Relapsing fever pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | ==Pathophysiology== | ||
*After entering the bloodstream, spirochetes replicate extracellularly and remain predominantly in the plasma space. Some organisms are found within circulating polymorphonuclear cells or reticuloendothelial cells, or Occasionally can be found in tissues such as liver, spleen, kidney, heart, or brain, with foci of perivascular inflammation, hemorrhage, and infarction at autopsy. | *After entering the bloodstream, [[spirochetes]] replicate extracellularly and remain predominantly in the [[plasma]] space. Some organisms are found within circulating polymorphonuclear cells or reticuloendothelial cells, or Occasionally can be found in tissues such as liver, spleen, kidney, heart, or brain, with foci of perivascular inflammation, hemorrhage, and infarction at autopsy. | ||
*Patients generally remain asymptomatic until high-level spirochetemia (104-108 organisms m!) develops, at which time symptoms begin abruptly. Although spirochetes are pyrogenic, they probably do not generate detectable endo- or exotoxins. Organisms are cleared predominantly by opsonizing antibodies with resolution of symptoms ( afebrile period), followed several days or weeks later by reemergence of a new antigenic strain, high-level spirochetemia, and recurrence of symptoms. | *Patients generally remain [[asymptomatic]] until high-level [[spirochetemia]] (104-108 organisms m!) develops, at which time symptoms begin abruptly. Although [[spirochetes]] are [[pyrogenic]], they probably do not generate detectable endo- or exotoxins. Organisms are cleared predominantly by opsonizing [[antibodies]] with resolution of symptoms ( [[afebrile]] period), followed several days or weeks later by reemergence of a new antigenic strain, high-level spirochetemia, and recurrence of symptoms. | ||
*This cyclical process of initially effective immune response followed by antigenic variation and immunologic escape is responsible for the relapsing nature of this illness | *This cyclical process of initially effective [[immune response]] followed by [[antigenic variation]] and [[immunologic]] escape is responsible for the relapsing nature of this illness. There are multiple genes in the spirochete encoding [[variable]] [[membrane]] [[proteins]]( [[VMPs]]). These '''VMPs''' determine the antigenic serotype of the organism. At any given time, each spirochete has VMP genes that are [[expressed]] and others that are [[silent]]. An antigenic switch occurs when a given VMP gene transposes from silent to an expressed locus. This mechanism of [[antigenic variation]] presumably leads to [[immunologic escape]] and relapse. | ||
*Specific serotypes can recur within an individual. Infection with a given strain of Borrelia may | *Specific serotypes can recur within an individual. Infection with a given strain of [[Borrelia]] may cause partial protection against subsequent infection by the same strain. In some highly endemic areas, relapsing fever is more severe in newcomers than natives. | ||
==References== | ==References== | ||
Revision as of 16:19, 9 August 2020
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Overview
Pathophysiology
- After entering the bloodstream, spirochetes replicate extracellularly and remain predominantly in the plasma space. Some organisms are found within circulating polymorphonuclear cells or reticuloendothelial cells, or Occasionally can be found in tissues such as liver, spleen, kidney, heart, or brain, with foci of perivascular inflammation, hemorrhage, and infarction at autopsy.
- Patients generally remain asymptomatic until high-level spirochetemia (104-108 organisms m!) develops, at which time symptoms begin abruptly. Although spirochetes are pyrogenic, they probably do not generate detectable endo- or exotoxins. Organisms are cleared predominantly by opsonizing antibodies with resolution of symptoms ( afebrile period), followed several days or weeks later by reemergence of a new antigenic strain, high-level spirochetemia, and recurrence of symptoms.
- This cyclical process of initially effective immune response followed by antigenic variation and immunologic escape is responsible for the relapsing nature of this illness. There are multiple genes in the spirochete encoding variable membrane proteins( VMPs). These VMPs determine the antigenic serotype of the organism. At any given time, each spirochete has VMP genes that are expressed and others that are silent. An antigenic switch occurs when a given VMP gene transposes from silent to an expressed locus. This mechanism of antigenic variation presumably leads to immunologic escape and relapse.
- Specific serotypes can recur within an individual. Infection with a given strain of Borrelia may cause partial protection against subsequent infection by the same strain. In some highly endemic areas, relapsing fever is more severe in newcomers than natives.