John Smith was admitted to UMass Medical Center at age 27 with pneumonia. This w

Question

John Smith was admitted to UMass Medical Center at age 27 with pneumonia. This was his 25th admission to the hospital in his life time. On previous admissions (since his first year of life) he had been treated for middle ear infection, pneumonia, sinusitis, skin abscesses and septicemia. On physical examination at his latest admission, John was found to be slightly obese but otherwise normally developed.

A urine analysis yielded normal results. His white cell count in blood was 6000 per microliter (normal range is 4,500 and 10,000). His platelet count was 240,000 per microliter (normal range is 150,000 to 450,000) and his blood clotted normally. His red blood cells gave a strong positive agglutination reaction with an antibody to C3 but no agglutination with an antibody to lgG or IgM. His serum lgG level was 9.15 mg/mL, IgA 4.75 mg/mL and IgM 1.35 mg/mL (all normal). John responded normally to an injection of tetanus vaccine, and showed a rise in serum antibody levels to the tetanus toxoid.

Serum levels of C3 were 2.7 mg/mL (normal values 9.7—20.4 mg/mL). The serum levels of all other complement components were normal except for factor B, which was undetectable. He also lacked complement regulatory factor I. His serum failed to kill a smooth strain of Salmonella newport, even after addition of C3 to the serum to render the C3 concentration normal.

A) Describe the mechanism that is leading to recurrent infections in Mr. Smith?

B) Can you suggest a specific therapy that will help Mr. Smith?

C) Mr. Smith’s clinical course has improved with age and he now has fewer infections than he had as a child and adolescent? How do you explain this?

D) Why did Mr. Smith’s red blood cells agglutinate with antibody to C3?

Explanation / Answer

A Ans. It's due to primary immunodeficiency which weaken the immune system, allowing infections to occur more easily.
Because they are born missing some of the body's immune defences which leaves them more susceptible to germs that can cause infections.

BAns. prolonged antibiotic therapy.

C) Previously in his childhood he had many infections but in his adolescent he has fewer infections which we can say with the help of reports. It's sure to as he lived longer his adaptive immunity started increasing. His adaptive immunity against these common bacteria becomes better and he has come to rely less on innate immune mechanisms for protection against infection.

D) He is producing large amounts of C3b. which binds to complement receptor 1 on RBC and leads to agglutination by anti-C3

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