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Untitled - D Ank Unlimited

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dinitrochlorobenzene (DNCB) 229 diphtheria toxin<br />

dinitrochlorobenzene (DNCB)<br />

A substance employed to test capacity to develop a cellmediated<br />

immune reaction. A solution of DNCB is applied<br />

to the skin of an individual not previously sensitized<br />

against this chemical, where it acts as a hapten, interacting<br />

with proteins of the skin. Re-exposure of this same individual<br />

to a second application of DNCB 2 weeks after the<br />

first challenge results in a T-cell-mediated, delayed-type<br />

hypersensitivity (contact dermatitis) reaction. Persons with<br />

impaired delayed-type hypersensitivity or cell-mediated<br />

immunity may reveal impaired responses. The 2,4-dinitro-<br />

1-chlorobenzene interacts with free α amino terminal<br />

groups in polypeptide chains and with side chains of<br />

lysine, tyrosine, histidine, cysteine, or other amino acid<br />

residues.<br />

dinitrofluorobenzene (2,4-dinitro-1-fluorobenzene)(DNFB)<br />

A chemical employed to prepare hapten–carrier conjugates.<br />

It inserts the 2,4-dinitrophenyl group into molecules containing<br />

free –NH 2 groups. When placed on the skin, it leads<br />

to contact hypersensitivity.<br />

dinitrophenyl (DNP) group<br />

Designation for 2,4-dinitrophenyl groups that become<br />

haptens after they are chemically linked to –NH 2 groups<br />

of proteins that interact with chlorodinitrobenzene, 2,4dinitrobenzene<br />

sulphonic acid, or dinitrofluorobenzene.<br />

These protein carrier–DNP hapten antigens are useful<br />

as experimental immunogens. Antibodies specific for<br />

the DNP hapten that are generated through immunization<br />

with the carrier–hapten complex interact with<br />

low molecular weight substances that contain the DNP<br />

groups.<br />

diphtheria and tetanus toxoids (adsorbed, injection)<br />

The preparation intended for pediatric use (DT) is indicated<br />

for active immunization against diphtheria and tetanus in<br />

infants and children from 2 months to 7 years of age, for<br />

whom the use of combined vaccine containing pertussis<br />

antigen is contraindicated. The vaccine should be administered<br />

intramuscularly. The potency of tetanus and diphtheria<br />

toxoids has been determined based on immunogenicity<br />

studies, with comparison to a serological correlate of protection<br />

(0.01 antitoxin units/mL) established by the Panel<br />

on Review of Bacterial Vaccines and Toxoids. Results of<br />

the study indicated protective levels of antibody were raised<br />

in more than 90% of the study population after primary<br />

immunization with both components. Booster injections<br />

were effective in 100% of individuals with pre-existing<br />

antibody responses.<br />

diphtheria and tetanus toxoids and acellular pertussis<br />

vaccine (adsorbed [DTaP], injection)<br />

Intended for active immunization against diphtheria, tetanus<br />

and pertussis simultaneously in infants and children<br />

6 weeks to 7 years of age (prior to seventh birthday).<br />

These preparations combine diphtheria and tetanus toxoids<br />

with acellular pertussis bacterial vaccine. The acellular<br />

pertussis antigens include pertussis toxin (PT), FHA,<br />

and pertactin. Immunization with diphtheria and tetanus<br />

toxoid is believed to confer protection lasting 10 years.<br />

Nevertheless, diphtheria toxoid does not prevent carriage<br />

of Corynebacterium diphtheriae in the pharynx, nose, or<br />

skin. Protection against pertussis lasts 4 to 6 years. Serum<br />

diphtheria and tetanus antitoxin levels of 0.l IU/mL and<br />

higher are considered protective. Efficacy of the pertussis<br />

component does not have a well established correlate of<br />

protection.<br />

diphtheria antitoxin<br />

An antibody generated by the hyperimmunization of<br />

horses against Corynebacterium diphtheriae exotoxin<br />

with injections of diphtheria toxoid and diphtheria toxins.<br />

When used earlier in the 20th century to treat children<br />

with diphtheria, many of the recipients developed serum<br />

sickness. It may be employed for passive immunization to<br />

treat diphtheria or for short-term protection during epidemics.<br />

Presently, pepsin digestion of the serum globulin<br />

fraction of the antitoxin yields F(ab′) 2 fragments of antibodies<br />

that retain their antigen-binding property but lose<br />

the highly antigenic Fc region. This process diminishes<br />

the development of serum sickness-type reactions and is<br />

called despecification.<br />

diphtheria immunization<br />

The repeated administration of diphtheria toxoids as alumprecipitated<br />

toxoids (APTs). Toxoid–antitoxin floccules<br />

(TAFs) constitute an alternate form for adults who show<br />

adverse reactions to adenosine triphosphate (APT). Besides<br />

this active immunization procedure, diphtheria antitoxin<br />

can also be given for passive immunization in the treatment<br />

of diphtheria.<br />

diphtheria toxin<br />

A 62-kDa protein exotoxin synthesized and secreted by<br />

Corynebacterium diphtheriae. The exotoxin, which is distributed<br />

in the blood, induces neuropathy and myocarditis<br />

in humans. Tryptic enzymes nick the single-chain diphtheria<br />

toxin. Thiols reduce the toxin to produce two fragments.<br />

The 40-kDa B fragment gains access to cells through their<br />

membranes, permitting the 21-kDa A fragments to enter.<br />

Whereas the B fragment is not toxic, the A fragment is<br />

toxic and it inactivates elongation factor 2, thereby blocking<br />

eukaryocytic protein synthesis. Guinea pigs are especially<br />

sensitive to diphtheria toxin, which causes necrosis at injection<br />

sites, hemorrhage of the adrenals, and other pathologic<br />

consequences. Animal tests developed earlier in the century<br />

consisted of intradermal inoculation of C. diphtheriae<br />

suspensions into the skin of unprotected guinea pigs compared<br />

to a control guinea pig that had been pretreated with<br />

passive administration of diphtheria antitoxin for protection.<br />

In later years, toxin generation was demonstrated in<br />

vitro by placing filter paper impregnated with antitoxin at<br />

right angles to streaks of C. diphtheriae microorganisms<br />

growing on media in Petri plates. Formalin treatment or<br />

storage converts the labile diphtheria toxin into toxoid. A<br />

secretory product of Corynebacterium diphtheriae, the<br />

etiologic agent of diphtheria, produces symptoms of the<br />

disease. Immunization requires the use of an inactive form<br />

of the toxin (diphtheria toxoid). Refer to diphtheria toxin<br />

and diphtheria toxoid.<br />

D

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