The occurrence of tetanus in the United States has
decreased dramatically from 560 reported cases in 1947, when national reporting
began, to a record low of 48 reported cases in 1987.1 The decline has resulted
from widespread use of tetanus toxoid and improved wound management, including
use of tetanus prophylaxis in emergency rooms.2
HyperTET S/D supplies passive immunity to those
individuals who have low or no immunity to the toxin produced by the tetanus
organism, Clostridium tetani. The antibodies act to neutralize the free form of
the powerful exotoxin produced by this bacterium. Historically, such passive
protection was provided by antitoxin derived from equine or bovine serum;
however, the foreign protein in these heterologous products often produced
severe allergic manifestations, even in individuals who demonstrated negative
skin and/or conjunctival tests prior to administration. Estimates of the
frequency of these foreign protein reactions following antitoxin of equine
origin varied from 5%–30%.3-6 If passive immunization is needed, human tetanus
immune globulin (TIG) is the product of choice. It provides protection longer
than antitoxin of animal origin and causes few adverse reactions.2
Several studies suggest the value of human tetanus
antitoxin in the treatment of active tetanus.7,8 In 1961 and 1962,
Nation et al,7 using Hyper-Tet treated 20 patients with tetanus
using single doses of 3,000 to 6,000 antitoxin units in combination with other
accepted clinical and nursing procedures. Six patients, all over 45 years of
age, died of causes other than tetanus. The authors felt that the mortality
rate (30%) compared favorably with their previous experience using equine
antitoxin in larger doses and that the results were much better than the 60%
national death rate for tetanus reported from 1951 to 1954.9 Blake
et al,10 however, found in a data analysis of 545 cases of tetanus
reported to the Centers for Disease Control from 1965 to 1971 that survival was
no better with 8,000 units of TIG than with 500 units; however, an optimal dose
could not be determined.
Serologic tests indicate that naturally acquired immunity
to tetanus toxin does not occur in the United States. Thus, universal primary
vaccination, with subsequent maintenance of adequate antitoxin levels by means
of appropriately timed boosters, is necessary to protect persons among all age
groups. Tetanus toxoid is a highly effective antigen; a completed primary
series generally induces protective levels of serum antitoxin that persist for 10 years.2
Passive immunization with HyperTET S/D may be undertaken
concomitantly with active immunization using tetanus toxoid in those persons
who must receive an immediate injection of tetanus antitoxin and in whom it is desirable
to begin the process of active immunization. Based on the work of Rubbo,11
McComb and Dwyer,12 and Levine et al,13 the physician may
thus supply immediate passive protection against tetanus, and at the same time
begin formation of active immunization in the injured individual which upon
completion of a full toxoid series will preclude future need for antitoxin.
Peak blood levels of IgG are obtained approximately 2
days after intramuscular injection. The half-life of IgG in the circulation of
individuals with normal IgG levels is approximately 23 days.14
In a clinical study in eight healthy human adults
receiving another hyperimmune immune globulin product treated with
solvent/detergent, Rabies Immune Globulin (Human), HyperRAB® S/D, prepared by
the same manufacturing process, detectable passive antibody titers were
observed in the serum of all subjects by 24 hours post injection and persisted
through the 21 day study period. These results suggest that passive immunization
with immune globulin products is not affected by the solvent/detergent
1. Tetanus — United States, 1987 and 1988, MMWR 39(3):
2. Diphtheria, Tetanus, and Pertussis: Recommendations
for Vaccine Use and Other Preventive Measures. Recommendations of the
Immunization Practices Advisory Committee (ACIP). MMWR 40 (RR-10): 1-28, 1991.
3. Moynihan NH: Tetanus prophylaxis and serum sensitivity
tests. Br Med J 1:260-4, 1956.
4. Scheibel I: The uses and results of active tetanus
immunization. Bull WHO 13:381-94, 1955.
5. Edsall G: Specific prophylaxis of tetanus. JAMA 171(4):417-27,
6. Bardenwerper HW: Serum neuritis from tetanus
antitoxin. JAMA 179(10):763-6, 1962.
7. Nation NS, Pierce NF, Adler SJ, et al: Tetanus: the
use of human hyperimmune globulin in treatment. Calif Med 98(6):305-6, 1963.
8. Ellis M: Human antitetanus serum in the treatment of
tetanus. Br Med J 1(5338):1123-6, 1963.
9. Axnick NW, Alexander ER: Tetanus in the United States:
A review of the problem. Am J Public Health 47(12):1493-1501, 1957.
10. Blake PA, Feldman RA, Buchanan TM, et al: Serologic
therapy of tetanus in the United States, 1965-1971. JAMA 235(1):42-4, 1976.
11. Rubbo SD: New approaches to tetanus prophylaxis. Lancet
12. McComb JA, Dwyer RC: Passive-active immunization with
tetanus immune globulin (human). N Engl J Med268(16):857-62, 1963.
13. Levine L, McComb JA, Dwyer RC, et al: Active-passive
tetanus immunization; choice of toxoid, dose of tetanus immune globulin and
timing of injections. N Engl J Med 274(4):186-90, 1966.
14. Waldmann TA, Strober W, Blaese RM: Variations in the
metabolism of immunoglobulins measured by turnover rates. In Merler E (ed.):
Immunoglobulins: biologic aspects and clinical uses. Washington, DC, Nat Acad
Sci, 1970, p. 33-51.