back 174

Varivax:live attenuated Oka strain, one dose for children at 12-18months with booster at 4-6 yrs. Two doses for susceptible older chidren and adults. May protect from shingles.

Front 175

Is there a vaccine for zoster?

Back 175

Zostavax.

Front 176

Trichinella spiralis is a _____.

Back 176

parasite.

Front 177

Describe the life cycle of trichinella spiralus.

Back 177

1. larva in muscle of host
2. muscle is eaten, larva freed by stomach acid and replicate in intestine.
3. larva seed in muscle via blood, increase in sized, coil, form cyst walls, eventually calcify.
4. dead end.

Front 178

How to treat Trichinella spiralis?

Back 178

no treatment for muscle phase.
bedrest, aspirin.

Front 179

A patient complains of fever, myalgia, weakness, periorbital edema. History shows that he had eaten pork the night before. What is the causative organism?

Back 179

Trichinella spiralis.