Microbiology

Question 1

Common cause and skin layer affected in impetigo:

Answer 1

Strep pyogenes and/or staph aureus

Superficial cutaneous infection affecting the epidermis only through cuts in the skin

Question 2

Common cause and skin layer affected in erysipelas

Answer 2

Strep pyogenes

Dermis

Question 3

Common cause and skin layer affected in folliculitis, boils and carbuncles

Answer 3

Staph aureus

Hair follicles

Question 4

Common cause and skin layer affected in necrotising fascitis

Answer 4

Anaerobes and microaerophils

Fascia

Question 5

Common cause and skin layer affected in myenecrosis gangrene

Answer 5

Clostridium perfringes

Muscle

Question 6

Causes and antibiotic therapy for boils, carbuncles, folliculitis

Answer 6

Cause: s. aureus

Usually pus drainage sufficient for minor lesions. For more severe lesions:

Staph aureus usually resistant to penicillin, therefore penicillin not used unless sensitivity proven.

Di/fluclox used orally if methicillin sensitive s. aureus (MSSA).

Cephalexin used orally if hypersensitivity to penicillins.

Question 7

Causes and antibiotic therapy for impetigo

Answer 7

Impetigo is caused by s. aureus and/or strep pyogenes.

Staph aureus usually resistant to penicillin, therefore penicillin not used unless sensitivity proven.

Di/fluclox used orally if methicillin sensitive s. aureus (MSSA).

Cephalexin used orally if hypersensitivity to penicillins.
In immediate hypersensitivity: clindamycin

Question 8

Causes and antibiotic therapy for erysipelas

Answer 8

Cause: Strep pyogenes

Di/fluclox orally
Hypersensitivity: cephalexin

Question 9

Causes and antibiotic therapy for cellulitis

Answer 9

Causes: strep pyogenes (>90% of cases), staph aureus. Emprical treatment with di/dluclox to cover both pathogens.

MILD: di/fluclox orally. Cephalexin if non-immediate hypersensitivity to penicillin.

SEVERE: di/fluclox intravenously.
Delayed hypersensitivity: cephalothin/cephazolin IV
Immediate hypersensitivity: clindamycin/lincomycin

In wound is dirty, add metronidazole to cover anaerobes.

Question 10

Antibiotic therapy for skin infections caused by MRSA

Answer 10

Treatment guided by susceptibility testing.
CA-MRSA usually susceptible to clindamycin, trithemoprim+sulfamethoxasole or doxycycline
HA-MRSA usually multi-resistant. Possible treatments: vancomycin, rifampicin + sodium fusidate, teicoplanin

Question 11

Common causes and skin layer affected in cellulitis

Answer 11

Strep pyogenes (>90%), staph aureus
Acute inflammation involving subcutaneous tissue and fat

Question 12

Treatment for impetigo

Answer 12

Small number of lesions: crusts should be sponged off with saline, soap water, aluminium acetate plus Mupirocin (topical cream used to treat staph and strep)
Large number of lesions/failure to resolve: use antibiotics + sponge off old crusts

Question 13

Epidemiology of GAS

Answer 13

Industrialised countries: common cause of pharyngitis and tonsilitis in children 5-15 years

Non-industrialised countries: most commonly associated with pyoderma (up to 70% of children in Indigenous communities)

Question 14

Prevalence of scabies in Indigenous communities

Answer 14

Up to 50% of children, 25% of adults

Question 15

Scabies aetiology

Answer 15

Infestation of skin by arthopod mite sacroptes scabei - lives in burrows within skin usually around hands/wrists.

Question 16

Treatment of scabies

Answer 16

Permethrin 5% cream topically, applied to whole body and face and left on for minimum 8 hours.
If allergic to permethrin, benzyl benzoate 25% emulsion in water for 24 hours.
Repeat in 7-14 days if severe infection.

Question 17

Causative agents of dermatophyte infections

Answer 17

Epidermaphyton
Trichophyton
Microsporum

Question 18

Clinical conditions caused by dermatophyte infections

Answer 18

Tinea (corporis, pedis, cruris) (known as ringworm)

Question 19

Treatment of dermatophyte infections

Answer 19

Terafine OR bifonazole OR clotrimazole (some others also) administered as a topical cream
If unresponsive: Terbanifine orally (2-6 weeks)

Question 20

Transdermal antimicrobials

Answer 20

Clindamycin, erthromycin, benzoyl peroxide for acne vulgaris

Mupirocin (protein synthesis inhibitor) for impetigo

Question 21

Transdermal antifungal

Answer 21

Permethrin for scabies

Question 22

Transdermal drugs

Answer 22

Clonidine (HT), fentanyl (pain), nicotine, nitroglycerine, scopolamine, testosterone (male hypogonadism)

Question 23

Types of plasmodium

Answer 23

P. falciparum (most life-threatening; mainly in Africa; constitutes 20% of cases in Australia)
P. vivax (commonest form; more benign/rarely life-threatening; 80% of cases in Australia)
P. ovale
P. malariae
P. knowlesi (Asia - Borneo; infects organgutans and now humans due to deforestation; like falciparum)

Transmitted via the female anopheles sp.
Malaria fever occurs every 48hours, except in malariae, it’s 72 hours.

Question 24

Malaria transmission

Answer 24

Malaria deposits parasite into circulation as a sporozoite. Goes to liver (latent stage - may stay there for 5 days - 4 weeks), asexual division to form merozoite. Enters blood stream, invades RBC. Asexual division 2, causes lysis of the RBC, infects more RBCs (symptomatic stage - takes 48 hours). Sexual reproduction only occurs in the mosquito.
Recurrence may occur with vivax and ovale as they may not divide in the liver immediately and become latent as hipnozoites. Falciparum may spill into bloodstream and adhere to endothelial cells instead of infecting RBCs, and stay there for up to 4 years.

Question 25

Treatment of malaria

Answer 25

Clinical cure: results in eradication of parasites from the blood, leading to resolution of clinical symptoms. Use: chloroquine (if sensitive), quinine, doxycycline, malarone, artemather

Severe: IV artesunate + quinine, cautious fluid replacement, anticonvulsants if needed. Corticosteroids CONTRAINDICATED.

Radical cure: For ovale and vivax. Gets rid of hipnozoites. Use primaquine.

Question 26

Life cycle of giardia

Answer 26

Ingested as cyst, excysts in duodenum, trophozoite released. Multiplies by longituidinal fission. Develops wall to survive outside body once secreted (cyst). Trophozoites will disintegrate outside body.

Question 27

Diagnosis of giardia

Answer 27

Stool - microscopy for cysts/trophozoites, antigen detection and PCR.

Question 28

Diagnosis of malaria

Answer 28

Peripheral blood smear for infected RBCs (thin for screening and thick for degree of paracythaemia), immunoassay can give reliable diagnosis.

Question 29

Diagnosis of cryptosporidium

Answer 29

Stool microscopy - modified acid fast stain

Question 30

Clinical features of amoebiasis

Answer 30

Infects and invades the LARGE bowel.
Asymptomatic - most common
Acute colitis (amoebic dysentry) - bloody diarrhoea, abdp pain, fever
Amoebic liver disease - RUQ pain, tender hepatomegaly, fever

Question 31

Clinical feature of giardia

Answer 31

Adheres to small bowel.
Asymptomatic (most common)
Acute infection - nausea, vomiting, watery diarrhoea, abdo pain (most will clear the infection)
Chronic infection (~1.3) - malabsorption syndrome

Question 32

Clinical features of cryptosporidium

Answer 32

Small bowel infection.
Normal host - watery diarrhoea for 1-2 weeks.
Immunocompromised host - chronic diarrhoea

Question 33

Diagnosis of amoebiasis

Answer 33

Stool tests (microscopy for cysts/trophozoites and antigen detection)
Colonoscopy - biopsy shows flask-shaped ulcers
Serology - invasive infection, esp. liver abscess.