Microbiology Flashcards
Common cause and skin layer affected in impetigo:
Strep pyogenes and/or staph aureus
Superficial cutaneous infection affecting the epidermis only through cuts in the skin
Common cause and skin layer affected in erysipelas
Strep pyogenes
Dermis
Common cause and skin layer affected in folliculitis, boils and carbuncles
Staph aureus
Hair follicles
Common cause and skin layer affected in necrotising fascitis
Anaerobes and microaerophils
Fascia
Common cause and skin layer affected in myenecrosis gangrene
Clostridium perfringes
Muscle
Causes and antibiotic therapy for boils, carbuncles, folliculitis
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.
Causes and antibiotic therapy for impetigo
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
Causes and antibiotic therapy for erysipelas
Cause: Strep pyogenes
Di/fluclox orally
Hypersensitivity: cephalexin
Causes and antibiotic therapy for cellulitis
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.
Antibiotic therapy for skin infections caused by MRSA
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
Common causes and skin layer affected in cellulitis
Strep pyogenes (>90%), staph aureus Acute inflammation involving subcutaneous tissue and fat
Treatment for impetigo
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
Epidemiology of GAS
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)
Prevalence of scabies in Indigenous communities
Up to 50% of children, 25% of adults
Scabies aetiology
Infestation of skin by arthopod mite sacroptes scabei - lives in burrows within skin usually around hands/wrists.
Treatment of scabies
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.
Causative agents of dermatophyte infections
Epidermaphyton
Trichophyton
Microsporum
Clinical conditions caused by dermatophyte infections
Tinea (corporis, pedis, cruris) (known as ringworm)
Treatment of dermatophyte infections
Terafine OR bifonazole OR clotrimazole (some others also) administered as a topical cream
If unresponsive: Terbanifine orally (2-6 weeks)
Transdermal antimicrobials
Clindamycin, erthromycin, benzoyl peroxide for acne vulgaris
Mupirocin (protein synthesis inhibitor) for impetigo
Transdermal antifungal
Permethrin for scabies
Transdermal drugs
Clonidine (HT), fentanyl (pain), nicotine, nitroglycerine, scopolamine, testosterone (male hypogonadism)
Types of plasmodium
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.
Malaria transmission
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.
Treatment of malaria
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.
Life cycle of giardia
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.
Diagnosis of giardia
Stool - microscopy for cysts/trophozoites, antigen detection and PCR.
Diagnosis of malaria
Peripheral blood smear for infected RBCs (thin for screening and thick for degree of paracythaemia), immunoassay can give reliable diagnosis.
Diagnosis of cryptosporidium
Stool microscopy - modified acid fast stain
Clinical features of amoebiasis
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
Clinical feature of giardia
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
Clinical features of cryptosporidium
Small bowel infection.
Normal host - watery diarrhoea for 1-2 weeks.
Immunocompromised host - chronic diarrhoea
Diagnosis of amoebiasis
Stool tests (microscopy for cysts/trophozoites and antigen detection)
Colonoscopy - biopsy shows flask-shaped ulcers
Serology - invasive infection, esp. liver abscess.
