Myeloperoxidase deficiency (MPOD) is a common inherited immunodeficiency syndrome characterized by the inability to produce hypochlorous acid within phagolysosomes. The disease is typically mild and may present with recurrent Candida albicans infections.
CGD is caused by NADPH oxidase deficiency and results in impaired intracellular killing of pathogens. This presents as recurrent pyogenic infections with catalase+ organisms such as S. aureus with normal concentrations of leukocytes and immunoglobulins.
So that is to say BOTH CGD(NADPH oxidase deficiency) AND Myeloperodiase deficiency predisposes to catalase-positive bug infection.
FA2020 P109 only emphasized on "CGD patient are at increased risk for infection by catalase+ species capable of neutralizing their own H2O2, leaving phagocytes without ROS for fighting infection". But apparently, according to this question, this statement holds true to Myeloperodiase deficiency as well
Why not superoxide dismutase? Its the step right in between NADPH (chronic granulomatous disease) and MPO
Myeloperoxidase is the only one actually involved in making free radicals. Catalase makes H2O2 into water, Superoxide dismutase eliminates oxygen radicals, LDH makes lactate (no role in bacterial killing), and NO synthase, makes NO.
why is ther hyperreflxia and a babinski sign meaning that there is an UMN lesion?
submitted by โitsalwayslupus(48)
From Pathoma Ch. 2 pg. 14: MPO deficiency results in defective conversion of H2O2 to HOCl. Increased risk for Candida infxns (although most patients asymptomatic). Nitroblue tetrazolium test is normal because the respiratory burst is actually still intact. This patient has candida infection and delayed, but still can kill staph a, which seemingly goes along with the fact that the respiratory burst is still intact, but without MPO it may be hindered a little.