Infections on Surfaces and Streptococci (pyogenes)

Question 1

What is a surface? Give examples of surfaces on patients.

Answer 1

An interface between a solid and a liquid/gas. There are many surfaces on a patient e.g. Skin - epithelium, hair, nails and mucosal surfaces - conjunctival, gastrointestinal, respiratory and genitourinary (ecological surfaces for microbes).

Question 2

Give some examples of skin viruses and bacteria.

Answer 2

Wide range of viruses: Papilloma (benign, but not commensal), Herpes simplex.
Bacteria: gram positive Staph aureus, Coagulase negative staphylococci, Corynebacterium and gram negative Enterobacteriaceae.

Question 3

Give some examples of skin fungi and parasites.

Answer 3

Fungi: yeasts, dermatophytes (Athlete’s foot may cause a break in skin).
Parasites: mites.

Question 4

Where might mucosal flora be found? Give some examples.

Answer 4

Eye e.g. Viridans group streptococci (problematic if cataract surgery), Nares e.g. Staph aureus, Nasopharynx e.g. Neisseria meningitidis (mostly commensal), Mouth, Stomach e.g. Helicobacter (1/3 people), Intestine e.g. Aerobic and anaerobic streptococci, Urethra e.g. Enterobacteriaceae and Vagina e.g. Lactobacilli (low pH keeping Candida at bay).

Question 5

People may get infections from themself, how?

Answer 5

Microbiota - ‘commensals’ - microorganisms carried on the skin and mucosal surfaces, normally harmless/beneficial, but when transferred to other sites, can be harmful: invasion, migration, inoculation, haematogenous.

Question 6

What are the 2 types of natural surface infections? Give examples.

Answer 6

External p: Cellulitis, Pharyngitis, UTIs, pneumonia etc) or …
Internal: Empyema, endocarditis/vasculitis, septic arthritis etc).

Question 7

What sort of things may patients get prosthetic surface infections from?

Answer 7

IV lines, dialysis catheters, prosthetic joints, cardiac valves, pacing wires, endovascular grafts or ventriculo-peritoneal shunts.

Question 8

Prosthetic valve endocarditis is usually caused by different organisms depending on whether it’s less than or over 1 year post-operative, what are they?

Answer 8

<1 year post-op = coagulase negative staphylococci.

>1 year post-op / native valve can be a range - cause vegetation to grow on valves, which may perforate.

Question 9

Prosthetic joint inactions and and those from cardiac pacing wires have the same causative organisms, which are what?

Answer 9

Coagulase negative streptococci and Staph aureus.

Question 10

Process in pathogenesis of infections at surfaces:
____________ to host cells/prosthetic surface, _________ formation, invasion and ___________, then host response - ___________ and granulomatous (modular inflammatory lesions).

Answer 10

Adherence
Biofilm
Multiplication
Pyogenic

Question 11

How do microorganisms usually achieve adherence?

Answer 11

Extracellular structures, such as pili or fimbriae (to the host cell membrane).

Question 12

What is a biofilm?

Answer 12

A common feature of cell surface infections, a thin but robust layer of mucilage adhering to a solid surface and containing a community of bacteria and other microorganisms. If bacteria think they’re alone, they’ll switch off biofilm production.

Question 13

What are Quorum sensing molecules and what are their uses?

Answer 13

Quorum sensing chemicals are released by bacteria/microorganisms to control sporulation, biofilm formation and virulence factor secretion. They have 3 principles: signalling molecules - autoinducers (AI), cell surface/cytoplasmic receptors and gene expression leading to cooperative behaviours and more AI production.

Question 14

Outline how microorganisms cause disease.

Answer 14

Exposure->adherence->invasion->multiplication->dissemination with Virulence factors of endotoxins (cytolytic, AB toxins, superantigens, enzymes) and exotoxins, leading to host cellular damage (direct or consequent to host immune response).

Question 15

What does diagnosis of an infection aim to do and state some challenges?

Answer 15

Aims to identify the infecting organism and its antimicrobial susceptibilities. A challenge is presented with adherent molecules and those with a low metabolic rate/small colony variants, as they grow poorly on agar plates. Try to blood culture and tissue/prosthetic material sonication and culture.

Question 16

What does treatment of an infection aim to do and state some challenges?

Answer 16

Aim to sterilise the tissue and reduce the bio burden e.g. With antibacterials, by removing prosthetic material or surgery to resect infectious material. Challenges arise when there’s poor antibacterial penetration into the biofilm, low metabolic activity of biofilm microorganisms as well as the dangers/difficulties of surgery.

Question 17

What are the aims of infection prevention on natural and prosthetic surfaces?

Answer 17

On natural surfaces: maintain surface integrity, prevent bacterial surface colonisation and remove colonising bacteria.
On prosthetic surfaces: prevent colonisation, inhibit surface colonisation and remove colonising bacteria.

Question 18

What do Streptococci look like under the microscope?

Answer 18

STReptococci look like STRing balls (chains).

Question 19

Streptococci may be classed by haemolytic into which categories? Give examples.

Answer 19

Alpha haemolysis: ‘Viridans’ streptococci partially break down blood agar, so it goes green e.g. Streptococcus pneumoniae.
Beta haemolysis: complete breakdown e.g. Streptococcus pyogenes (makes pus/abscess).
Non-haemolytic-gamma: e.g. Enterococcus faecalis.

Question 20

Streptococci have ___S ribosomal ____ sequences. Lancefield Serological classification is based on _____ ______ antigens eg S. pyogenes, is class A (beta) pyogenic, so virtually synonymous to _______ ___ ____________.

Answer 20

16
RNA
Cell wall
Class A Streptococcus

Question 21

Streptococcus pyogenes is a Lancefield group A beta-haemolytic streptococcus. Some of its virulence factors include hyaluronic acid, M proteins and adhesins. Explain/describe them.

Answer 21

M proteins are a family of proteins, with nucleotide variants, that inhibit the activation of the alternative complement pathway and so resist phagocytosis and also assist adhesion and stick out of the cell.Adhesions, including M proteins, are the first step in colonisation/infection.

Question 22

Streptococcus pyogenes is a Lancefield group A beta-haemolytic streptococcus. Some of its virulence factors include Streptolysins, Dnases, capsule and Hyaluronidase. Explain/describe them.

Answer 22

Streptolysins O and S are involved in the lysis of RBCs, neutrophils and platelets. Dnases A, B, C and D degrade DNA.
The hyaluronic acid capsule inhibits phagocytosis and is a poor immunogen (similar to connective tissue).
Hyaluronidase degrades connective tissue hyaluronic acid.

Question 23

Streptococcus pyogenes is a Lancefield group A beta-haemolytic streptococcus. Some of its virulence factors include Streptokinase and exotoxins. Explain/describe them.

Answer 23

Streptokinase converts plasminogen into plasma, resulting is the dissolution of clots.
Streptococcal pyogenic exotoxins cleave IgG bound to Strep A and are a member of the super antigenic family.

Question 24

Streptococcal pharyngitis has a peak incidence with those aged __ to ___ and has __________ spread, so is associated with overcrowding. Untreated patients develop a ___ _________ specific antibody (so don’t give antibodies, since it doesn’t shorten _________).

Answer 24

5 to 15
Droplet
M protein
Duration

Question 25

What are the clinical features of Streptococcal pharyngitis?

Answer 25

Abrupt onset sore throat, malaise, fever, headache, lymphoid hyperplasia, tonsilopharyngeal exudates. Throat swabs show Group A Strep (pus shows it's not viral).

Question 26

Scarlet fever is a complication of Streptococcal pharyngitis, explain how and list some clinical features.

Answer 26

Due to infection with a Streptococcal pyogenic exotoxins strain of S. pyogenes - local of haematogenous spread. High fever, sepsis, arthritis, jaundice, typical pink appearance.

Question 27

Peritonsillar cellulitis/abscess, retropharyngeal abscess, mastoiditis, sinusitis, otitis media, meningitis (and rarely) brain abscesses, are all what type of complication of Streptococcal pharyngitis?

Answer 27

Suppurative complications (pus forming).

Question 28

What is Acute Rheumatic Fever and suggest some possible mechanism?

Answer 28

Inflammation of the heart/joints/CNS triggered by rheumatogenic M types (specific type not prevalent in Britain). Possible mechanisms: autoimmune, serum sickness, binding of M proteins to collagen, ASO/ASS induced tissue injury.

Question 29

What is Acute post-Streptococcal glomerulonephritis?

Answer 29

Acute inflammation of renal glomerulus, M type specific (not the same as Acute Rheumatic Fever), antigen-antibody complexes in glomerulus.

Question 30

What are the differences in what Acute Rheumatic Fever and Acute post-Streptococcal glomerulonephritis may follow?

Answer 30

While both diseases can be complications of Streptococcal pharyngitis, Acute Rheumatic Fever may only follow the pharyngitis, whereas Acute post-Streptococcal glomerulonephritis may follow any Strep infection.

Question 31

What skin infections may Streptococcus pyogenes cause?

Answer 31

Impetigo, Erysipelas, Cellulitis or Necrotising fasciitis.

Question 32

Impetigo, most commonly seen in people aged __ to __, has initial skin colonisation leading to intradermal inoculation. No Acute Rheumatic Fever can be caused by it, but it is the most common cause of _________________.

Answer 32

2 to 5 | Glomerulonephritis

Question 33

Erysipelas, which may be preceded by a Group A Step sore throat (___________) is a dermis infection with ___________ involvement on the _____ and lower limbs. The latter infection is usually secondary to invasion of the skin via _______/skin disease/local _______ infection. There are ________ edges and the fascial lesions have a ________ colour.

Answer 33

``` Pharyngitis Lymphatic Face Trauma Fungal Raised Salmon ```

Question 34

What is cellulitis, who's at risk and how might it be distinguished clinically from Erysipelas?

Answer 34

Cellulitis is an infection of the skin and subcutaneous tissue. Those with impaired lymphatic drainage and illicit injecting drug users have risk factors. Unlike the presentation of Erysipelas, there are no raised edged on the skin.

Question 35

What is Necrotising fasciitis?

Answer 35

Infection of deep subcutaneous tissue and fascia. It's extensive necrosis (may produce gas) and rapid, usually secondary to a skin break. There's severe pain even before gross clinical changes: high fever, fulminant course and high mortality (operate to debride and give antibiotics).

Question 36

What combines to make Streptococcal toxic shock syndrome?

Answer 36

A deep tissue infection with Streptococcus pyogenes + Bacteraemia + vascular collapse + organ failure.

Question 37

Streptococcal toxic shock syndrome can make a person go from health to death in a matter of hours, what process facilitates this?

Answer 37

Entry of group A Strep to deeper tissues and the bloodstream, Streptococcal pyogenic exotoxins stimulate T cells by binding to MHC class II APCs and V-beta region of T cell receptor inducing monocytes cytokines (TNF alpha, IL1beta, IL6) and lymphokines (TNF-beta, IL2, IFN-gamma), M protein fibrinogen complex formation. Superantigenic activity - cloning of T cells leads to cytokines etc leading to vascular collapse as BP drops.