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ooster phenomenon 112 botulinum toxin
a recall or anamnestic response through stimulation of
memory cells that encountered the same antigen previously.
Booster injections are given after a passage of time sufficient
for a primary immune response specific for the immunogen
to have developed. Booster injections are frequently
given to render the subject immune prior to the onset of a
particular disease or protect the individual when exposed to
subjects infected with the infectious disease agent against
which immunity is desired.
booster phenomenon
An expansion in the diameter of a tuberculin reaction following
the administration of a subsequent PPD skin test
for tuberculosis. The reaction is usually larger than 6 mm
and shows an increase in size from below 10 mm to more
than 10 mm in diameter following the secondary challenge.
A positive test suggests an increased immunologic
recall as a consequence of either previous infection with
Mycobacterium tuberculosis or other mycobacteria. It is
seen in older subjects with previous M. tuberculosis infections
who fail to convert to active disease.
booster response
The secondary antibody response produced during immunization
of subjects primed by earlier exposure to the same antigen.
Also called anamnestic response and secondary response.
Jules Jean Baptiste Vincent Bordet.
Bordet, Jules Jean Baptiste Vincent (1870–1961)
Belgian physician who graduated from the University of
Brussels as a doctor of medicine. He served as a preparateur
in Metchnikoff’s laboratory at the Institut Pasteur from
1894 to 1901 where he discovered immune hemolysis and
elucidated the mechanisms of complement-mediated bacterial
lysis. He and Gengou described complement fixation
and pointed to its use in the diagnosis of infectious diseases.
Their technique was subsequently used by von Wassermann
to develop a complement fixation test for syphilis that
enjoyed worldwide popularity. Bordet’s debates with Paul
Ehrlich on the nature of antigen–antibody–complement
interactions stimulated much useful research. He was
awarded the 1919 Nobel Prize in Medicine or Physiology
for his studies on immunity. (Refer to Traite de l’Immunite
dans les Maladies Infectieuses, 1920.)
Bordetella immunity
Bordetella pertussis produces the respiratory disease known as
whooping cough or pertussis. Both humoral and cell-mediated
immune responses follow infection. The neutralizing antibodies
believed to be the principal protective mechanism against
infection with B. pertussis are formed against the B. pertussis
antigens PT, FHA, PRN, and fimbriae associated with protection
against pertussis. Pertussis infection can lead to long-lasting
immunity against subsequent pertussis. Patients recovering
from the infection develop anti-B. pertussis immunoglobulin
A (IgA) in serum and saliva, pointing to the role of mucosal
antibodies. Cell-mediated immunity is also believed to be
significant, as T H1 cells specific for the microorganism occur
in persons following either infection or vaccination. High-titer
IgG antibodies may clear bacteria in respiratory infections,
as revealed by animal studies, but cell-mediated immunity is
necessary to completely eliminate the microorganism from
mouse lungs. In humans, immunity that follows infection may
prevent respiratory colonization, whereas immunity that follows
vaccination may protect against toxin-mediated disease.
B. pertussis antigens suppress the host response to pertussis
both in vitro and in vivo. The whole-cell vaccine comprised
of killed, whole, virulent B. pertussis has been replaced with
an acellular preparation combined with diphtheria and tetanus
toxoid in the currently used DTaP vaccine. It provides fewer
and milder side effects than the whole-cell vaccine preparation
and is more effective in inducing serum antibody
responses and protection from pertussis.
Bordetella pertussis
The etiologic agent of whooping cough in children. Killed
Bordetella pertussis microorganisms are administered in a
vaccine together with diphtheria toxoid and tetanus toxoid
as DPT. The endotoxin of B. pertussis has an adjuvant
effect that can facilitate antibody synthesis.
Borrelia immunity
Relapsing fever and Lyme disease are produced by
members of this genus. Borrelia burgdorferi sensu lato
spirochetes are the causative agents of Lyme disease. These
microorganisms are covered by a slime layer comprised of
self molecules that block immune recognition. The slime
layer acting as a capsule prevents phagocytosis, but the
microbe is killed when it is incubated with specific antibody
in complement. The principal surface proteins in the exterior
cell membrane include A, B, C, D, E, and F, which are
designated as outer surface proteins (Osps). The proteins
are heterogeneous, but their function remains to be determined.
Spirochetes that cause Lyme disease upregulate or
downregulate Osp A and Osp C during the course of human
infection. Other antigens in the outer membrane of Borrelia
burgdorferi sensu lato include 16-, 27-, 55-, 60-, 66-, and
83-kDa proteins. Osp A is the principal candidate for a
Lyme disease vaccine. Soon after infection with Borrelia
burgdorferi sensu lato, the microorganisms become refractory
to the action of bactericidal antibodies.
botulinum toxin
A toxin formed by Clostridium botulinum. The 150-kDa,
type A toxin is available in purified form and is employed
to treat neuromuscular junction diseases such as dystonias.
It acts by combining with the presynaptic cholinergic nerve
terminals where it is internalized and prevents exocytosis of