Infectious diseases

Question 1

How does strep associated HUS present?

Answer 1

5% of cases of HUS
Caused by toxin neuraminidase which damages endothelial cells.
The bacteria remove N-acetylneuraminic acid from cell-surface glycoproteins and expose the normally hidden T-antigen (Thomsen-Friedenreich antigen) on erythrocytes, platelets, and glomeruli.
Blood serum has anti-T immunoglobulin M (IgM), which can react with the antigen and cause damage to red blood cells and the kidneys

Classic sx of : Haemolytic anaemia, low platelets, uraemia (with raised Cr)

Question 2

What are the main features of Cutaneous leishmaniasis?

Answer 2

Found in America, North Africa, Middle East and Asia
Caused by protazoa leishmaniasis
• Acquired through bite of
infected sandfly
• Erythematous papule enlarges to
nodule to ulcerating lesion months
with raised indurated borders
• May spontaneously resolve
over months/years
• Biopsy to confirm diagnosis
• Various therapeutic options

Question 3

What are the main features of Cutaneous larva migrans?

Answer 3

AKA “creeping eruption”
• Most frequent skin disease among travellers returning from tropical countries (esp from beaches)
• Animal hookworms (contact with dog/cat faeces)
– Ancylostoma braziliense (cat)
– Ancylostoma caninum (dog)
• Incubation period usually short
• Advancing serpiginous tracts in skin with associated intense pruritus
• Eventually self limiting
• Treatment
– Oral albendazole, or ivermectin
• Complications
– Impetigo
– Local and generalised allergic reactions
– hypereosinophilia

Question 4

GAS

Answer 4

• gram +ve bacteria (NO endotoxins as this is gram -ve only bacteria

GAS induces disease by at least three mechanisms:

• Suppuration, as in pharyngitis, pyoderma, or abscesses
• Toxin elaboration (superantigen-mediated), as in strep toxic shock syndrome
• Non-suppurative, immune-mediated inflammatory mechanisms, as in acute renal failure, acute glomerulonephritis, and, possibly, reactive arthritis

Question 5

ESBL

Answer 5

Not long after cefotaxime came into clinical use in Europe, strains of Klebsiella pneumoniae were discovered in Germany with transferable resistance to the oxyimino-cephalosporins (e.g. cefotaxime, ceftazidime, and ceftriaxone).

ESBLs arose by amino acid substitutions that allowed narrower spectrum enzymes to attack the new oxyimino-beta-lactams.

ESBLs vary in activity against different oxyimino-beta-lactam substrates but cannot attack the cephamycins (cefoxitin, cefotetan and cefmetazole) and the carbapenems (imipenem, meropenem and ertapenem).

They are also generally susceptible to beta-lactamase inhibitors, such as clavulanate, sulbactam, and tazobactam, which consequently can be combined with a beta-lactam substrate to test for the presence of this resistance mechanism.

ESBLs have been found exclusively in Gram-negative organisms, primarily in Klebsiella pneumoniae, Klebsiella oxytoca, and Escherichia coli.

But also in Acinetobacter, Burkholderia, Citrobacter, Enterobacter, Morganella, Proteus, Pseudomonas, Salmonella, Serratia, and Shigella spp.

ESBL-producing isolates typically show greater than average resistance to other agents including aminoglycosides and fluoroquinolones.

A review of 85 episodes of bacteremia with ESBL-producing K. pneumonia showed that:
◾All isolates were susceptible to imipenem or meropenem,
◾ While 71% were resistant to gentamicin, 47% to piperacillin-tazobactam, and 20% to ciprofloxacin.

Question 6

Erythema multiforme

Answer 6

Erythema multiforme is an immune-mediated condition characterised by the appearance of distinctive target-like lesions on skin. If involving mucosa, it is erythema multiforme major.

Target lesions - round erythematous papules that evolve with a dusky central area or blister, dark red inflammatory zone surround by pale ring of oedema with an erythematous halo on extreme periphery of lesion. It most commonly appears in symmetrical distribution on the extensor surfaces of acral (distal)extremities, and subsequently spreads in a centripetal manner.

It usually appears over 3-5 days and resolves within two weeks. Lesions do not scar but post-inflammatory hyperpigmentation may remain for months after resolution

Causes
◾Infections (viral, bacterial or fungal à 90% of cases). HSV infection is most common precipitator. Mycoplasma pneumoniae is also common.
◾Medications (<10%): NSAIDs; sulfonamides; antiepileptics; antibiotics
◾Malignancy
◾Autoimmune disease
◾Immunisations
◾Radiation
◾Sarcoidosis
◾Menstruation

Question 7

Ramsay hunt syndrome

Answer 7

Ramsay Hunt syndrome (herpes zoster oticus) occurs when a shingles outbreak affects the facial nerve near one of your ears. In addition to the painful shingles rash, Ramsay Hunt syndrome can cause facial paralysis and hearing loss in the affected ear