Vaccination rates for children aged 13–17 with one or more TDaP shots was 90.2% in 2019. Only 43.6% of adults (older than 18) have received a TDaP shot in the last 10 years. The CDC aims to increase vaccination rate among 2 year olds from 80.4% to 90.0%

Combination vaccines with acellular pertussis
DTaP and Tdap are both combination vaccines against diphtheria, tetanus, and pertussis. The lower-case "d" and "p" indicate smaller concentrations of diphtheria toxoids and pertussis antigens, and "a" in "ap/aP" indicates that the pertussis toxoids are acellular. DTaP
DTaP (also DTPa and TDaP) is a combination vaccine against diphtheria, tetanus, and pertussis, in which the pertussis component is acellular. This is in contrast to whole-cell, inactivated DTP (DTwP). The acellular vaccine uses selected antigens of the pertussis pathogen to induce immunity. Because it uses fewer antigens than the whole-cell vaccines, it is considered to cause fewer side effects, but it is also more expensive. Research suggests that the DTP vaccine is more effective than DTaP in conferring immunity, because DTaPs narrower antigen base is less effective against current pathogen strains. Tdap
Tdap, (also dTpa), is a tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine. It was licensed in the United States for use in adults and adolescents on 10 June 2005. Two Tdap vaccines are available in the US. In January 2011, the US Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices (ACIP) recommended the use of Tdap in adults of all ages, including those age 65 and above.
Respiratory distress can be caused by an underdeveloped trachea which collapses on inhalation or by insufficient rib cage development. Genetics
CMD is commonly caused by chromosomal abnormalities in or around the gene SOX9 on the long arm of chromosome 17, specifically at position 17q24, generally spontaneously arising or de novo mutations. Also, numerous single nucleotide variants been identified involving the SOX9 gene that cause some form of CMD. The SOX9 gene codes for a protein transcription factor which, when expressed at the embryonic stage, plays an important role in determining sexual characteristics and greatly influences skeletal development. When the SRY gene of the Y chromosome is expressed in human embryos, a cascade of gene interactions controlled by SOX9 begins and ultimately leads to male gender.. Any mutation within the coding region of SOX9 can cause campomelic dysplasia and 75% of the reported mutations lead to sex reversal. Four major classes of heterozygous SOX9 mutations can cause CMD: amino acid substitutions in the HMG-box, truncations or frameshifts that alter the C-terminal end, mutations at the splice junction, and chromosomal translocations. Additionally, mutations upstream from SOX9 can also cause CMD. Several researchers have reported cis-acting control elements upstream of SOX9. Translocation breakpoints scattered over 1Mb proximal to SOX9 indicate the presence of an extended control region.The lack of correlation between specific genetic mutations and observed phenotype, particularly with regard to sex reversal, give clear evidence of the variable expressivity of the disease.