Clinical Conditions

Question 1

What is cellulitis?

Answer 1

Inflammation of subcutaneous connective tissue.

Question 2

How may a patient present with cellulitis?

Answer 2

Rubor and tumor of affected tissues. Low grade fever. High WBC and CRP. They may have an open wound, apparent on examination.

Question 3

What are the main bacterial causes of cellulitis?

Answer 3

Staphylococcus Aureus or Streptococcus pyogenes (both gram positive)

Question 4

How would a patient with cellulitis be treated?

Answer 4

Flucoxacillin (a Beta-lactam which is given via IV or orally)

Question 5

How would you decide which antibiotic to use in a patient with cellulitis, which was caused by a staph infection?

Answer 5

Flucoxacillin (resistant to staphylococcal B-lactamase) and B-lactamse combinations (Co-amoxiclav with tazocin) can be used. If the staph is flucoxacillin resistant (e.g. MRSA), then we use glycopeptides (e.g. vancomycin).

Question 6

For a patient with cellulitis, why might there be no blood culture growth after 48 hours?

Answer 6

Cellulitis is the bacterial infection of the subcutaneous connective tissue. At this point the infection has not disseminated into the blood (there will be no septicaemia).

Question 7

What condition presents similarly to cellulitis in its early stages?

Answer 7

Necrotising fasciitis (an example of toxic shock syndrome).

Question 8

How could you differentiate cellulitis and the other infection that initially mimics its presentation?

Answer 8

With necrotising fasciitis, the patient has severe, constant pain out of proportion to the physical signs. The inflammation will also have poorly-defined outer margins.

Question 9

What is the most common cause of necrotising fascitiis?

Answer 9

Group A ß-haemolytic streptococci - normally Strep. pyogenes (gram positive)

Question 10

On what basis are streptococci divided into Þ and ß-haemolytic?

Answer 10

They produce haemolysin which breaks down haemoglobin.

ß-haemolytic streps break down the haemoglobin completely. This means in an agar plate there are clear circles around the bacteria.
This is in contrast to Þ-haemolytic streps which only break down the haemoglobin partially. A green colour is left behind due to the presence of biliverdin (released due to the partial haem catabolism). Strep viridans is an Þ-haemolytic strep.

Question 11

Patients with necrotising fasciitis can develop toxic shock syndrome. What should be done to treat these patients who go on to develop sepsis? (Hint: Sepsis Six)

Answer 11

High flow O2
Microscopy, cultures and antibiotic sensitivity
IV fluid resuscitation
Antibiotic of choice
Measure serum lactate
Measure urine output accurately

Question 12

How would you treat necrotising fasciitis through surgical intervention?

Answer 12

A doctor must undertake an initial fasciotomy to assess deep tissues. Depending on the extent of the damage amputation may be necessary.

Question 13

How would you treat necrotising fascitiis caused by a streptoccocal infection?

Answer 13

Beta-lactams & glycopeptides are active against streps (gram positive cocci). If the disease is toxin-mediated we should give high dose human immunoglobulin and give antibiotics that prevent protein synthesis e.g. clindamycin (a lincosamide, similar to macrolides)

The empiric treatment is tazocin + clindamycin
If group A streptococci identified benzylpenicillin replaces tazocin. High dose immunoglobulin is considered.

Question 14

How can adenovirus be categorised?

Answer 14

It is a DNA non-enveloped virus.

Question 15

What are some of the symptoms of an infection caused by adenovirus?

Answer 15

Sore throat with a blocked nose (nasal congestion) Fever. Coughs are common. Occasionally a patient may develop conjunctivitis (a red eye).

Question 16

How is adenovirus usually spread?

Answer 16

Inhalation.

Question 17

What is SIRS? How does this differ from Sepsis?

Answer 17

It is systemic inflammatory response syndrome (SIRS). It is diagnosed when a person has 2 or more of the following: Temperature >38°C; HR >90/min RR >20/min (or pCO2 <4.3kPa); WBC <4 or >12 x10⁹/L

Sepsis is where there is SIRS AND there is a documented or presumed infection.

Question 18

When does sepsis become severe sepsis? What is septic shock?

Answer 18

Severe sepsis is sepsis with organ dysfunction or hypoperfusion (hypotension = decreased urine output)

Septic shock is severe sepsis with persistently low BP DESPITE IV fluid resuscitation

Question 19

How can sepsis lead to a reduction in blood pressure? (Hint: BP = TPR * CO)

Answer 19

There is a release of endotoxins which result in severe vasodilation. This serves to decrease TPR.

Question 20

Why would a septic patient become tachycardic?

Answer 20

Decreased TPR means there will be a lower venous return. Thus venous pressure falls… HR increases (baroreceptor response to fall in BP). SV decreases however so CO stays the same.

Question 21

E. Coli can be a causative pathogen of sepsis. Classify E. Coli.

Answer 21

Gram negative bacilli.

Question 22

Pneumonia can result in SIRS. What organisms may cause this infection?

Answer 22

Classical: Streptococcus pneumoniae (gram positive cocci), Haemophilus influenzae (gram negative coccobacilli - very short rods which look like cocci), Moraxella Catarhallis (gram negative cocci). Atypical: Mycobacterium, Legionella pneumophila (gram negative bacilli), Chlamydia (gram negative, pneumoniae)

Question 23

How would you treat pneumonia?

Answer 23

Specific treatments such as antibiotics are given.
If typical, amoxicillin (possibly with clavulanic acid to cover ß-lactamase inhibitors); if atypical, doxycycline or clarithromycin is often used.

Supportive treatment e.g. ventilation and fluids are given if required.

Question 24

C. Diff. is an example of a hospital acquired infection. Classify C. Diff.

Answer 24

Gram positive bacilli. It is an opportunistic pathogen.
Infection will normally present as gastroenteritis.

Question 25

Is C. Diff. part of the normal flora of the body?

Answer 25

Yes. It is normal flora in the large intestines.

Question 26

How can C. Diff. cause infection?

Answer 26

C. Diff. is a small component of the normal flora of the large intestine. Use of antibiotics, specifically those that decrease the amount of harmless bacteria in the gut, can help C. Diff. to outcompete these ‘harmless bacteria’. This leads to infection.

Question 27

With which antibiotics is C. Diff. closely associated with?

Answer 27

Amoxicillin (a penicillin - ß-lactam)

Cephalosporins (e.g. ceftriaxone - ß-lactam)
ß-lactams affects cell wall synthesis

Quinolones (e.g. ciprofloxacin, used as a broad-spectrum antibiotic)
Affect DNA synthesis

Question 28

Why are ß-lactams so effective against gram positive bacteria?

Answer 28

They affect cell wall synthesis - the outermost peptidoglycan membrane of a gram positive bacteria.
Thus they damage the structural integrity of these cells.

Question 29

How does C. Diff. exert its pathological effects?

Answer 29

By producing toxins: C. Diff. Toxin A and B - enterotoxin and cytotoxin respectively. They cause the diarrhoea and inflammation.

Question 30

How do bacteria become antibiotic resistant?

Answer 30

Conjugation: plasmid (genetic material) transfer through cell-to-cell contact or a bridge-like structure.
Transduction: DNA transfer via a viral vector (phage)
Transformation: uptake of exogenous DNA from the environment.

Normally DNA transfer from one bacterium to another.

Question 31

Classify norovirus.

Answer 31

RNA single-stranded virus.

Question 32

How is norovirus spread? Is it a healthcare infection?

Answer 32

Aerosol: inhalation or droplet transmission; Direct contact; Faecal-oral route.

Yes. Due to its route of transmission and high level of virulence.