Escherichia Coli, Influenza & Streptococci *on IMs

Question 1

• describe what type of bacteria e-coli is. where does it normally reside?
• ecoli are diverse w many different antigens like O,H,K,F. How can we distinguish between the different types?
• name the different types of infections e-coli can cause.

Answer 1

• gram negative rods (stains pink), lactose fermenting, anaerobic, often motile. Normally found as part of large bowel microbiota.
• serology using antibodies to find different bacterial antigens, metabolic profiling.
• intestinal infections eg diarrhoea, toxin mediated disease, extra-intestinal infections eg UTIs.

Question 2

• how does e-coli cause diarrhoea? how do you manage & treat this?
• what is shiga toxin producing e-coli? what symptoms can it cause?
• extra intestinal pathogenic e-coli cause disease outside of the intestinal tract. Name some virulence factors.

Answer 2

• there are 6 pathotypes of diarrhoeagenic ecoli. One type, enterotoxigenic E. coli (ETEC), is an important cause of bacterial diarrhoea. Faeco-oral transmission and common in LEDCs. ETEC produces 2 toxins; heat stable toxin (ST) and heat labile toxin (LT), these toxins then enter the villi cells. This stimulates the lining of the intestines causing them to secrete excess fluid producing watery diarrhoea. Onset 1-3 days, lasts 4 days. Manage=a valid foods and drink contaminated, treat=most recover themselves, fluids, oral rehydration solutions, NO ABX.
• aka EHEC, type of E. coli, causes bloody diarrhoea and haemolytic uraemia syndrome ( pa triad=acute renal failure, haemolytic anaemia, thrombocytopenia)
• adhesins, toxins.

Question 3

• describe how e-coli can cause a UTI. give some symptoms. & treatment.
• give some causal factors of E. coli bacterial infection in the bloodstream. Treatment?

Answer 3

• more common in women because the urethra is shorter so bacteria’s journey is shorter, the e-coli transfers from the rectum to the urethra and then migrated to the bladder. Symptoms=freq and urgent urination, dysuria. To treat= empirical Abx eg trimethoprim & nitrofurantoin.
• 50% have had previous UTIs so could be linked to ineffective Abx treatment, urinary catheters. Treat=Abx but increasing resistance .

Question 4

• describe viruses in terms of payload and delivery system.
• describe the structure of the influenza virus.
• describe the 3 different types of influenza virus.

Answer 4

• delivery=protects the virus against degradation in the environment and contains structures it uses to bind to hosts. Payload=contains the genome and enzymes necessary to initiate the virus replicating.
• part of the orthomyxovirus family, spherical, enveloped, containing (neg)-ssRNA. 2 surface antigens= (Haemagglutinin) H which binds to host cells, (Neuraminidase) N which releases the virus from the host.
• 1)Influenza A=antigenic shift & drift, may cause large pandemics and kill YP, mainly spread in birds.2) Influenza B=antigenic drift only, severe disease in older adults, no pandemics, main,y spread by kids.3) Influenza C=antigenic drift only, mild disease

Question 5

• how does the influenza virus replicate?
• give 3 ways the influenza virus transmitted.
• give 3 barriers to entry of influenza virus through the respiratory route.

Answer 5

• the neg ssRNA is converted to +ssRNA and mRNAs. The mRNA forms viral proteins which are assembled into nucleocapsids which the -ssRNA is inserted into.
• spread via the respiratory route, 3 potential modes: 1=small particle aerosols, remain suspended in air for hrs. 2=larger particles or droplets, infect w direct contact. 3=particles on surfaces, spreads via indirect contact.
• 1=resp epithelial cells are covered by a thick mucus that traps viruses. 2= ciliates resp epithelia sweep mucus from lower down upwards to be coughed out. 3=immunologic defences in the lung including secretory IgA, MK cells and macrophages.

Question 6

• how does the influenza virus enter cells?
• how does the influenza virus then leave cells?
• give symptoms and possible complications of influenza.

Answer 6

• the virus has H protein on the surface. This binds to sialic acid residues on a glycoproteins/glycolipid then enters the host via receptor-mediated endocytosis.
• the H that’s bound to sialic acid residues is cleaved off by N antigen to allow the release of the virus from the host surface after mRNA insertion.
• symptoms=fever, dry cough,sore throat, nausea, fatigue, no symptoms. Complications=meningitis/encephalitis, bronchitis, pneumonia.

Question 7

• how long does influenza typically incubate for?
• in which groups is risk of serious complications greater?
• how can influenza be diagnosed?
• how can flu kill?

Answer 7

• typically for 1-5 days
• children under 6 months, older ppl, those w underlying health conditions eg immunosuppressed, pregnant, morbidly obese.
• usually via symptoms & clinical assessment only, but can use rapid influenza diagnostic tests.
• symptoms are caused by the immune systems response to virus, it could overreact and T cells attack tissue the virus is replicating in eg lungs, OR opportunistic 2nd infection eg bacterial esp in lungs.

Question 8

• give 3 types of treatment for influenza.
• describe antigenic drift.
• describe antigenic shift. How does this reassortment happen?

Answer 8

• 1=antivirals eg rimantadine, inhibit viral undo sting after uptake. (A) 2=neuraminidase inhibitors eg oseltamivir (tamiflu), inhibits viral release from host, aggregates viral particles (A & B). 3=prevention via vaccine (inactivated for A&B or live attenuated in kids -also A&B)
• antigenic drift=minor changes (natural mutations) in the genes of flu viruses (in H & N proteins) that happen gradually over time ie cause seasonal epidemics.
• antigenic shift=major changes in the gene of flu viruses (H & N proteins) that happen suddenly when 2 or more diff strains combine, results in new subtype and can cause pan/epidemics. ONLY in influenza A!
• between viruses in diff animal and avian species, an animal can be infected w both and mRNAs encoding H&N antigens can be reassorted into unique combos.

Question 9

• describe streptococci.
• describe streptococcal pharyngitis incl the microorganism, clinical features, type of spread, peak incidence and what can happen if it’s untreated.

Answer 9

• a bacteria, gram positive cocci, (strep = string of pills, staph= grapes).
• classified by haemolysis of blood agar that the bacteria will break down- a measure of how fast the bacteria grows. 1)Alpha haemolysis=partial breakdown of RBCs in agar eg strep ‘viridans’- means green bc turns green. 2)beta haemolysis=complete breakdown of blood agar eg strep pyogenes. 3)non-haemolytic= sometimes called gamma haemolysis. Lancefield class=group A strep.
• caused by strep pyogenes, symptoms=abrupt onset sore throat, malaise, lymphoid hyperplasia, tonsil exudate, fever. Throat swab gives group A strep. Droplet spread, peaks in 5-15 yrs, if untreated= develop M protein specific antibody.

Question 10

-describe the following complications of streptococcal pharyngitis: scarlet fever, suppurative complications, acute rheumatic fever, acute post-strep glomerulonephritis.

Answer 10

• scarlet fever=local or haematogenous spread, high fever, sepsis, jaundice, rash all over body.
• suppurative complications= peritonsillar abcess, retropharyngeal abcess, mastoiditis, meningitis.
• acute rheumatic fever=inflammation of heart, joints, CNS. Following pharyngitis. Causes=autoimmune.
• acute post-strep glomerulonephritis=acute inflammation of renal glomerulus.

Question 11

• give 4 examples of skin infections caused by strep pyogenes.
• outline streptococcal toxic shock syndrome.

Answer 11

• 1=impetigo, childhood infection (2-5yrs), initially skin colonisation followed by I trader also innoculation.
• 2=erysipelas, dermis infection w lymphatic involvement, face and lower limbs, facial lesions and redness
• 3=cellulitis, skin and subcutaneous tissue infection, impaired lymph drainage, injecting drugs is a major RF.
• 4=necrotising fasciitis, infection of deeper subcutaneous tissue and fascia, rapid and extensive necrosis, usually after a skin break eg after surgery, high fever + severe pain, high mortality (20-70%)
• streptococcal TSS= deep tissue infection w strep pyogenes + bactaraemia + vascular collapse + organ failure. Where strep A get into deeper tissues and blood. Health-> death in hrs.