Medical Microbiology

Question 1

Give the difference defense mechanisms of the skin.

Answer 1

Mechanical
Chemical
Inflammatory cells
Normal Flora

Question 2

What constitutes Skin Flora

Answer 2

Bacteria, Eukarya and Viruses

Question 3

Give the different types of bacteria which are part of the skin flora

Answer 3

Cutibacterium acnes
Corynebacterium species
Streptococcus species
Micrococcus species
Coagulase-negative-staphylococcus

Question 4

Give the different types of Eukarya

Answer 4

Malassezia species
Dermatophytes
Candida parasilosis

Question 5

modes of infections?

Answer 5

i)Breach of intact skin
ii)Skin manifestation of systemic infections
iii)Damage of the skin by toxins

Question 6

Virulence Factors of Staphylococcus aureus

State the different types of virulence factors and specify the factors and give biological activity of the factor.

Answer 6

Structural factors, divided into two
i) has a slime layer on the surface which facilitates adherence to foreign bodies, and inhibits phagocytosis
ii) Fibronectin binding protein- which binds to fibronectin on human cells( It is an adhesin which enables Staphylococcus aureus (S. aureus) to adhere to host cells of another organism, and an invasin facilitating its internalisation into these cells.)

TOXINS
divided into four types:
i) Cytotoxins- Lyses erythrocytes, leukocytes, macrophages, platelets
ii) Exfoliative toxin- Splits intercellular brigdes in epidermis
iii) Enterotoxins- Superantigen produces- Diarrhoea
iiii) Toxic shock syndrome toxin 01- Superantigen- produces toxic shock and multi organ failure

ENZYMES
i) Coagulase: Converts fibrinogen to fibrin
ii) Hydrolyses hyaluronic acid in connective tissue- promotes spread
iii) DNAse- Hydro lysis of DNA

Question 7

Outline the infection of hair follicles, Sebaceous gland and Sweat Glands

Answer 7

Folliculitis(minor infection of the hair follicles) (S aureus)
Furencle(boil)- Small abscesses that develop in the region of a hair follicle. (S aureus)
Carbuncle(mulltiple boils/furencles) Abscesses involving more than one hair follicle.

Question 8

Give the names of dermatophyte fungi,

Answer 8

Trichophyton, Microsporum and Epidermophyton species

Question 9

Diagnosis for infection of keratinized layers

Answer 9

Skin scrapings sent to lab
* KOH preparation
* Hyphae or spores detected
* Culture
* PCR

Question 9

Treatment for infection of keratinized layers

Answer 9

Oral terbinafine, fluconazole, itraconazole, griseofulvin
* Topical preparations for mild infections(medications applied directly to the skin)
* Oral anti-fungals for more extensive infectio

Question 10

What is the treatment for impetigo

Answer 10

Topical antibiotic therapy (Mupirocin)
* If complicated, systemic manifestations or part of outbreak – treat with cloxacillin, amoxicillinclavulanate or cefuroxime

• Most common bacterial infection in kids
• Very contagious/ highly infectioius
• S. pyogenes is the main cause, followed by S. aureus
• Secondary skin infections of existing lesions may occur
• Can be bullous or non-bullous
• Diagnosis based on history and clinical findings

Question 11

What are the treatment for erysipelas

Answer 11

Requires immediate treatment with penicillin or
erythromycin

Rapidly spreading infection of deeper layers of dermis
* Caused by S. pyogenes, sometimes groups B, C, or G
streptococci.
* Clinical – erythema, pain, fever, lymphadenopathy
* Complications – septicaemia or local necrosis of skin

Question 12

What is the treatment of Cellulitis

Answer 12

Treatment
* Oral antibiotics: penicillin, cefuroxime, erythromycin
* IV antibiotics: penicillin G, flucloxacillin, cefazolin
* Elevate limb

• A diffuse, spreading infection/inflammation of the subcutaneous connective tissue
• Extends deeper than erysipelas
• May have marked constitutional signs and symptoms
• May be fatal if not treated correctly
• Often no history of a wound
• Sometimes an accidental wound or draining lesion is present
• Most commonly caused by S. aureus and S. pyogenes

Question 13

What is the pathogenesis, Clinincal, Diagnosis and Treatment of Necrotizing Fasciitis

Answer 13

Pathogenesis
* Occlusion of blood vessels results in necrosis

Clinical
* Intense pain, area is red, hot, swollen
* Bullae, crepitus (from soft tissue gas) and gangrene may develop
* Spread to adjacent tissues
* Acutely ill, high fever, tachycardia, confusion, hypertension
* May develop Streptococcal toxic shock syndrome

Diagnosis
* History and clinical exam
* Raised white cell count, increased CRP, soft tissue gas on Xray, positive blood or tissue cultures
Treatment
* Surgical debridement and antibiotics

Question 14

What is the treatment of F. Pyomyositis

Answer 14

• Treatment: – Surgical drainage – IV anti-staphylococcal antibiotics (cloxacillin, vancomycin)

Localized collection of pus in the muscle tissue – Staphylococcus aureus
* It is characterized by: – Muscle pain, fever, swelling, and “wood-like” induration
* Secondary to transient bacteraemia – Diabetic and immunocompromi

Question 15

What is the treatment for Clostridial Myonecrosis(gas gangrene)

Answer 15

• Emergency surgical exploration and debridement
• Empirical antibiotic therapy with piperacillin– tazobactam
• Definitive treatment: penicillin and clindamycin.
• Life-threatening rapidly progressive infection of skeletal muscle, due to
  Clostridia (primarily C. perfringens).
• Develops either contiguously or by haematogenous spread.
• Anaerobic environment
• Initial muscle pain out of proportion to physical findings, tense muscle
  swelling, crepitation, overlying skin discoloration, bullae and subsequent
  systemic toxicity.
• large, gram-variable bacilli at the site of injury.
• Notable absence of

Question 16

Symptons of Scalded Skin Syndrome(SSSS)?

Answer 16

Fever and Lethargy

Question 17

What is the treatment of Scalded Skin Syndrome?

Answer 17

antiseptic wound dressing, fluid support, antibiotic therapy

Caused by: Exfoliatin A or B
* Toxin is produced by S.aureus locally, passes through the body and localises at the
level of the stratum granulosum (specific cell membrane ganglioside GM4 – only
present in young children & certain adults) * Toxins act by direct effect on stratum granulosum of the keratinized epidermis * The toxin destroys intercellular connections and separates layers within the
epidermis. In severe cases, the whole skin separates leaving typical scalded
appearance
* Mucosa are never involved
Prognosis in children is good, adults have high mortality

Question 18

What is the treatment for Toxic Shock Surgery

Answer 18

MANAGEMENT: * Antibiotics therapy narrowly targeting GAS is achieved wih penicillin +
clindamycin. Broader coverage may be warranted until streptococcal
infection has been confirmed. * Mortality: 20% - 45%

• Caused by the production of Staphylococcal exotoxins.
• These include a unique group of exotoxins that are referred to
  as superantigens because of their ability to cause widespread
  non-antigen specific activation of T-lymphocytes.
• The activation produced by these superantigens results in rapid
  release of cytokines by lymphocytes and macrophages.
• First recognized in women
  using highly absorptive
  tampons
• May be caused by S. aureus
  infection from non-genital
  sites
• Involves multiple organ systems
• Characterized by:
• Fever
• Hypotension
• Diffuse macular
  erythematous rash
• After the rash there is
  desquamation of skin (also
  soles and palms)
• Streptococcal Toxic Shock Syndrome
• A complication of invasive GAS disease characterized by shock and
  multiorgan failure; it occurs because of capillary leak and tissue damage due
  to release of inflammatory cytokines induced by streptococcal toxins. * Rash is less pronounced in STSS than TSS. * Blood culture may be positive.
  MANAGEMENT: * Antibiotics therapy narrowly targeting GAS is achieved wih penicillin +
  clindamycin. Broader coverage may be warranted until streptococcal
  infection has been con

Question 19

Antimicrobial Stewardship

Answer 19

The right antibiotic, for the right patient, at the right time, with the right dose, and the right route, causing the least harm to the patient and future patients.

Question 20

What are the goals of antimicobial stewardship

Answer 20

Improving patient care
Reducing collateral damage- meaning in the short term there is less toxicity in the intermidiate term(weeks/months) it causes reduced antimicrobial use and in the long term(years) it causes less resistance.
Impacting costs- in the intermidiate term it results in less costs due to less collateral damage and in the long term it leads to antimicrobial savings.

Question 21

What are the optional bacterial mobile elements of a bacteria.

Answer 21

Plasmids
Bacteriophages
Transposons

Question 22

Give the three different types of horizontal gene transfer.

Answer 22

Conjugation
Transduction
Transformation

Question 23

What causes intrinsic resistance

Answer 23

Due to genetic properties inherent in all members of specific species of bacteria

Question 24

What causes acquired resistance

Answer 24

Acquired resistance
* Bacteria acquire new genetic material leading to development of resistance
* Mutation
* Point mutations: changes in single nucleotides which alter the triplet code and may or may not
result in a change in translated protein
* Changes in a number of bases, e.g. deletion, replacement, insertion or inversion
* Horizontal gene transfer
* Very important in the spread of antibiotic resistance
* Conjugation
* Transduction
* Transformation

Question 25

Bactericidal vs bacteriostatic

Answer 25

• Bactericidal  antibiotic actually kills organism
• Bacteriostatic  antibiotic prevents growth of bacteria without killing
  them  bacteria could regrow once antibiotic removed 
  bactericidal antibiotics preferred, particularly for serious infections

Question 26

How do we classify bacteria?

Answer 26

.According to whether they are bactericidal or bacteriostatic
* By chemical structure
* By target site or mechanism of action
* By spectrum of activity i.e. narrow or broad spectrum