Psychiatric comorbidity is extensive in the general population (Kessler et al., 1994 Kessler et al., 2005), and in clinical samples poly-diagnosis is the rule rather than the exception (Zimmerman & Mattia, 1999). This complicates clinical communication, treatment selection, and frustrates efforts to uncover the pathophysiology, etiology, and maintenance mechanisms of mental illness (Hyman, 2010). One promising approach for resolving these issues involves using formal statistical modeling to clarify the natural structure of mental disorders (Krueger & Markon, 2006; Wright & Zimmermann, 2015). This approach has been profitably applied to both child(Achenbach, 1966; Lahey et al., 2008) and adult (Kotov et al., 2011; Krueger, 1999; Markon & Krueger, 2006) disorders. In adult psychopathology, a well-replicated structure has emerged based on the clustering of disorders and their symptoms into internalizing (e.g., unipolar mood disorders, anxiety disorders), externalizing (e.g., substance use, antisocial behavior), and thought disorder/psychosis (e.g., psychotic disorders, schizotypal personality disorder) spectra (Kotov et al., 2010; Markon, 2010; Wolf et al., 1988; Wright et al., 2013). This structure has demonstrated strong empirical and statistical evidence for its validity; importantly the resulting spectra or domains appear to predict treatment response and match genetic models of these disorders (Kendler et al., 2003; Kendler et al., 2011). Recently developed quantitative models of psychopathology have expanded the basic internalizing, externalizing, and thought disorder/psychosis structure by incorporating additional diagnoses, most notably personality disorders (PDs), and have begun to uncover additional spectra. To date only four published studies have explored the structure of psychopathology using a broad suite of clinical syndromes and personality disorders (Blanco et al., 2013; Kotov et al., 2011; Markon, 2010; Roysamb et al., 2011).1 Although each resultant model is necessarily unique given differences in the precise admixture of disorders (e.g., some do not include indicators of psychosis), sampling strategy (e.g., clinical vs. epidemiological), and other features (e.g., disorder-level vs. symptom-level analyses), two additional domains appear reasonably replicable across studies. First, Markon (2010) and Roysamb and colleagues (2011) each identified a new spectrum they respectively termed pathological or anhedonic introversion. In both cases, avoidant and dependent PDs were strong markers of the factor, although Roysamb et al. also found that schizoid and depressive PDs loaded strongly on the factor, which accounts for the slight difference in conceptualization. Blanco and colleagues (2013) also found evidence for a factor with the strongest loadings from avoidant and dependent PDs and social phobia. Second, in three studies (Blanco et al., 2013; Kotov et al., 2011; Roysamb et al., 2011), a domain related to antagonism, as labeled by Kotov and colleagues, has emerged. Again, slight differences emerge in the makeup of this domain across studies, although narcissistic and histrionic PDs consistently exhibit the strongest loadings. Additional markers for this domain, but varying slightly across studies, include obsessive-compulsive, borderline, paranoid, and (to a lesser extent) antisocial PDs. What these disorders share to varying degrees is an antagonistic interpersonal style that puts afflicted individuals at odds with others. Notably, introversion and antagonism, which emerge with the addition of PDs, each deal with maladaptive social/interpersonal functioning, consistent with the view that the PDs reflect the interpersonal disorders (Benjamin, 1996; Hill, Pilkonis, Bear, 2011; Hopwood et al., 2013; Meyer & Pilkonis, 2005; Pincus, 2005). Therefore, based on this initial accumulation of studies that have included PDs in structural models of psychopathology and a strong theoretical rationale, the domains of introversion and antagonism appear to be good candidates to include alongside internalizing, externalizing, and thought disorder/psychosis as broad, replicable domains of psychopathology. Taken together, these domains bear a remarkable conceptual resemblance to the pathological personality trait domains included in DSM-5 Section III system of PDs (American Psychiatric Association, 2013). The five domains outlined in this system include Negative Affectivity, Antagonism, Detachment, Disinhibition, and Psychoticism, and were empirically derived from quantitative modeling of more specific PD features (i.e., clinical specifiers) outlined by the DSM-5 Personality and PD workgroup (Krueger et al., 2011; 2012). Compared to this PD trait framework, the psychopathology spectra of internalizing, antagonism, anhedonic/pathological introversion, externalizing, and thought disorder, respectively, reflect strong conceptual matches. However, although intuitively compelling, these putative matches between psychopathology spectra and personality domains have not been empirically demonstrated. Notably, an empirical demonstration that the major spectra underlying psychiatric comorbidity in common clinical syndromes and PDs align with the domains of pathological personality trait models would represent a major advance in clarifying the phenotypic structure of psychopathology. A model such as this would provide the foundation for a comprehensive bridge between mental disorders and elementary domains of individual differences in basic functioning. For example, the DSM-5 pathological trait model has been linked empirically to a large scientific literature on structural models of normal personality and temperament (De Fruyt et al., 2013; Gore & Widiger, 2013; Thomas et al., 2013; Watson et al., 2013; Wright et al., 2012; Wright & Simms, 2014), which builds on a larger literature linking pathological and basic personality traits (e.g., Markon et al., 2005). Adding to the strength of our proposal, that the structures underlying traits and much of psychopathology align, basic trait domains demonstrate strong associations to clinical syndromes (Kotov et al., 2010) and PDs (Samuel & Widiger, 2008; Saulsman & Page, 2004) in meta-analyses. Based on these accumulated findings, some have suggested that there is potential to organize both basic domains of individual differences and psychopathology using a finite number of functional domains or spectra rooted in basic psychological and physiological systems (e.g., Harkness, Reynolds, & Lilienfeld, 2013; Siever & Davis, 1991). This parallels efforts in the broader DSM-5 development process aimed at developing crosscutting dimensions of pathology (Narrow et al., 2012) and in the National Institute of Mental Health's Research Domain Criteria (RDoC; Insel et al., 2010; Sanislow et al., 2010). Further, an empirically based dimensional structure increases the potential to link with biological correlates, genetic liabilities, and leads to more replicable and accurate etiological research (Orfat & Krueger, 2012; Plomin et al., 2009) The potential for an organizing metastructure that encompasses basic and pathological functioning would go a long way towards linking disparate scientific literatures and in so doing provide an organizing scheme for refining the study of psychopathology. In the current study, we tested whether such a model was viable by examining the joint structure of mental disorders and the DSM-5 pathological personality traits. We hypothesized that a factor analysis of interview-diagnosed major clinical syndromes and PDs and patient-reported pathological trait scales in a large general psychiatric outpatient sample would result in five easily interpretable dimensions that closely resemble the aforementioned internalizing, externalizing/disinhibition, thought disorder/psychoticism, antagonism, and introversion/detachment domains. Specifically, we use exploratory structural equation modeling (ESEM; Asparouhov & Muthen, 2009; see also Marsh et al. 2010 for an applied example) to examine the joint structure of DSM-5 pathological personality traits, clinical syndromes, and personality disorders, while accounting for method variance across instruments. We hypothesize that disorders that mark the internalizing spectrum (e.g., mood, anxiety disorders) will load on the same factor as traits that indicate Negative Affectivity (e.g., Emotional Lability, Separation Insecurity), and that markers of Externalizing (e.g., alcohol use, antisocial PD) and Disinhibition (e.g., Risk Taking, Implusivity), antagonism (e.g., narcissistic PD and histrionic PD) and trait Antagonism (e.g., callousness, manipulativeness), pathological introversion (e.g., avoidant PD, schizoid PD) and Detachment (e.g., Withdrawal, Restricted Affectivity), and Thought Disorder (e.g., psychotic symptoms, schizotypal PD) and Psychoticism (e.g., Unusual Beliefs, Perceptual Dysregulation) will load together on the same factors, respectively.