Infection

Question 1

Cellulitis

Answer 1

severe inflammation of dermal and subcutaneous layers of the skin

Question 2

Candidiasis

Answer 2

Candida albicans and other Candida species

infections have various manifestations, depending on the site and the degree of immune-incompetence of the patient.

Question 3

Oral candidiasis (thrush)

Answer 3

yeast Candida albicans and other Candida species

raised, white plaques on the oral mucosa, tongue, or gums. The plaques can become confluent and ulcerated and spread to the throat

treated topically with nystatin or clotrimazole

Question 4

Vaginal candidiasis

Answer 4

yeast Candida albicans and other Candida species

itching and burning pain of the vulva and vagina, accompanied by a white discharge.

treated topically with nystatin or clotrimazole

Question 5

Pneumonia

• Definition
• Pathenogenesis
• Clinical features

Answer 5

Pneumonia is infection of the terminal air sacs (“alveoli”) and tissue of the lung.

Pneumococci, characteristically in pairs (diplococci), multiply rapidly in alveolar spaces and induce extensive oedema =incite an acute inflammatory
response in which neutrophils and congestion are prominent. As the inflammatory process progresses, macrophages replace the neutrophils and ingest debris. The
process usually resolves.

fever, malaise, tachypnea (increased respiratory rate),
and tachycardia, cough

Question 6

Pneumonia

• Definition
• Pathenogenesis
• Clinical features

Answer 6

Pneumonia is infection of the terminal air sacs (“alveoli”) and tissue of the lung.

Pneumococci, characteristically in pairs (diplococci), multiply rapidly in alveolar spaces and induce extensive oedema =incite an acute inflammatory
response in which neutrophils and congestion are prominent. As the inflammatory process progresses, macrophages replace the neutrophils and ingest debris. The process usually resolves.

fever, malaise, tachypnea (increased respiratory rate),
and tachycardia, cough

Question 7

Community-Acquired Pneumonia

Answer 7

pneumonia (infection of the lung parenchyma seen on chest X-ray) which develops outside the hospital

2 years old+: S.pneumoniae
Under 2 years old: Respiratory syncytial virus (RSV)
No causative agent is found in up to 40% of patients with CAP.

Question 8

X ray patterns of acute pneumonia

Answer 8

Lobar pneumonia is pulmonary consolidation demarcated by border of lung segment or lobe.
 Bronchopneumonia is seen as patchy consolidation around the larger airways
 Interstitial pneumonia is demonstrated by fine areas of shadowing in the lung fields and there is usually no sputum production at presentation. It is usually seen in mycoplasma, legionella, and viral pneumonia

Question 9

Meningitis

Answer 9

Meningitis is inflammation of the meningeal lining of the brain and spine.

A patient will have:
 General features of an infection such as fever, increased pulse rate
 Symptoms and signs due to inflammation of the meninges:
a. headache
b. photophobia (difficulty looking at bright lights)
c. vomiting
d. neck stiffness on flexion of the neck
e. irritable (progressing to reduced level of consciousness)
f. Other findings dependent on severity (e.g. sepsis) or complications.

Question 10

Sepsis

Answer 10

a syndrome of life-threatening organ dysfunction caused by a dysregulated host response to infection. It is usually caused by a bacterial infection.

Septic shock: subset of sepsis where particularly profound circulatory, cellular and metabolic abnormalities substantially increase mortality.

Causative agents depend on the syndrome, host and clinical context. Gram-negative infections account for an increasingly large proportion of cases,
particularly of healthcare-associated infections

Common presenting syndromes include pneumonia, intra-abdominal and urinary sepsis, and skin and soft tissue infections.

Management and treatment: prompt recognition, early appropriate
antimicrobial therapy and supportive treatment- Sepsis 6 bundle

Question 11

Neisseria meningitidis infection

Answer 11

Neisseria meningitidis is a Gram negative diplococcus that may be found within polymorphonuclear leukocytes (neutrophils)

Rates of meningococcal disease are highest for young children and increase again
for adolescents and young adults.

Neisseria meningitidis causes both meningitis and septicaemia. They can occur
together or separately.

Question 12

Septicaemia

Answer 12

the bacteria in the blood

Neisseria meningitidis in the blood triggers an intense host immune response.
- Fever:
- Sepsis: reduced level of consciousness, tachycardia, low blood pressure, poor peripheral circulation,
reduced urine output.
- Disseminated Intravascular Coagulation (DIC)
- Non-blanching Rash (30-75% pts)

Management:
Early recognition
 Early administration of antibiotics. 
 Urgent investigation
 Supportive care, often in an intensive care unit to manage organ
dysfunction and DIC.
 Notify Public Health
 Prevention

Treatment: ceftriaxone

Question 13

Disseminated Intravascular Coagulation (DIC)

Answer 13

syndrome of widespread intravascular activation of coagulation.

Question 14

Clostridioides difficile infection

Answer 14

gram-positive, anaerobic, spore-forming bacillus that is
responsible for the development of antibiotic-associated diarrhoea and colitis
(bowel inflammation).

Spore (faecal-oral) transmission

The diagnosis of C. difficile colitis should be suspected in any patient with
diarrhoea who has received antibiotics within the previous 3 months, has been
recently hospitalised, and/or has an occurrence of diarrhoea within 48 hours or more after hospitalisation

CDI clinical picture can vary from the asymptomatic carrier state to life-threatening colitis

Treatment:
-Asymptomatic carriers: No necessary treatment
-Mild, antibiotic-associated diarrhoea without fever, abdominal pain, or
leucocytosis: Cessation of antibiotic(s) may be the only treatment
necessary
-Mild to moderate diarrhoea or colitis: Metronidazole (P.O or IV)
or vancomycin (oral) for 10 days
-Severe or complicated disease: Vancomycin is considered to produce faster symptom resolution and fewer treatment failures than metronidazole; in
fulminant cases, combined therapy with IV metronidazole and
oral vancomycin may be considered

Question 15

MRSA

Answer 15

a type of Staphylococcus aureus that is resistant to most beta-lactam antibiotics, antistaphylococcal penicillins (e.g., methicillin, oxacillin), and
cephalosporins.

Skin to skin transmission

Treatment:

Question 16

Norovirus

Answer 16

a small, non-enveloped single stranded RNA virus that is a major cause of acute gastroenteritis outbreaks.

There is no specific treatment available so
treatment consists of supportive measures.

Transmission is mainly faecal-oral and also thought to be respiratory. Can be spread following ingestion of contaminated food, direct person-to-person contact or through contact with contaminated surfaces.

Question 17

HIV

Answer 17

Retrovirus that infects cells with CD4 surface receptor. It destroys the cell, causes inflammation and spreads to/infects to more cells

Clinical features: oral candidiasis, Kaposi’s sacroma, PCP

Transmission: contact of infected bodily fluids with mucosal tissue/blood/broken skin

Treatments: anti-retroviral drugs

Question 18

Malaria

Answer 18

One of the most common and deadly infections

Vector transmission: female Anopheles mosquito

Presentation: headache, fever, fatigue, pain, chill, pallor, sweating, dry cough, splenomegaly, nausea, vomiting] bite marks, low BP, high HR (110bpm)

Treatment dependant of species:
P. faciparum= artesunate, quinine + doxycycline
P. vivax, ovale, malariae = chloroquine,

Question 19

Endocarditis

Answer 19

Formation of vegetation that binds to valves or mural endocardium. Aberrant flow predisposes to a collection of fibrin, platelets and scant inflammatory cells

Clinical features of Endocarditis
 Fever
 Heart murmur
 Other cardiac complications
 Embolic features: These are small bits of the vegetation (or biofilm) that become loose and travel to small capillaries where they can block the
capillary or cause local infection at that site.
e.g Janeway lesions, splinter haemorrhages, roth spots in the eye, oslers nodes

Question 20

Chicken pox/shingles

Answer 20

Chicken pox: varicella
Shingles: Herpes zoster

Presentation: fever, malaise, headache, and abdominal pain. The exanthem begins on the scalp, face, or trunk as erythematous macules, which evolve into virus-containing vesicles that begin to crust over after about 48 hours

Treatment: acyclovir

Question 21

Examples of disease caused by healthcare infection viruses

Answer 21

blood borne viruses (hepatitis B, C, HIV)
norovirus
influenza
chickenpox

Question 22

Examples of disease caused by healthcare infection bacteria

Answer 22

Staph aures including MRSA
Clostridium difficle
Escherichia coli, Klebsiella pneumoniae
Pseudomonas aeruginosa
Mycobacterium tuberculosis

Question 23

Describe the role of E.coli in health and disease

Answer 23

Gra m-negative rods, typically lactose-fermenting, facultatively anaerobic

normal part of large bowel microbiota

Possibly protects against invasion by pathogenic species

Can cause:
intestinal infections
toxin-mediated disease
extra-intestinal infections

disease is linked to the presence of virulence factors, frequently restricted to specific E.coli strains

Question 24

Hepatitis B

Answer 24

Inflammation of the liver
Chronic: persistence of HBsAg after 6 months

Double-stranded eveloped DNA virus

Transmission: vertical (75% cases globally), sexual contact, drug injection, needlestick injuries

Presentation: jaundice, fatigue, abdominal pain, anorexia/nausea/vomiting, arthralgia

Treatment: no cure, life-long anti-virals
Vaccine available

Question 25

Pharyngitis

Answer 25

Streptococcus pyogenes ``` • Peak incidence 5-15 years • Droplet spread • Association with overcrowding • Untreated patients develop M protein specific antibody ``` ``` Clinical features Abrupt onset sore throat Malaise, fever, headache Lymphoid hyperplasia Tonsillopharyngeal exudates Throat swab -> Group A strep ```

Question 26

Scarlet fever

Answer 26

``` Due to infection with streptococcal pyrogenic exotoxin strain of S.pyogenes • Local or haematogenous spread • High fever, sepsis, arthritis, jaundice ```

Question 27

Typhoid and paratyphoid (enteric fever)

Answer 27

Systemic disease Salmonella typhi, Salmonella paratyphi= rod shaped Gram-negative bacteria Faecal-oral transmission from contaminated food/water -poor sanitation, limited access to clean water Presentation: fever headache, abdominal discomfort, dry cough, relative bradycardia ``` Treatment: fluoroquinolones (increasing resistance), IV ceftriaxone or azithormycin for 7-14days Vaccine available (50-75% effective) ```

Question 28

Dengue fever

Answer 28

commonest arbovirus Vector transmission: Aedes aegytpo Presentation: first infection ranges from asymptomatic to non-specific febrile illness

Question 29

Dengue fever

Answer 29

commonest arbovirus Vector transmission: Aedes aegytpo Presentation: first infection ranges from asymptomatic to non-specific febrile illness - lasts 1-5 days: intense headache, fever, muscle/joint pain, widespread red rash Supportive treatment only: paracetamol, fluids

Question 30

Schistosomaisis/bilharzia

Answer 30

Parasitic worms in fresh water snails (cercariae) - Schistosoma mansoni Presentation: fever, chills, cough, muscle aches, rash, itchy skin Treatment: praziquantel

Question 31

Ebola

Answer 31

Filovirus Presentation: flu-like illness with vomiting, diarrhoea, headaches, confusion, rash, internal/external bleeding at 5-7 day Transition: direct contact with body fluids

Question 32

Zika virus

Answer 32

Arbovirus (flavivrius) Vector transmission: Aedes mosquito and sexual transmission Presentation: 20% get symptoms which are mild, dengue-like No treatment, no vaccine

Question 33

Primary immunodeficiency disease

Answer 33

due to intrinsic gene defect: missing protein, missing cell, non-functional components

Question 34

Secondary immunodeficiency disease

Answer 34

due to an underlying disease/treatment:

Question 35

Primary immunodeficiency disease

Answer 35

due to intrinsic gene defect: missing protein, missing cell, non-functional components 65% caused by Ab defects

Question 36

Secondary immunodeficiency disease

Answer 36

due to an underlying disease/treatment: decrease production/function of immune components, increased loss of catabolism of immune components

Question 37

X-linked agammaglobulinaemia

Answer 37

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components Patient lacks B cells- defect in B cell development

Question 38

Primary immunodeficiency disease

Answer 38

due to intrinsic gene defect: missing protein, missing cell, non-functional components Presentation: age of symptom onset, type of microbes/sites Management: supportive treatment (infection prevention, nutritional support), specific treatment ( regular Ig therapy), comorbidities

Question 39

Common Variable Immunodeficiency (CVID)

Answer 39

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components Patient has B cells but do not produce any antibodies

Question 40

Selective IgA deficiency

Answer 40

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components Most common - slight raised risk of autoimmune conditions 90% of patients are asymptomatic prevalence 1:100 to 1:1000

Question 41

Hyper-IgM syndrome

Answer 41

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components no type switching in B cells= IgG is not produced. IgM continues to be produced leading to unusually high levels in serum

Question 42

Severe combined immunodeficiency (SCID)

Answer 42

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components T cells are defective. B cells are not activated

Question 43

Di George syndrome (thymus)

Answer 43

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components 5-10% of all PID deletion syndrome on chr22p11.2 absence of hypoplastic thymus= no T cell maturation

Question 44

Chronic granulomatous disease (CGD)

Answer 44

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components ~10% of all PIDs

Question 45

Chronic granulomatous disease (CGD)

Answer 45

Primary immunodeficiency disease due to intrinsic gene defect: missing protein, missing cell, non-functional components ~10% of all PIDs phagocytes lack killing machinery and are ineffective as a result

Question 46

Describe the serological antigensof E.coli

Answer 46

``` Capsule (K) LPS (O) Cell membrane Fimbriae (F) Flagella (H) production of toxins ```

Question 47

Describe E. coli as a cause of diarrhoea including its pathogenesis, role of toxins and clinical features

Answer 47

Enterotoxigenic E.coli (ETEC) is the most important cause of bacterial diarrohoeal illness Faeco-oral transmission ETEC produces two toxins, a heat-stable toxin (ST) and heat-labile toxin (LT) Toxins stimulate the lining of the intestines to secreted excessive fluid =watery diarrhoea and abdominal cramping other less common features: fever, nausea, chills, loss of appetite, headache, muscle aches and bloating

Question 48

Cystistis

Answer 48

Lower UTI Risk factors: female, history UTI, secual activity, vaginal infection, diabetes, obesity, genetic susceptibilyt Clinical features: frequent and urgent urination, dysuria, suprapubic pain, nocturia, hematuria, malaise Causative organisms: Uropathogenic E.coli (UPEC) Virulence factors: Adhesins (type 1 & other chaperone-usher pili_ toxins (HIyA, CNF1) Siderophores (aerobactin, enterobactin, yersinabactin) capsule

Question 49

Pyelonephritis

Answer 49

Upper UTI Risk factors: diabetes, HIV/AIDS, iatrogenic immunosuppression Clinical symptoms: back and/or flank pain fever, chills, malaise, nausea, vomiting, anorexia Causative organisms: Uropathogenic E.coli (UPEC) ``` Virulence factors: Adhesins (type 1 & P pili) toxins (HIyA, CNF1) Siderophores flagella ```

Question 50

Describe UPEC virulence factors

Answer 50

Adhesins: Type 1 fimbriae have adhesive tips that bind to alpha-D-mannosylated proteins on uroepithelium= adhesion, invasion of uroepitheilum and the formation of intracellular bacterial communities (IBCs) Toxins: Lipopolysaccharide (LPS) alpha-Hameolysin (HIyA) is a secreted, pore-forming toxin, cytotoic towards epithelial cells in the urinary tract bacteria produce their own iron-complexing proteins (siderophores) to acquire iron

Question 51

Describe E. coli as a cause of blood stream infections and sepsis

Answer 51

E.coli are the commonest cause of bacterial bloodstream infection in England ~50% of E.coli bloodstream infections occur in patients older than 75 years

Question 52

Describe the management of E. coli infections - Diarrhoea

Answer 52

Prevention: avoid contaminated food and water eating raw fruits, veg, seafood or undercooked meat or poultry in areas lacking adequate chlorinate Treatment: most recover without any specific treatments, clear liquids to prevent deydration oral rehydration solutions avoid antibiotics

Question 53

Describe the management of E. coli infections - UTI

Answer 53

Antibiotics: trimethoprim and nitrofurantoin

Question 54

Describe the management of E. coli infections - bloodstream infections

Answer 54

increasing resistance to a wide range of antibiotic classes

Question 55

Describe the management of E. coli infections - bloodstream infections

Answer 55

increasing resistance to a wide range of antibiotic classes

Question 56

Describe the structure of the Influenza virus

Answer 56

orthomyxovirus- spherical, enveloped viruses containing a segmented, negative strand RNA genome Genetic material: • (-) ssRNA – 8 genes • encoding 11 proteins • include 3 RNA polymerases (high error rates) Two surface antigens: • Haemagglutinin (H) – 18 types – binds to cells of the infected person • Neuraminidase (N) – 11 types - releases the virus from the host cell surface

Question 57

Define the concept of an animal reservoir for type A influenza (including poultry, horses, pigs, and other animals) and its major surface antigens - hemagglutinin (HA) and neuraminidase (NA)

Answer 57

a) influenza type A viruses in many animals, including horses, pigs, and wild migrating waterfowl. b) reassortment can occur between influenza A viruses that infect different animal and avian species, e.g., pigs can be infected by human- and avian-specific influenza viruses c) In environments where pigs, birds and humans coexist, it is possible for a pig to be simultaneously infected with multiple influenza subtypes. d) “Reassortants” can, therefore, be produced within one host animal (the pig), in which the mRNAs encoding the H and N antigens have been reassorted into unique combinations. e)The reassortant virus then has the potential to spread among humans, birds, and pigs.

Question 58

Describe the clinical symptoms and complications of influenza infection

Answer 58

headache, high fever, sore throat, runny nose, muscle aches and pains complications of influenza: viral pneumonia, secondary (bacterial) pneumonia, central nervous system syndromes, or Reye syndrome

Question 59

Describe how you would diagnose flu in a clinical setting

Answer 59

sample from a nasopharyngeal swab

Question 60

Briefly outline the management of influenza including treatment options and prevention Treatment and prevention including vaccination and how this is determined by WHO each year

Answer 60

antivirals NA inhibitors- Tamiflu Prevention: formalin-activated vaccine by injection influenza A&B live, attenuated, cold-adapted vaccine by nasal spray Influenza A&B

Question 61

Define the concepts of antigenic shift (acquisition of a novel HA and NA by the virus) and antigenic drift (yearly accumulation of mutations in the HA and NA)

Answer 61

antigenic shift= acquisition of a novel HA and NA by the virus antigenic drift =yearly accumulation of natural mutations in the HA and NA - this causes seasonal epidemics

Question 62

Define the concepts of antigenic shift (acquisition of a novel HA and NA by the virus) and antigenic drift (yearly accumulation of mutations in the HA and NA)

Answer 62

antigenic shift= major changes in the genes of flu vruses that occur suddenly when two or more different strains combine. Acquisition of a novel HA and NA by the virus- cause widespread epidemics/pandemics antigenic drift =yearly accumulation of natural mutations in the HA and NA - this causes seasonal epidemics

Question 63

Define the concepts of pandemics and epidemics (seasonality) and how these may arise in relation to influenza.

Answer 63

Antigentic shift phenomenon can be easily explained by the reassortment of different RNA segments from each species in a new capsid. Occurs infrequently - maybe every 10 or 20 years Only influenza type A viruses show antigenic shift May not have been seen in circulation in population for many years Immune systems of many individuals have no defence against this new subtype Epidemic - Prevalent among a people or a community at a special time, and produced by some special causes not generally present in the affected locality Pandemic - epidemic over a very large area; affecting a large proportion of a population – often the world

Question 64

Suppurative complications of streptococcal | pharyngitis

Answer 64

* Peritonsillar cellulitis/abscess * Retropharyngeal abscess * Mastoiditis, sinusitis, otitis media * Meningitis, brain abscess

Question 65

Acute rheumatic fever

Answer 65

Complications of streptococcal pharyngitis ``` Inflammation of heart, joints, CNS • Follows on from pharyngitis • Rheumatogenic M types • Possible mechanisms: – Auto-immune – Serum sickness – Binding of M protein to collagen – ASO, ASS induced tissue injury ```

Question 66

Acute post-streptococcal | glomerulonephritis

Answer 66

Complications of streptococcal pharyngitis Acute inflammation of renal glomerulus • M type specific but NOT same as ARF M types • Antigen-antibody complexes in glomerulus

Question 67

Impetigo

Answer 67

Streptococcus pyogenes skin infections Childhood infection, 2-5 years – Initial skin colonisation, followed by intradermal innoculation – No ARF but impetigo is most common cause of glomeruonephritis

Question 68

Erysipelas

Answer 68

Streptococcus pyogenes skin infections – Dermis infection with lymphatic involvement – Face, lower limbs – Facial lesions frequently preceded by pharyngitis – Lower limb infection usually secondary to invasion of skin via trauma, skin disease or local fungal infection

Question 69

Cellulitis

Answer 69

Streptococcus pyogenes skin infections Skin and subcutaneous tissue infection – Impaired lymphatic drainage and illicit injecting drug use important risk factors

Question 70

Necrotising fasciitis

Answer 70

Streptococcus pyogenes skin infections ``` Infection of deeper subcutaneous tissues and fascia. – Rapid, extensive necrosis – Usually secondary to skin break – Severe pain, even before gross clinical changes – High fever, fulminant course, high mortality (20-70%) ```

Question 71

Streptococcal toxic shock syndrome

Answer 71

Deep tissue infection with Strep pyogenes AND Bacteraemia AND Vascular collapse AND Organ failure From health to death in hours Entry of group A strep into deeper tissues and bloodstream Streptococcal pyrogenic exotoxins stimulate T-cells through binding to MHC class II antigen-presenting cells and V-β region of T-cell receptor, inducing monocyte cytokines (TNF-α, IL-1β, IL-6) and lymphokines (TNF-β, IL-2, IFN-γ). M-protein fibrinogen complex formation