METHODS FOR IMAGING BACTERIAL INFECTIONS CLAIM OF PRIORITY This application claims priority to U.S. Provisional Patent Application Serial No.63/045,234, filed on June 29, 2020, the entire contents of which are hereby incorporated by reference. STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH OR DEVELOPMENT This invention was made with government support under HL139598 and HL114477 awarded by National Institutes of Health. The government has certain rights in the invention. TECHNICAL FIELD This invention relates to conjugates of thrombin inhibitor dabigatran, and to methods of using these conjugates for detecting thrombin-associated diseases or conditions in organs and tissues of patients. In one example, the conjugates are useful to diagnose bacterial endocarditis in the heart of the patient. BACKGROUND Bacterial endocarditis is an often lethal infection of the heart valves and surrounding endocardium. Major challenges to clinically managing endocarditis include identifying the causal pathogens, timing surgical interventions and rising bacterial resistance to antibiotics. Staphylococcus aureus (S. aureus) is the most common cause of acute endocarditis in patients, likely because these bacteria produce potent factors promoting bacterial virulence and survival. Historically, S. aureus has been differentiated from other pathogens, such as S. epidermidis, through its distinct ability to clot blood. This directly results from S. aureus’ production of the two redundant prothrombin activators staphylocoagulase (“SC”) and von Willebrand factor-binding protein (“vWBp”). SC and vWBp both bind active prothrombin through N-terminal interactions and stay locked into the vegetation through independent C-terminal binding interactions. This anchoring mechanism essentially paints vegetations with layers of thrombin-like proteolytic activity. As a consequence, a fibrin-rich wall shields the bacterial colony against drugs and immune cells. SUMMARY Provided herein are dabigatran conjugates labeled with either a near-infrared fluorochrome or a positron emission tomography (PET) isotope (e.g., fluorine-18). These compounds are useful as fluorescent imaging agents in noninvasive fluorescence tomography and intravital microscopy to assess the relative distribution of thrombin activity in growing vegetations. As the experimental results presented herein show, the dabigatran conjugates of this disclosure are advantageously useful in integrated PET/magnetic resonance (MR) imaging for detecting of S. aureus endocarditis in mice and piglets. Furthermore, and importantly here, the compounds are useful for monitoring treatment of endocarditis using, for example, an immunotherapy that neutralizes SC and vWBp in mice that have the condition. The imaging with the conjugates of this disclosure showed that the immunotherapy reduced thrombin deposition, boosted innate immune cell defense and impeded vegetation formation. In one general aspect, the present disclosure provides a compound of Formula (I): or a pharmaceutically acceptable salt thereof, wherein L ¹ , n, and R ¹ are as described herein. In another general aspect, the present disclosure provides a pharmaceutical composition comprising a compound of Formula (I), or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier. In another general aspect, the present disclosure provides a method of imaging an organ or tissue of a subject, the method comprising (i) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising same; (ii) waiting a time sufficient to allow the compound to accumulate in the organ or tissue to be imaged; and (iii) imaging the imaging the organ or tissue with an imaging technique. In another general aspect, the present disclosure provides a method of diagnosing a bacterial infection in an organ or tissue of a subject, the method comprising (i) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising same; (ii) waiting a time sufficient to allow the compound to accumulate in the organ or tissue to be imaged; and (iii) imaging the imaging the organ or tissue with an imaging technique, wherein observing an image attributable to the fluorophore or the radioisotope within the compound of Formula (I) is indicative of the bacterial infection in the organ or tissue of the subject. In another general aspect, the present disclosure provides a method of monitoring treatment of a bacterial infection in a subject, the method comprising (i) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising same; (ii) waiting a time sufficient to allow the compound to accumulate in an organ or tissue of the subject; (iii) imaging the organ or tissue of the subject with an imaging technique; (iv) administering to the subject a therapeutic agent in an effective amount to treat the bacterial infection; (v) after iv), administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising same; (vi) waiting a time sufficient to allow the compound to accumulate in the organ or tissue of the subject; (vii) imaging the organ or tissue of the subject with an imaging technique; and (viii) comparing the image of step iii) and the image of step vii). Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which the present application belongs. Methods and materials are described herein for use in the present application; other, suitable methods and materials known in the art can also be used. The materials, methods, and examples are illustrative only and not intended to be limiting. All publications, patent applications, patents, sequences, database entries, and other references mentioned herein are incorporated by reference in their entirety. In case of conflict, the present specification, including definitions, will control. Other features and advantages of the present application will be apparent from the following detailed description and figures, and from the claims. DESCRIPTION OF DRAWINGS FIG.1. Imaging agent synthesis and validation. (A) Synthesis scheme of a near infrared fluorescent dabigatran derivative (DAB-VT680XL) and a positron emission tomography fluorine-18 tracer ¹⁸ F-dabigatran ( ¹⁸ F-DAB), both prepared in 2 steps from dabigatran. (B) LC-MS analysis of DAB-VT680XL showing the [M - 2H ⁺ ] ^2- /2 (917.66 m/z) and [M - 3H ⁺ ] ^3- /3 (611.41 m/z) ions and (C) ¹⁹ F-DAB showing the [M + H ⁺ ] ⁺ (724.60 m/z). (D) Preparative HPLC chromatograms (radio, top trace) and ultraviolet (UV) absorbance at 254 nm (bottom trace). The collection window is highlighted in red. (E) Analytical HPLC chromatograms of the ¹⁸ F-succinimidyl fluorobenzoate ( ¹⁸ F-SFB) prosthetic group, ¹⁸ F-DAB crude conjugation reaction mixture and HPLC purified ¹⁸ F-DAB. (F) Analytical HPLC chromatograms of ¹⁸ F- DAB and stable-isotope standard ¹⁹ F-DAB (blue). Since the two detectors are connected in series, there is a 0.2 min delay between UV and radio signals. (G) Thrombin activity assay with argatroban (Arg), dabigatran (DAB) and ¹⁹ F-dabigatran ( ¹⁹ F-DAB). (H) Clearing ¹⁸ F-DAB from mouse blood (n=3). The half-life in blood is 2.0±0.6 minutes. (I) Bio-distribution of ¹⁸ F-DAB in mice (n=3-8). Data are shown as mean ± s.e.m.. FIG.2. In vivo DAB-VT680XL or control probe binding to thrombi in mice. (A) Intravital microscopy of a FeCl3-induced thrombosis of the femoral artery 90 min after injection of DAB-VT680XL or (B) an unspecific control fluorochrome (VT680XL). Aggregating platelets are stained with anti-CD41 monoclonal antibody. The experiments were repeated twice with the same result (n=3 per group). FIG.3. DAB-VT680XL targeting of endocarditic vegetations in mice. (A) Gram stain of aortic root after inducing endocarditis in mice shows S. aureus in dark purple. Arrow heads indicate aortic valve leaflet. (B) High magnification view of boxed area in (A). (C, D) Adjacent sections of the endocarditic vegetation 90 min after DAB-VT680XL injection. DAPI indicates 4′,6-diamidino-2-phenylindole. DAB-VT680XL imaging signal (E) highlights the intersection of bacterial vegetations (F) with the host. Staining for CD11b (G) illustrates the distribution of myeloid cells, which are unable to enter the bacterial colony. The experiment was repeated twice with the same result. FIG.4. Noninvasively imaging mouse endocarditis. (A) In vivo FMT/CT images and (B) fluorescence quantification in the aortic roots of mice with S. aureus endocarditis (right) and sham controls (left) (n=5-8 mice per group; P = 0.0055). (C) Ex vivo fluorescence reflectance imaging (FRI) and bioluminescence imaging (BLI, insets) illustrate macroscopic co-localization of bacterial colonies with DAB- VT680XL imaging signal. (D) Quantification of fluorescence as target to background ratio (TBR) (n=5-8 mice per group, P = 0.0286). (E) Quantification of BLI signal derived from bioluminescent S. aureus strain Xen29 (n=5-8 mice per group, P = 0.0095). (F) PET/CT imaging after injection of ¹⁸ F-DAB. Arrows indicate signal from S. aureus vegetations on the aortic valves and the suture in the brachiocephalic artery. (G) In vivo quantification of PET signal in the aortic root (SUV, standardized uptake value, n=6-10 mice per group, data from four separate experiments, P = 0.0095). (H) Ex vivo scintillation counting of aortic roots (%IDGT, percent injected dose per gram tissue, n=5-12 mice per group, P = 0.0052). (I) Autoradiography of dissected aortas. Left panel, sham-operated mouse with absent ¹⁸ F-DAB signal and absent bioluminescent signal indicating lack of bacteria; right panel with ¹⁸ F-DAB signal with co-localized bioluminescent bacterial colonies in the ascending aorta (inset). (J) Quantification of autoradiography (TBR, target to background ratio, n=5-7 mice per group, three separate experiments, P = 0.037). Unpaired, two-tailed t-test was used and data are shown as mean ± s.e.m.. *P < 0.05, **P < 0.01. FIG.5. S. aureus endocarditis in piglets. (A) H&E staining of right-sided piglet endocarditis vegetation indicating immune response to the S. aureus Xen 36 infection. (B) Gram staining of an adjacent section showing the pathogen in the piglet heart. (C) Short axis stacks of black blood MRI from a pig 10 days after induction of right-sided endocarditis. Arrows indicate vegetations. (D) View of the open right ventricle in piglet with right-sided endocarditis. Inset shows magnified view. (E) Bioluminescence image of (D) illustrates location of Xen 36 S. aureus. (F) Fluorescence reflectance image (FRI) of (D) and (E) indicates DAB-VT680XL imaging signal after intravenous injection of the near infrared imaging agent. (G) Ex vivo quantification of bacterial bioluminescence from multiple vegetations of 12 piglets with right-sided endocarditis. Unpaired, two-tailed t-test was used and data are shown as mean ± s.e.m., ****P < 0.0001. (H) FRI in a DAB-VT680XL-injected subset of piglet demonstrates accumulation of the imaging probe (n=3 piglets per group, one-way ANOVA for multiple comparison, Barlett’s test, **P < 0.01. (I) Long and (J) short axis MRI of piglet after induction of left-sided endocarditis. (K) Cardiac MRI-derived ejection fraction (EF) of the right and left ventricle (RV and LV, respectively) and the end-diastolic volumes (EDV), comparing left- with right-sided endocarditis (n=6 piglets with tricuspid right-sided and n=4 with aortic left-sided disease, two tailed t test, *P < 0.05). (L) Bioluminescence imaging demonstrates bacterial infection, with signal arising from vegetations (arrows) identified on autopsy (M) and FRI (N). (O) Ex vivo quantification of bacterial bioluminescence in 8 piglets with left-sided endocarditis, two-tailed t test., ***P < 0.001. (P) Quantification of fluorescence signal arising from aortic valve vegetations (n=5 piglets, one-way ANOVA for multiple comparison with ****P < 0.0001, Barlett’s test). FIG.6. PET/MR imaging S. aureus endocarditis in piglets. (A) Left-sided endocarditis target to background ratio (TBR) of PET signal, calculated with either myocardium (control) or vegetation-bearing aortic root as target and the skeletal muscle as background (n=3 piglets, two-sided Student’s t test, *P < 0.05). (B) PET/MR images illustrating the imaging signal in aortic valve with endocarditis lesion (arrow). Color scale depicts becquerels/mL. (C) Right-sided endocarditis TBR, calculated as above (n=3 piglets, two-sided Student’s t test, *P < 0.05). (D) PET/MR images illustrating the imaging signal in tricuspid valve endocarditis lesion (arrow). Color scale depicts becquerels/mL. (E) Ex vivo autoradiography of aortic valve indicates radioactive signal in the aortic valve vegetations, which were verified on autopsy (F) and a source of bioluminescence (G) arising from S. aureus (arrows). F ^{IG. 7. Immunotherapy neutralizing virulence factors disrupts} vegetations and improves survival. (A-C) Specificity of monoclonal antibodies by immunoblotting against vWBp-(1-263) in lane 1; vWBp-(1-474) in lane 2; SC-(1- 325) in lane 3; SC-(1-660) in lane 4. Lane 5 contains protein standards with the indicated molecular weights. The indicated antibodies, in panel A GMA-2510 monoclonal [anti-von Willebrand factor-binding protein (anti-vWBp)] and in panel B GMA-2105 monoclonal [anti-staphylocoagulase (anti-SC)], are specific for their respective targets. Panel C shows probing for total mouse IgG (anti-IgG polyclonal against both the heavy and light chains of murine IgG) and reflects the bound antibodies shown in panels A and B. (D) Increase in turbidity as measured by absorbance change at 450 nm for mixtures of 1.5 mg/mL fibrinogen and 75 nM prothrombin complexed to vWBp-(1-263) (ProT●vWBp) complex in the absence of GMA-2510 antibody (anti-vWBp Ab; black line), in the presence of 300 nM anti- vWBp Ab or 1.5 µM anti-vWBp Ab. (E) Similar reactions for 15 nM prothrombin complexed to SC-(1-325) (ProT●SC) are shown in the absence of GMA-2105 antibody (anti-SC Ab), in the presence of 50 nM anti-SC ab or 250 nM anti-SC ab. (F) In vivo FMT/CT images of S. aureus endocarditis in mice after injection of DAB- VT680XL treated with either isotype control antibody or antibodies neutralizing SC and vWBp. (G) In vivo fluorescence quantitation of vegetation thrombin in aortic roots following DAB-VT680XL injection (n=10-12 mice per group, three separate experiments; unpaired, two-sided t-test was used and data are shown as mean ± s.e.m. ***P < 0.001). (H) Kaplan-Meier survival curves of S. aureus endocarditis mice treated with isotype control antibody or combination therapy with anti-SC and anti- vWBp antibodies (n=15 mice per group, mice received a single intraperitoneal injection of their respective antibody treatment 6 hrs post surgery). (I) Intravital microscopy of femoral S. aureus vegetation 24 hours after intravenous injection of S. aureus ^RFP+ and combination treatment with both anti-SC and anti-vWBp or (J) isotype control antibody. In vivo DAB-VT680 microscopy of the vegetation wall surrounding RFP ⁺ bacteria and Ly6g ⁺ neutrophils. FIG.8. Blocking experiment indicates specificity of DAB-VT680XL. (A) Bioluminescent signal in aortic vegetations in respective experimental groups (Naive n=2, DAB-VT680XL n=7, Dabigatran n=8, one-way ANOVA for multiple comparison, Barlett’s test). (B) In vivo FMT/CT images obtained in mice with S. aureus endocarditis after injection of DAB-VT680XL, and with preceding injection of non-fluorescent dabigatran. (C) Quantification of DAB-VT680XL concentration in vegetations with fluorescent molecular tomography (FMT) (DAB-VT680XL n=7, Dabigatran n=8, two-tailed Student’s t test, **P < 0.01). (D) Ex vivo fluorescence reflectance imaging (FRI) confirms in vivo observation of lower signal after blocking (DAB-VT680XL n=7, Dabigatran n=8, two-tailed Student’s t test, *P < 0.05). FIG.9. DAB-VT680XL does not enrich in acute myocardial infarcts. (A) FMT/CT images obtained in mice 5 days after coronary ligation show no signal in the apical infarct (right panel) compared to endocarditis (left panel). (B) Quantification of FMT signal in comparison to endocarditis cohort (endocarditis n=9, MI n=7, two- tailed Student’s t test). (C) Ex vivo imaging of myocardial rings. Highlighted area shows infarct. (D) Target to background ratio obtained in (C), using remote myocardium as background area (saline n=5, DAB-VT680XL n=7, two-tailed Student’s t test, ***P < 0.001). FIG.10. FMT in mice with endocarditis induced by S. epidermidis Xen43. (A) In vivo FMT quantification of DAB-VT680XL concentration in vegetation, in comparison with S. aureus strain Xen29 (Xen29 n=10, Xen43 n=6, two-tailed Student’s t test, *P < 0.05). (B) Ex vivo fluorescence reflectance imaging (FRI) returns a lower target to background ratio (TBR) for the Xen43 strain (Xen29 n=10, Xen43 n=7, two-tailed Student’s t test, *P < 0.05). FIG.11 Fluorescence imaging of renal S. aureus infection with DAB- VT680XL. (A) Bioluminescent imaging shows hot spots in the lower back of the mouse, consistent with bacterial accumulation. (B) These areas were fluorescent after intravenous injection of DAB-VT680XL. (C, D) Same as (A, B) with ex vivo opened situs, confirming that signal arises from kidneys. (E) In vivo bioluminescence signal in kidneys (n=4 mice per group, two-tailed Student’s t test). (F) In vivo fluorescence reflectance imaging in mice injected with DAB-VT680XL (n=4 mice per group, two- tailed Student’s t test, ***P = 0.0006). (G) Ex vivo imaging of isolated kidneys confirms that optical signal is arising from this organ. FIG.12. DAB-VT680XL correlates with bacterial bioluminescence. (A) Comparison of DAB-VT680XL fluorescence signal (n=3 piglets per group) and (B) bioluminescence arising from left- versus right-sided endocarditis (n=5-6 piglets per group). Threshold on vegetations signal was set at 2e4 radiance units for bioluminescence. Unpaired, two-tailed t-test was used and data are shown as mean ± s.e.m., *P = 0.0163 and ***P = 0.0007, respectively. (C) Correlation of bioluminescence with fluorescence signal for identical regions of interests. Each dot corresponds to one endocarditis vegetation or region of developing vegetations with bioluminescence with < 2e4 radiance units. Only datasets with both fluorescence and bioluminescence collected under identical instrument settings were used for the correlation. A total of 6 piglets (3 aortic and 3 tricuspid cases) were used. Dashed lines represent the 95% confidence interval in the linear regression analysis. DETAILED DESCRIPTION Acute bacterial endocarditis is a rapid, difficult to manage and frequently lethal disease. Potent antibiotics often cannot efficiently kill Staphylococcus aureus (S. aureus) that colonizes the heart’s valves. S. aureus relies on virulence factors to evade therapeutics and the host’s immune response, usurping the host’s clotting system by activating circulating prothrombin with staphylocoagulase and von Willebrand factor-binding protein. An insoluble fibrin barrier then forms around the bacterial colony, shielding the pathogen from immune cell clearance. Provided herein are small-molecule optical and positron emission tomography (PET) reporters targeting active thrombin in the fibrin-rich environment of bacterial colonies. The imaging agents, based on the clinical thrombin inhibitor dabigatran, bound to heart valve vegetations in mice. Using optical imaging, it is possible to monitor treatment therapy for endocarditis, for example with antibodies neutralizing staphylocoagulase and von Willebrand factor binding protein. This treatment deactivated bacterial defenses against innate immune cells, decreased in vivo imaging signal (compared to the signal taken at the beginning of the treatment) and improved survival. Aortic or tricuspid S. aureus endocarditis in piglets was also successfully imaged with clinical PET/magnetic resonance imaging (MRI). Therapeutic compounds In some embodiments, the present disclosure provides a compound of Formula (I): or a pharmaceutically acceptable salt thereof, wherein: n is an integer selected from 1 to 10; each L ¹ is independently selected from C(=O), N(R ^N ), O, (-C _1-3 alkylene-O-)x, (-O-C _1-3 alkylene-)x, and -C _1-6 alkylene-, wherein each x is independently an integer from 1 to 10 and eachC _1-6 alkylene is optionally substituted with 1, 2, or 3 substituents independently selected from OH, NO ² , CN, halo, amino, and carboxy; each R ^N is independently selected from H and C _1-3 alkyl; and R ¹ is selected from a fluorophore, C _1-6 alkyl, C _6-10 aryl, C _3-10 cycloalkyl, 5-14 membered heteroaryl, and 4-10 membered heterocycloalkyl, wherein each of said C _1-6 alkyl, C _6-10 aryl, C _3-10 cycloalkyl, 5-14 membered heteroaryl, and 4-10 membered heterocycloalkyl is optionally substituted with 1, 2, or 3 substituents independently selected halo, OH, NO ₂ , CN, halo, amino, C _1-3 alkylamino, di(C _1-3 alkyl)amino, carboxy, carbamyl, C _1-6 alkylcarbamyl, di(C _1-6 alkyl)carbamyl, C _1-6 alkyl, C _1-4 haloalkyl, C _1-6 alkoxy, C _1-6 haloalkoxy, and C _1-6 alkoxycarbonyl; and wherein said C _1-6 alkyl, C _6-10 aryl, C _3-10 cycloalkyl, 5-14 membered heteroaryl, and 4-10 membered heterocycloalkyl of R ¹ comprise at least one radioisotope. In some embodiments, at least one L ¹ is C(=O). In some embodiments, at least one L ¹ is NH. In some embodiments, at least one L ¹ is O. In some embodiments, at least one L ¹ is -C _1-6 alkylene-. In some embodiments, at least one L ¹ is (-C _1-3 alkylene-O-)x. In some embodiments, at least one L ¹ is (-ethylene-O-)x. In some embodiments, at least one L ¹ is (-isopropylene-O-)x. In some embodiments, at least one L ¹ is (-O-C _1-3 alkylene-)x. In some embodiments, at least one L ¹ is (-O-ethylene-)x. In some embodiments, at least one L ¹ is (-O-isopropylene-)x. In some embodiments, n is an integer from 2 to 10. In some embodiments, n is an integer from 2 to 8. In some embodiments, n is 2, 3, 4, 5, 6, 7, 8, 9, or 10. In some embodiments, x is an integer from 1 to 5. In some embodiments, x is 1, 2, or 3. In some embodiments, the moiety (L ¹ )n has formula: . In some embodiments, the moiety (L ¹ )n has formula: . In some embodiments, the compound of Formula (I) has formula: , or a pharmaceutically acceptable salt thereof. In some embodiments, the compound of Formula (I) has formula: , or a pharmaceutically acceptable salt thereof. In some embodiments, R ¹ is a fluorophore. Suitable examples of fluorophores include any fluorescent chemical compound that can re-emit light upon light excitation. The fluorophores can by excited by a light of a wavelength form about 300 nm to about 800 nm, and then emit light of a wavelength from about 350 nm to about 770 nm (e.g., violet, blue, cyan, green, yellow, orange or red light), which can be detected by fluorescent imaging devices, including the ability to measure the intensity of the fluorescence. In some embodiments, R ¹ is a near-infrared fluorophore (e.g., absorbing and/or emitting light from about 400 nm to about 1700 nm, from about 700 nm to about 1700 nm, or from about 1000 nm to about 1700 nm). Suitable examples of fluorophores include VT680XL, 680XL, MB, indocyanine green, IRDye800CW, cyanine dyes (including non-sulfonated, zwitterionic, phosphonated, and quaternium ammonium dyes), BODIPY, CH1055, AF488, hydroxycoumarin blue, methoxycoumarin blue, Alexa fluor blue, aminocoumarin blue, Cy2 green (dark), FAM green (dark), alexa fluor 488 green (light), Fluorescein FITC green (light), Alexa fluor 430 green (light), Alexa fluor 532 green (light), HEX green (light), Cy3 yellow, TRITC yellow, alexa fluor 546 yellow, Alexa fluor 5553 yellow, R- phycoerythrin (PE) 480; yellow, rhodamine red-X orange, tamara red, Cy3.5581 red, rox red, alexa fluor 568 red, Red 613 red, texas red red, alexa fluor 594 red, alexa fluor 633 red, allophycocyanin red, alexa fluor 633 red, Cy5 red, Alexa fluor 660 red, Cy5.5 red, truRed red, Alexa fluor 680 red, Cy7 red, and Cy7.5. Absorbance and emission wavelengths of these fluorophores are well known in the art. In some embodiments, R ¹ is selected from C _6-10 aryl, C _3-10 cycloalkyl, 5-14 membered heteroaryl, and 4-10 membered heterocycloalkyl, each of which is optionally substituted with at least one substituent selected from halo, C1-4 haloalkyl, C _1-6 alkoxy, and C _1-6 haloalkoxy, wherein said halo, C1-4 haloalkyl, C _1-6 alkoxy, and C1- 6 haloalkoxy comprise at least one radioisotope. In some embodiments, R ¹ is C _6-10 aryl, substituted with at least one substituent selected from halo, C1-4 haloalkyl, C _1-6 alkoxy, and C _1-6 haloalkoxy, wherein said halo, C1-4 haloalkyl, C _1-6 alkoxy, and C _1-6 haloalkoxy comprise at least one radioisotope. In some embodiments, said C _6-10 aryl is phenyl. In some embodiments, said C _6-10 aryl is substituted with at least one halo. In some embodiments, said C _6-10 aryl is substituted with at least one C _1-4 haloalkyl. In some embodiments, said C _6-10 aryl is substituted with at least one C _1-6 alkoxy. In some embodiments, said C _6-10 aryl is substituted with at least one C _1-6 haloalkoxy. In some embodiments, the at least one radioisotope is a positron emitter. In some embodiments, the positron emitter is selected from the group consisting of ¹¹ C, ¹³ N, ¹⁵ O, ¹⁸ F, ^34m Cl, ³⁸ K, ⁴⁵ Ti, ⁵¹ Mn, ^52m Mn, ⁵² Fe, ⁵⁵ Co, ⁶⁰ Cu, ⁶¹ Cu, ⁶² Cu, ⁶⁴ Cu, ⁶⁶ Ga, ⁶⁸ Ga, ⁷¹ As, ⁷² As, ⁷⁴ As, ⁷⁵ Br, ⁷⁶ Br, ⁸² Rb, ⁸⁶ Y, ⁸⁹ Zr, ⁹⁰ Nb, ^94m Tc, ^110m In, ¹¹⁸ Sb, ¹²⁰ I, ¹²¹ I, ¹²² I, and ¹²⁴ I. In some embodiments, the radioisotope is ¹¹ C or ¹⁸ F. In some embodiments, the radioisotope is ¹¹ C. In some embodiments, the radioisotope is ¹⁸ F. In some embodiments, the compound of Formula (I) is selected from any one of the following compounds: , , or a pharmaceutically acceptable salt thereof. In some embodiments, the compound of Formula (I) is selected from any one of the following compounds: , , or a pharmaceutically acceptable salt thereof. Pharmaceutically acceptable salts In some embodiments, a salt of any one of the compounds of the present disclosure is formed between an acid and a basic group of the compound, such as an amino functional group, or a base and an acidic group of the compound, such as a carboxyl functional group. According to another embodiment, the compound is a pharmaceutically acceptable acid addition salt. In some embodiments, acids commonly employed to form pharmaceutically acceptable salts of the compounds include inorganic acids such as hydrogen bisulfide, hydrochloric acid, hydrobromic acid, hydroiodic acid, sulfuric acid and phosphoric acid, as well as organic acids such as para-toluenesulfonic acid, salicylic acid, tartaric acid, bitartaric acid, ascorbic acid, maleic acid, besylic acid, fumaric acid, gluconic acid, glucuronic acid, formic acid, glutamic acid, methanesulfonic acid, ethanesulfonic acid, benzenesulfonic acid, lactic acid, oxalic acid, para- bromophenylsulfonic acid, carbonic acid, succinic acid, citric acid, benzoic acid and acetic acid, as well as related inorganic and organic acids. Such pharmaceutically acceptable salts thus include sulfate, pyrosulfate, bisulfate, sulfite, bisulfite, phosphate, monohydrogenphosphate, dihydrogenphosphate, metaphosphate, pyrophosphate, chloride, bromide, iodide, acetate, propionate, decanoate, caprylate, acrylate, formate, isobutyrate, caprate, heptanoate, propiolate, oxalate, malonate, succinate, suberate, sebacate, fumarate, maleate, butyne-1,4-dioate, hexyne-l,6-dioate, benzoate, chlorobenzoate, methylbenzoate, dinitrobenzoate, hydroxybenzoate, methoxybenzoate, phthalate, terephthalate, sulfonate, xylene sulfonate, phenylacetate, phenylpropionate, phenylbutyrate, citrate, lactate, β-hydroxybutyrate, glycolate, maleate, tartrate, methanesu1fonate, propanesulfonate, naphthalene-1-sulfonate, naphthalene-2- sulfonate, mandelate and other salts. In one embodiment, pharmaceutically acceptable acid addition salts include those formed with mineral acids such as hydrochloric acid and hydrobromic acid, and especially those formed with organic acids such as maleic acid. In some embodiments, bases commonly employed to form pharmaceutically acceptable salts of the compounds include hydroxides of alkali metals, including sodium, potassium, and lithium; hydroxides of alkaline earth metals such as calcium and magnesium; hydroxides of other metals, such as aluminum and zinc; ammonia, organic amines such as unsubstituted or hydroxyl-substituted mono-, di-, or tri- alkylamines, dicyclohexylamine; tributyl amine; pyridine; N-methyl, N-ethylamine; diethylamine; triethylamine; mono-, bis-, or tris-(2-OH-(C1-C6)-alkylamine), such as N,N-dimethyl-N-(2-hydroxyethyl)amine or tri-(2-hydroxyethyl)amine; N-methyl-D- glucamine; morpholine; thiomorpholine; piperidine; pyrrolidine; and amino acids such as arginine, lysine, and the like. Methods of use In one general aspect, the compounds of the present disclosure are useful in imaging techniques (e.g., as described below), and more specifically in diagnosing and/or monitoring treatment of bacterial infections and associated inflammation, as well as other conditions where fibronectin is implicated. Certain embodiments of the imaging techniques, bacterial infections, the fibronectin-associated conditions, and other aspects of these diagnostic and monitoring methods are described below. It is estimated that about 65% of all bacterial infections are associated with bacterial biofilms. These include both, device- and non-device-associated infections. Native valve endocarditis (NVE) is an inflammation caused by interaction of bacteria with the vascular endothelium and pulmonic valves of the heart. This is usually the result of Streptococci, Staphylococci, gram negative bacteria, and/or fungal infections. In this condition microbial cells gain access to the heart and blood through the gastrointestinal tract, urinary tract and/or through the oropharynx. As the intact valve endothelium gets damaged by the microorganisms that attach to it, even after the bacteria have been cleared by the immune system or an antibiotic therapy, a non- bacterial thrombotic endocarditis (NBTE) develops at the injury location, as a result a thrombus formation occurs, a condition where platelets, red blood cells and fibrin are aggregated. Biofilms may also occur on or within indwelling medical devices such as contact lenses, central venous catheters, mechanical heart valves, peritoneal dialysis catheters, prosthetic joints, pacemakers, urinary catheters. These biofilms may be composed of only a single or of different types of microbial species. In this case, microbial cells attach and produce biofilm on mechanical heart valves and surrounding tissues, a condition known as prosthetic valve endocarditis. Examples of bacteria responsible for this unpleasant condition are Streptococcus species, S. aureus, S. epidermidis, gram-negative Bacillus, Enterococcus and Candida spp. The origin of these micro-organisms may be from the skin or from other indwelling devices like central venous catheters or dental work. At the time of surgical implantation of prosthetic heart valves, tissue damage may occur as a result of accumulation of platelets and fibrin at the location of suture and on the devices. Microbial cells have better ability to colonize these locations. Additional examples of bacteria that form biofilms (including fibrin-containing biofilms) and that can be detected using the compounds of this disclosure for diagnostic or monitoring treatment purposes include Enterococcus faecalis, Staphylococcus aureus, Streptococcus mutans (a bacteria that is known to be responsible for dental caries and may enter blood stream and lead to endocarditis), Staphylococcus epidermidis, Streptococcus viridans, E. coli, Klebsiella pneumoniae, Proteus mirabilis, and Pseudomonas aeruginosa. In some embodiments, the compounds of this disclosure can be used for diagnosing or monitoring treatment of a bacterial infection and associated inflammation of the heart. Examples of such infections include endocarditis (e.g., native valve endocarditis or non-bacterial thrombotic endocarditis). The infection (or inflammation) may be located in a particular heart segment, such as right atrium, pulmonary valve, right ventricle, tricuspid valve, left ventricle, mitral valve, aortic valve, or left atrium. The compounds are particularly useful to detect inflammation of the heart’s valves, such as pulmonary valve, aortic valve, mitral valve, or tricuspid valve. In some embodiments, the compounds of this disclosure can be used for diagnosing or monitoring treatment of a bacterial infection and associated inflammation of the kidney. A non-limiting example of such a condition includes renal S. aureus lesions. In some embodiments, the compounds of this disclosure can be used for diagnosing or monitoring treatment of a bacterial infection of an organ or tissue selected from: artery (e.g., aorta, pulmonary artery, umbilical artery, brachiocephalic artery, carotid artery, subclavian artery), vein (e.g., inferior vena cava, abdominal vena cava, subclavian vein), lung, liver, kidney, skin, brain, eye, bone, intestine, gallbladder, pancreas, trachea, bladder, uterus, spleen, cartilage, muscle (e.g., smooth muscle, cardiac muscle, skeletal muscle), cartilage, epithelium, tendon, and ligament. In some embodiments, the organ or tissue is a heart. In some embodiments, the organ or tissue is kidney. In some embodiments, the bacterial infection is selected from nosocomial infection, skin infection, respiratory infection, wound infection, endovascular infection, CNS infection, abdominal infection, blood stream infection, urinary tract infection, pelvic infection, invasive systemic infection, gastrointestinal infection, dental infection, and connective tissue infection. Any of these infections can be caused by one or more of the biofilm-forming bacteria described herein (e.g., S. aureus including MRSA). Suitable examples of specific bacterial infections include pneumonia, tuberculosis, obstructive pulmonary disease, sinusitis, gastroenteritis, meningitis, arthritis, osteomyelitis, endocarditis, and conjunctivitis. For example, osteomyelitis is a disease of bones, which may be caused by bacterial cells or fungi. Bacteria enter the bones through the bloodstream, trauma or through previous infections. When microbes enter through the bloodstream and the metaphysis of the bone becomes infected, this leads to the recruitment of white blood cells (WBCs) to the site. These WBCs attempt to phagocytose or lyse the pathogens by secreting enzymes. These enzymes may lyse the bone, which results in the formation of pus, and spread through the bone blood vessels, thus stopping the proper flow of blood and causing tissue damage and deterioration of the function of the affected bone areas. In addition to diagnosing bacterial infections of organs and tissues (such as endocarditis), the compounds and compositions described here are useful for diagnosing any disease where fibrosis, blood clotting, and/or thrombosis may be implicated, such as cancers (e.g., lung, brain, pancreatic, melanoma, prostate, colon cancers), cardiovascular disease (e.g., myocardial infarction, atherosclerosis, arterial thrombosis), autoimmune diseases (e.g., multiple sclerosis, diabetes, irritable bowel syndrome, Celiac disease, Crohn’s disease), and pelvic inflammatory disease. In some embodiments, the present disclosure provides a method of diagnosing (e.g., detecting) a bacterial infection and/or a condition in which thrombin is implicated in an organ or a tissue of a subject (e.g., the subject in need thereof). In some embodiments, the subject in need of diagnosis and/or treatment is determined by a treating physician. The condition can be suspected by the physician, for example, by detecting specific biomarkers of the disease in a blood or a serum of the subject, or as a result of a physical exam. The diagnosing can be attained, for example, by imaging the organ or tissue of the subject by an imaging technique, for example, as described herein. A method of imaging the organ or tissue comprises (i) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising same; (ii) waiting a time sufficient to allow the compound to accumulate in the organ or tissue to be imaged (e.g., 1 min, 5 min, 10 min, 15 min, or 30 min), and (iii) imaging the organ or tissue with an imaging technique. When the compound of Formula (I) comprises ¹⁸ F or ¹¹ C radioisotope, the suitable imaging techniques include positron emission tomography (PET) and its modifications. As such, the imaging technique may be selected from positron emission tomography (PET) imaging, positron emission tomography with computer tomography (PET/CT) imaging, and positron emission tomography with magnetic resonance (PET/MRI) imaging, as well as other suitable methods. In some embodiments, observing an image attributable to the fluorophore or the radioisotope within the compound of Formula (I) is indicative of the condition being diagnosed (e.g., bacterial infection) in the organ or tissue of the subject. In some embodiments, the present disclosure provides a method of monitoring treatment of a bacterial infection and/or a condition in which thrombin is implicated in a subject, the method comprising (i) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising same, (ii) waiting a time sufficient to allow the compound of Formula (I) to accumulate in an organ or tissue of the subject (e.g., 5 min, 15 min, or 30 min); (iii) imaging the organ or tissue of the subject with an imaging technique; (iv) administering to the subject a therapeutic agent in an effective amount to treat the disease or condition (e.g., an FDA-approved or an experimental drug substance for treating a bacterial infection); (v) after (iv), administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof; (vi) waiting a time sufficient to allow the compound of Formula (I) to accumulate in the organ or tissue of the subject (e.g., 5 min, 15 min, or 30 min); (vii) imaging the organ or tissue of the subject with an imaging technique; and (viii) comparing the image of step (iii) and the image of step (vii). In one example, attaining decrease in amount of bacteria in the organ or tissue of the subject, as determined by comparing the images, is indicative of successful treatment of the disease or condition as described herein. Antibiotic agents In some embodiments, the compounds of this disclosure are useful to monitor treatment of a bacterial infection using one or more antibiotic agents or antibiotic therapies. In some embodiments, the antibiotic therapy is an immunotherapy which includes administering to a patient antibodies specific to virulence factors that bacteria (e.g., S. aureus) employs to activate the clotting cascade resulting in a biofilm with a fibrin wall protecting the bacterial colony from the host’s immune system. In some embodiments, the antibiotic is a cationic antimicrobial peptide (CAMP). In some aspects of these embodiments, the cationic antimicrobial peptide is a defensin peptide (e.g., defensin 1 such as beta-defensin 1 or alpha-defensin 1), or cecropin, andropin, moricin, ceratotoxin, melittin, magainin, dermaseptin, bombinin, brevinin (e.g., brevinin-1), esculentin, buforin II (e.g., from amphibians), CAP18 (e.g., from rabbits), LL37 (e.g., from humans), abaecin, apidaecins (e.g., from honeybees), prophenin (e.g., from pigs), indolicidin (e.g., from cattle), brevinins, protegrin (e.g., from pig), tachyplesins (e.g., from horseshoe crabs), or drosomycin (e.g., from fruit flies). In some embodiments, the antibiotic is selected from the quinolone class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of levofloxacin, norfloxacin, ofloxacin, ciprofloxacin, perfloxacin, lomefloxacin, fleroxacin, sparfloxacin, grepafloxacin, trovafloxacin, clinafloxacin, gemifloxacin, enoxacin, sitafloxacin, nadifloxacin, tosulfloxacin, cinnoxacin, rosoxacin, miloxacin, moxifloxacin, gatifloxacin, cinnoxacin, enoxacin, fleroxacin, lomafloxacin, lomefloxacin, miloxacin, nalidixic acid, nadifloxacin, oxolinic acid, pefloxacin, pirimidic acid, pipemidic acid, rosoxacin, rufloxacin, temafloxacin, tosufloxacin, trovafloxacin, and besifloxacin. In some embodiments, the antibiotic is selected from a β-lactam, a monobactam, oxazolidinone, and lipopeptide. In some embodiments, the antibiotic is selected from the cephalosporin class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of cefazolin, cefuroxime, ceftazidime, cephalexin, cephaloridine, cefamandole, cefsulodin, cefonicid, cefoperazine, cefoprozil, and ceftriaxone. In some embodiments, the antibiotic is selected from the penicillin class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of penicillin G, penicillin V, procaine penicillin, and benzathine penicillin, ampicillin, and amoxicillin, benzylpenicillin, phenoxymethylpenicillin, oxacillin, methicillin, dicloxacillin, flucloxacillin, temocillin, azlocillin, carbenicillin, ricarcillin, mezlocillin, piperacillin, apalcillin, hetacillin, bacampicillin, sulbenicillin, mecicilam, pevmecillinam, ciclacillin, talapicillin, aspoxicillin, cloxacillin, nafcillin, and pivampicillin. In some embodiments, the antibiotic is selected from the carbapenem class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of thienamycin, tomopenem, lenapenem, tebipenem, razupenem, imipenem, meropenem, ertapenem, doripenem, panipenem (betamipron), and biapenem. In some embodiments, the antibiotic is selected from the lipopeptide class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of polymyxin B, colistin (polymyxin E), and daptomycin. In some embodiments, the antibiotic is selected from the aminoglycoside class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of gentamicin, amikacin, tobramycin, debekacin, kanamycin, neomycin, netilmicin, paromomycin, sisomycin, spectinomycin, and streptomycin. In some embodiments, the antibiotic is selected from the glycopeptide class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of vancomycin, teicoplanin, telavancin, ramoplanin, daptomycin, decaplanin, and bleomycin. In some embodiments, the antibiotic is selected from the macrolide class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of azithromycin, clarithromycin, erythromycin, fidaxomicin, telithromycin, carbomycin A, josamycin, kitasamycin, midecamycin/midecamycinacetate, oleandomycin, solithromycin, spiramycin, troleandomycin, tylosin/tylocine, roxithromycin, dirithromycin, troleandomycin, spectinomycin, methymycin, neomethymycin, erythronolid, megalomycin, picromycin, narbomycin, oleandomycin, triacetyl-oleandomycin, laukamycin, kujimycin A, albocyclin and cineromycin B. In some embodiments, the antibiotic is selected from the ansamycin class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of streptovaricin, geldanamycin, herbimycin, rifamycin, rifampin, rifabutin, rifapentine and rifamixin. In some embodiments, the antibiotic is selected from the sulfonamide class of antibiotic compounds. In some aspects of these embodiments, the antibiotic is selected from the group consisting of sulfanilamide, sulfacetarnide, sulfapyridine, sulfathiazole, sulfadiazine, sulfamerazine, sulfadimidine, sulfasomidine, sulfasalazine, mafenide, sulfamethoxazole, sulfamethoxypyridazine, sulfadimethoxine, sulfasymazine, sulfadoxine, sulfametopyrazine, sulfaguanidine, succinylsulfathiazole and phthalylsulfathiazole. In some embodiments, the antibiotic is selected from the group consisting of quinolones, fluoroquinolones, β-lactams, cephalosporins, penicillins, carbapenems, lipopeptide antibiotics, glycopeptides, macrolides, ansamycins, sulfonamides, and combinations of two or more thereof. Positron emission tomography PET has become an important clinical diagnostic and research modality, and also a valuable technology in drug discovery and development. PET offers picomolar sensitivity and is a fully translational technique that requires specific probes radiolabeled with a usually short-lived positron-emitting radionuclide. Carbon-11 (radioactive half-life (t ^1/2 ) = 20.4 min) and fluorine-18 (t ^1/2 = 109.7 min) are the most commonly used radionuclides in PET imaging. PET has provided the capability of measuring biological processes at the molecular and metabolic levels in vivo by the detection of the photons formed as a result of the annihilation of the emitted positrons. As a noninvasive medical and molecular imaging technique and a powerful tool in cardiovascular research, PET offers the possibility of visualizing and analyzing complex physiological and pathophysiological conditions. PET has often been used to detect disease-related biochemical changes before the disease-associated anatomical changes can be found using standard medical imaging modalities. Positron emission tomography–computed tomography (PET/CT) Positron emission tomography–computed tomography (PET/CT) is a medical imaging technique using a device that combines in a single gantry system both a positron emission tomography (PET) scanner and an x-ray computed tomography (CT) scanner. The compounds of this disclosure, appropriately labeled, can be used to generate PET images of in a diseased or injured tissue, such as a tissue or an organ infected with bacteria producing a biofilm. Useful reporter groups that may be introduced to the compound of the present disclosure include radioactive isotopes, such as ¹¹ C, ¹³ N, ¹⁵ O, ¹⁸ F, ⁶⁴ Cu, ⁶⁸ Ga, ⁸¹ mKr, ⁸² Rb, ⁸⁶ Y, ⁸⁹ Zr, ¹¹¹ In, ¹²³ I, ¹²⁴ I, ¹³³ Xe, ²⁰¹ Tl, ¹²⁵ I, ³⁵ S ¹⁴ C, ³ H. Images acquired from both devices can be taken sequentially, in the same session, and combined into a single superposed (co-registered) image. Thus, functional imaging obtained by PET, which depicts the spatial distribution of metabolic or biochemical activity in the body can be more precisely aligned or correlated with anatomic imaging obtained by CT scanning. Two- and three- dimensional image reconstruction may be rendered as a function of a common software and control system. PET/CT scans can be used to diagnose a health condition in human and animal subjects. In a typical setting of performing PET/CT scans on for research animals such as mice, rats, and even larger animals, the animals are anesthetized, e.g., by isoflurane, prior to imaging, and anesthesia is maintained during the process. CT acquisition precedes PET and lasts approximately 4 minutes, acquiring 360 cone beam projections with a source power and current of 80 keV and 500 μA, respectively. Projections are reconstructed into three-dimensional volumes. The imaging bed then moves into the PET gantry. In some other embodiments, imaging is carried out in about 1-4 hours after the compound is administered to the patient. A high-resolution Fourier re-binning algorithm is used to re-bin sinograms, followed by a filtered back-projection algorithm for reconstruction. The reconstructed PET image, through dynamic framing of the sinograms, is composed of a series of 1, 3, and 5 minute frames. PET and CT reconstructed images are then fused using Inveon Research Workplace (IRW) software (Siemens). Positron Emission Tomography–Magnetic Resonance Imaging (PET-MRI) Positron emission tomography–magnetic resonance imaging (PET-MRI) is a hybrid imaging technology that incorporates magnetic resonance imaging (MRI) soft tissue morphological imaging and positron PET functional imaging. PET/MRI scans can be used to diagnose a health condition in humans and animals, e.g., for research and agricultural purposes. The compounds and compositions of this disclosure, when appropriately labelled with a radioisotope, can be used in PET/MRI. For imaging a particular organ, such as the heart, a fusion approach is implemented using external fiducial landmarks provided by a “vest” optimized for the particular organ, e.g., for cardiac imaging. The vest surrounds the subject’s chest to create a frame that follows minor movements due to transfer between scanners or light anesthesia. The tubes are filled with 15% iodine in water, rendering them visible in MRI. Subject motion is minimized with an imaging bed that can be used in both imaging systems. In Vivo Fluorescence-Molecular Tomography-Computed Tomography (FMT- CT) FMT-CT imaging is performed at 680/700 nm excitation/emission wavelength at specified time (e.g., 2, 4, 8, 24, or 48 hours) after injection of the compound of the present disclosure comprising a fluorochrome. Total imaging time for FMT acquisition is typically 5 to 8 minutes. Data are post-processed using a normalized Born forward equation to calculate three- dimensional fluorochrome concentration distribution. CT angiography can immediately follow FMT to robustly identify the aortic root. Pharmaceutical compositions The present application also provides pharmaceutical compositions comprising an effective amount of a compound of the present disclosure, or a pharmaceutically acceptable salt thereof; and a pharmaceutically acceptable carrier. The pharmaceutical composition may also comprise any one of the additional therapeutic agents described herein. In certain embodiments, the application also provides pharmaceutical compositions and dosage forms comprising any one the additional therapeutic agents described herein. The carrier(s) are “acceptable” in the sense of being compatible with the other ingredients of the formulation and, in the case of a pharmaceutically acceptable carrier, not deleterious to the recipient thereof in an amount used in the medicament. Pharmaceutically acceptable carriers, adjuvants and vehicles that may be used in the pharmaceutical compositions of the present application include, but are not limited to, ion exchangers, alumina, aluminum stearate, lecithin, serum proteins, such as human serum albumin, buffer substances such as phosphates, glycine, sorbic acid, potassium sorbate, partial glyceride mixtures of saturated vegetable fatty acids, water, salts or electrolytes, such as protamine sulfate, disodium hydrogen phosphate, potassium hydrogen phosphate, sodium chloride, zinc salts, colloidal silica, magnesium trisilicate, polyvinyl pyrrolidone, cellulose-based substances, polyethylene glycol, sodium carboxymethylcellulose, polyacrylates, waxes, polyethylene-polyoxypropylene-block polymers, polyethylene glycol, and wool fat. The compositions or dosage forms may contain any one of the compounds and therapeutic agents described herein in the range of 0.005% to 100% with the balance made up from the suitable pharmaceutically acceptable excipients. The contemplated compositions may contain 0.001%-100% of any one of the compounds and therapeutic agents provided herein, in one embodiment 0.1-95%, in another embodiment 75-85%, in a further embodiment 20-80%, wherein the balance may be made up of any pharmaceutically acceptable excipient described herein, or any combination of these excipients. Routes of administration and dosage forms The pharmaceutical compositions of the present application include those suitable for any acceptable route of administration. Acceptable routes of administration include, but are not limited to, buccal, cutaneous, endocervical, endosinusial, endotracheal, enteral, epidural, interstitial, intra-abdominal, intra- arterial, intrabronchial, intrabursal, intracerebral, intracisternal, intracoronary, intradermal, intraductal, intraduodenal, intradural, intraepidermal, intraesophageal, intragastric, intragingival, intraileal, intralymphatic, intramedullary, intrameningeal, intramuscular, intranasal, intraovarian, intraperitoneal, intraprostatic, intrapulmonary, intrasinal, intraspinal, intrasynovial, intratesticular, intrathecal, intratubular, intratumoral, intrauterine, intravascular, intravenous, nasal, nasogastric, oral, parenteral, percutaneous, peridural, rectal, respiratory (inhalation), subcutaneous, sublingual, submucosal, topical, transdermal, transmucosal, transtracheal, ureteral, urethral and vaginal. Compositions and formulations described herein may conveniently be presented in a unit dosage form, e.g., tablets, sustained release capsules, and in liposomes, and may be prepared by any methods well known in the art of pharmacy. See, for example, Remington: The Science and Practice of Pharmacy, Lippincott Williams & Wilkins, Baltimore, MD (20th ed.2000). Such preparative methods include the step of bringing into association with the molecule to be administered ingredients such as the carrier that constitutes one or more accessory ingredients. In general, the compositions are prepared by uniformly and intimately bringing into association the active ingredients with liquid carriers, liposomes or finely divided solid carriers, or both, and then, if necessary, shaping the product. In some embodiments, any one of the compounds and therapeutic agents disclosed herein are administered orally. Compositions of the present application suitable for oral administration may be presented as discrete units such as capsules, sachets, granules or tablets each containing a predetermined amount (e.g., effective amount) of the active ingredient; a powder or granules; a solution or a suspension in an aqueous liquid or a non-aqueous liquid; an oil-in-water liquid emulsion; a water-in- oil liquid emulsion; packed in liposomes; or as a bolus, etc. Soft gelatin capsules can be useful for containing such suspensions, which may beneficially increase the rate of compound absorption. In the case of tablets for oral use, carriers that are commonly used include lactose, sucrose, glucose, mannitol, and silicic acid and starches. Other acceptable excipients may include: a) fillers or extenders such as starches, lactose, sucrose, glucose, mannitol, and silicic acid, b) binders such as, for example, carboxymethylcellulose, alginates, gelatin, polyvinylpyrrolidinone, sucrose, and acacia, c) humectants such as glycerol, d) disintegrating agents such as agar-agar, calcium carbonate, potato or tapioca starch, alginic acid, certain silicates, and sodium carbonate, e) solution retarding agents such as paraffin, f) absorption accelerators such as quaternary ammonium compounds, g) wetting agents such as, for example, cetyl alcohol and glycerol monostearate, h) absorbents such as kaolin and bentonite clay, and i) lubricants such as talc, calcium stearate, magnesium stearate, solid polyethylene glycols, sodium lauryl sulfate, and mixtures thereof. For oral administration in a capsule form, useful diluents include lactose and dried corn starch. When aqueous suspensions are administered orally, the active ingredient is combined with emulsifying and suspending agents. If desired, certain sweetening and/or flavoring and/or coloring agents may be added. Compositions suitable for oral administration include lozenges comprising the ingredients in a flavored basis, usually sucrose and acacia or tragacanth; and pastilles comprising the active ingredient in an inert basis such as gelatin and glycerin, or sucrose and acacia. Compositions suitable for parenteral administration include aqueous and non- aqueous sterile injection solutions or infusion solutions which may contain antioxidants, buffers, bacteriostats and solutes which render the formulation isotonic with the blood of the intended recipient; and aqueous and non-aqueous sterile suspensions which may include suspending agents and thickening agents. The formulations may be presented in unit-dose or multi-dose containers, for example, sealed ampules and vials, and may be stored in a freeze dried (lyophilized) condition requiring only the addition of the sterile liquid carrier, for example water for injections, saline (e.g., 0.9% saline solution) or 5% dextrose solution, immediately prior to use. Extemporaneous injection solutions and suspensions may be prepared from sterile powders, granules and tablets. The injection solutions may be in the form, for example, of a sterile injectable aqueous or oleaginous suspension. This suspension may be formulated according to techniques known in the art using suitable dispersing or wetting agents and suspending agents. The sterile injectable preparation may also be a sterile injectable solution or suspension in a non-toxic parenterally-acceptable diluent or solvent, for example, as a solution in 1,3-butanediol. Among the acceptable vehicles and solvents that may be employed are mannitol, water, Ringer's solution and isotonic sodium chloride solution. In addition, sterile, fixed oils are conventionally employed as a solvent or suspending medium. For this purpose, any bland fixed oil may be employed including synthetic mono- or diglycerides. Fatty acids, such as oleic acid and its glyceride derivatives are useful in the preparation of injectables, as are natural pharmaceutically-acceptable oils, such as olive oil or castor oil, especially in their polyoxyethylated versions. These oil solutions or suspensions may also contain a long-chain alcohol diluent or dispersant. The pharmaceutical compositions of the present application may be administered in the form of suppositories for rectal administration. These compositions can be prepared by mixing a compound of the present application with a suitable non-irritating excipient which is solid at room temperature but liquid at the rectal temperature and therefore will melt in the rectum to release the active components. Such materials include, but are not limited to, cocoa butter, beeswax, and polyethylene glycols. The pharmaceutical compositions of the present application may be administered by nasal aerosol or inhalation. Such compositions are prepared according to techniques well-known in the art of pharmaceutical formulation and may be prepared as solutions in saline, employing benzyl alcohol or other suitable preservatives, absorption promoters to enhance bioavailability, fluorocarbons, and/or other solubilizing or dispersing agents known in the art. See, for example, U.S. Patent No.6,803,031. Additional formulations and methods for intranasal administration are found in Ilium, L., J Pharm Pharmacol, 56:3-17, 2004 and Ilium, L., Eur J Pharm Sci 11:1-18, 2000. The topical compositions of the present disclosure can be prepared and used in the form of an aerosol spray, cream, emulsion, solid, liquid, dispersion, foam, oil, gel, hydrogel, lotion, mousse, ointment, powder, patch, pomade, solution, pump spray, stick, towelette, soap, or other forms commonly employed in the art of topical administration and/or cosmetic and skin care formulation. The topical compositions can be in an emulsion form. Topical administration of the pharmaceutical compositions of the present application is especially useful when the desired treatment involves areas or organs readily accessible by topical application. In some embodiments, the topical composition comprises a combination of any one of the compounds and therapeutic agents disclosed herein, and one or more additional ingredients, carriers, excipients, or diluents including, but not limited to, absorbents, anti-irritants, anti-acne agents, preservatives, antioxidants, coloring agents/pigments, emollients (moisturizers), emulsifiers, film-forming/holding agents, fragrances, leave- on exfoliants, prescription drugs, preservatives, scrub agents, silicones, skin- identical/repairing agents, slip agents, sunscreen actives, surfactants/detergent cleansing agents, penetration enhancers, and thickeners. The compounds and therapeutic agents of the present application may be incorporated into compositions for coating an implantable medical device, such as prostheses, artificial valves, vascular grafts, stents, or catheters. Suitable coatings and the general preparation of coated implantable devices are known in the art and are exemplified in U.S. Patent Nos.6,099,562; 5,886,026; and 5,304,121. The coatings are typically biocompatible polymeric materials such as a hydrogel polymer, polymethyldisiloxane, polycaprolactone, polyethylene glycol, polylactic acid, ethylene vinyl acetate, and mixtures thereof. The coatings may optionally be further covered by a suitable topcoat of fluorosilicone, polysaccharides, polyethylene glycol, phospholipids or combinations thereof to impart controlled release characteristics in the composition. Coatings for invasive devices are to be included within the definition of pharmaceutically acceptable carrier, adjuvant or vehicle, as those terms are used herein. According to another embodiment, the present application provides an implantable drug release device impregnated with or containing a compound or a therapeutic agent, or a composition comprising a compound of the present application or a therapeutic agent, such that said compound or therapeutic agent is released from said device and is therapeutically active. Dosages and regimens In the pharmaceutical compositions of the present application, a compound of the present disclosure is present in an effective amount (e.g., a therapeutically effective amount). Effective doses may vary, depending on the diseases treated, the severity of the disease, the route of administration, the sex, age and general health condition of the subject, excipient usage, the possibility of co-usage with other therapeutic treatments such as use of other agents and the judgment of the treating physician. In some embodiments, an effective amount of the compound can range, for example, from about 0.001 mg/kg to about 500 mg/kg (e.g., from about 0.001 mg/kg to about 200 mg/kg; from about 0.01 mg/kg to about 200 mg/kg; from about 0.01 mg/kg to about 150 mg/kg; from about 0.01 mg/kg to about 100 mg/kg; from about 0.01 mg/kg to about 50 mg/kg; from about 0.01 mg/kg to about 10 mg/kg; from about 0.01 mg/kg to about 5 mg/kg; from about 0.01 mg/kg to about 1 mg/kg; from about 0.01 mg/kg to about 0.5 mg/kg; from about 0.01 mg/kg to about 0.1 mg/kg; from about 0.1 mg/kg to about 200 mg/kg; from about 0.1 mg/kg to about 150 mg/kg; from about 0.1 mg/kg to about 100 mg/kg; from about 0.1 mg/kg to about 50 mg/kg; from about 0.1 mg/kg to about 10 mg/kg; from about 0.1 mg/kg to about 5 mg/kg; from about 0.1 mg/kg to about 2 mg/kg; from about 0.1 mg/kg to about 1 mg/kg; or from about 0.1 mg/kg to about 0.5 mg/kg). In some embodiments, an effective amount of a compound is about 0.1 mg/kg, about 0.5 mg/kg, about 1 mg/kg, about 2 mg/kg, or about 5 mg/kg. The foregoing dosages can be administered on a daily basis (e.g., as a single dose or as two or more divided doses, e.g., once daily, twice daily, thrice daily) or non-daily basis (e.g., every other day, every two days, every three days, once weekly, twice weekly, once every two weeks, once a month). Kits The present invention also includes pharmaceutical kits useful, for example, in the treatment of disorders, diseases and conditions referred to herein, which include one or more containers containing a pharmaceutical composition comprising a therapeutically effective amount of a compound of the present disclosure. Such kits can further include, if desired, one or more of various conventional pharmaceutical kit components, such as, for example, containers with one or more pharmaceutically acceptable carriers, additional containers, etc. Instructions, either as inserts or as labels, indicating quantities of the components to be administered, guidelines for administration, and/or guidelines for mixing the components, can also be included in the kit. The kit may optionally include an additional therapeutic agent as described herein. Definitions As used herein, the term "about" means "approximately" (e.g., plus or minus approximately 10% of the indicated value). At various places in the present specification, substituents of compounds of the invention are disclosed in groups or in ranges. It is specifically intended that the invention include each and every individual subcombination of the members of such groups and ranges. For example, the term “C _1-6 alkyl” is specifically intended to individually disclose methyl, ethyl, C3 alkyl, C4 alkyl, C5 alkyl, and C6 alkyl. At various places in the present specification various aryl, heteroaryl, cycloalkyl, and heterocycloalkyl rings are described. Unless otherwise specified, these rings can be attached to the rest of the molecule at any ring member as permitted by valency. For example, the term “a pyridine ring” or “pyridinyl” may refer to a pyridin-2-yl, pyridin-3-yl, or pyridin-4-yl ring. The term “aromatic” refers to a carbocycle or heterocycle having one or more polyunsaturated rings having aromatic character (i.e., having (4n + 2) delocalized π (pi) electrons where n is an integer). The term “n-membered” where n is an integer typically describes the number of ring-forming atoms in a moiety where the number of ring-forming atoms is n. For example, piperidinyl is an example of a 6-membered heterocycloalkyl ring, pyrazolyl is an example of a 5-membered heteroaryl ring, pyridyl is an example of a 6- membered heteroaryl ring, and 1,2,3,4-tetrahydro-naphthalene is an example of a 10- membered cycloalkyl group. As used herein, the phrase “optionally substituted” means unsubstituted or substituted. The substituents are independently selected, and substitution may be at any chemically accessible position. As used herein, the term “substituted” means that a hydrogen atom is removed and replaced by a substituent. A single divalent substituent, e.g., oxo, can replace two hydrogen atoms. It is to be understood that substitution at a given atom is limited by valency. Throughout the definitions, the term “Cn-m” indicates a range which includes the endpoints, wherein n and m are integers and indicate the number of carbons. Examples include C _1-4 , C _1-6 , and the like. As used herein, the term “Cn-m alkyl”, employed alone or in combination with other terms, refers to a saturated hydrocarbon group that may be straight-chain or branched, having n to m carbons. Examples of alkyl moieties include, but are not limited to, chemical groups such as methyl, ethyl, n-propyl, isopropyl, n-butyl, tert- butyl, isobutyl, sec-butyl; higher homologs such as 2-methyl-1-butyl, n-pentyl, 3- pentyl, n-hexyl, 1,2,2-trimethylpropyl, and the like. In some embodiments, the alkyl group contains from 1 to 6 carbon atoms, from 1 to 4 carbon atoms, from 1 to 3 carbon atoms, or 1 to 2 carbon atoms. As used herein, the term “Cn-m haloalkyl”, employed alone or in combination with other terms, refers to an alkyl group having from one halogen atom to 2s+1 halogen atoms which may be the same or different, where “s” is the number of carbon atoms in the alkyl group, wherein the alkyl group has n to m carbon atoms. In some embodiments, the haloalkyl group is fluorinated only. In some embodiments, the alkyl group has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. As used herein, the term “Cn-m alkylene”, employed alone or in combination with other terms, refers to a divalent alkyl linking group having n to m carbons. Examples of alkylene groups include, but are not limited to, ethan-1,1-diyl, ethan-1,2- diyl, propan-1,1,-diyl, propan-1,3-diyl, propan-1,2-diyl, butan-1,4-diyl, butan-1,3- diyl, butan-1,2-diyl, 2-methyl-propan-1,3-diyl, and the like. In some embodiments, the alkylene moiety contains 2 to 6, 2 to 4, 2 to 3, 1 to 6, 1 to 4, or 1 to 2 carbon atoms. As used herein, the term “Cn-m alkoxy”, employed alone or in combination with other terms, refers to a group of formula -O-alkyl, wherein the alkyl group has n to m carbons. Example alkoxy groups include, but are not limited to, methoxy, ethoxy, propoxy (e.g., n-propoxy and isopropoxy), butoxy (e.g., n-butoxy and tert-butoxy), and the like. In some embodiments, the alkyl group has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. As used herein, “Cn-m haloalkoxy” refers to a group of formula –O-haloalkyl having n to m carbon atoms. An example haloalkoxy group is OCF3. In some embodiments, the haloalkoxy group is fluorinated only. In some embodiments, the alkyl group has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. As used herein, the term “amino” refers to a group of formula –NH2. As used herein, the term “Cn-m alkylamino” refers to a group of formula -NH(alkyl), wherein the alkyl group has n to m carbon atoms. In some embodiments, the alkyl group has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. Examples of alkylamino groups include, but are not limited to, N-methylamino, N-ethylamino, N- propylamino (e.g., N-(n-propyl)amino and N-isopropylamino), N-butylamino (e.g., N- (n-butyl)amino and N-(tert-butyl)amino), and the like. As used herein, the term “di(Cn-m-alkyl)amino” refers to a group of formula - N(alkyl)2, wherein the two alkyl groups each has, independently, n to m carbon atoms. In some embodiments, each alkyl group independently has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. As used herein, the term “Cn-m alkoxycarbonyl” refers to a group of formula -C(O)O-alkyl, wherein the alkyl group has n to m carbon atoms. In some embodiments, the alkyl group has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. Examples of alkoxycarbonyl groups include, but are not limited to, methoxycarbonyl, ethoxycarbonyl, propoxycarbonyl (e.g., n-propoxycarbonyl and isopropoxycarbonyl), butoxycarbonyl (e.g., n-butoxycarbonyl and tert-butoxycarbonyl), and the like. As used herein, the term “carbamyl” to a group of formula –C(O)NH2. As used herein, the term “Cn-m alkylcarbamyl” refers to a group of formula -C(O)-NH(alkyl), wherein the alkyl group has n to m carbon atoms. In some embodiments, the alkyl group has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. As used herein, the term “di(Cn-m-alkyl)carbamyl” refers to a group of formula –C(O)N(alkyl)2, wherein the two alkyl groups each has, independently, n to m carbon atoms. In some embodiments, each alkyl group independently has 1 to 6, 1 to 4, or 1 to 3 carbon atoms. As used herein, the term “carboxy” refers to a -C(O)OH group. As used herein, “halo” refers to F, Cl, Br, or I. In some embodiments, a halo is F, Cl, or Br. As used herein, the term "aryl," employed alone or in combination with other terms, refers to an aromatic hydrocarbon group, which may be monocyclic or polycyclic (e.g., having 2, 3 or 4 fused rings). The term "Cn-m aryl" refers to an aryl group having from n to m ring carbon atoms. Aryl groups include, e.g., phenyl, naphthyl, anthracenyl, phenanthrenyl, indanyl, indenyl, and the like. In some embodiments, aryl groups have from 6 to 10 carbon atoms. In some embodiments, the aryl group is phenyl or naphtyl. As used herein, “cycloalkyl” refers to non-aromatic cyclic hydrocarbons including cyclized alkyl and/or alkenyl groups. Cycloalkyl groups can include mono- or polycyclic (e.g., having 2, 3 or 4 fused rings) groups and spirocycles. Ring- forming carbon atoms of a cycloalkyl group can be optionally substituted by 1 or 2 independently selected oxo or sulfide groups (e.g., C(O) or C(S)). Also included in the definition of cycloalkyl are moieties that have one or more aromatic rings fused (i.e., having a bond in common with) to the cycloalkyl ring, for example, benzo or thienyl derivatives of cyclopentane, cyclohexane, and the like. A cycloalkyl group containing a fused aromatic ring can be attached through any ring-forming atom including a ring-forming atom of the fused aromatic ring. Cycloalkyl groups can have 3, 4, 5, 6, 7, 8, 9, or 10 ring-forming carbons (C _3-10 ). In some embodiments, the cycloalkyl is a C _3-10 monocyclic or bicyclic cyclocalkyl. In some embodiments, the cycloalkyl is a C3-7 monocyclic cyclocalkyl. Example cycloalkyl groups include cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, cyclopentenyl, cyclohexenyl, cyclohexadienyl, cycloheptatrienyl, norbornyl, norpinyl, norcarnyl, adamantyl, and the like. In some embodiments, cycloalkyl is cyclopropyl, cyclobutyl, cyclopentyl, or cyclohexyl. As used herein, “heteroaryl” refers to a monocyclic or polycyclic aromatic heterocycle having at least one heteroatom ring member selected from sulfur, oxygen, and nitrogen. In some embodiments, the heteroaryl ring has 1, 2, 3, or 4 heteroatom ring members independently selected from nitrogen, sulfur and oxygen. In some embodiments, any ring-forming N in a heteroaryl moiety can be an N-oxide. In some embodiments, the heteroaryl is a 5-10 membered monocyclic or bicyclic heteroaryl having 1, 2, 3 or 4 heteroatom ring members independently selected from nitrogen, sulfur and oxygen. In some embodiments, the heteroaryl is a 5-6 monocyclic heteroaryl having 1 or 2 heteroatom ring members independently selected from nitrogen, sulfur and oxygen. In some embodiments, the heteroaryl is a five- membered or six-membereted heteroaryl ring. A five-membered heteroaryl ring is a heteroaryl with a ring having five ring atoms wherein one or more (e.g., 1, 2, or 3) ring atoms are independently selected from N, O, and S. Exemplary five-membered ring heteroaryls are thienyl, furyl, pyrrolyl, imidazolyl, thiazolyl, oxazolyl, pyrazolyl, isothiazolyl, isoxazolyl, 1,2,3-triazolyl, tetrazolyl, 1,2,3-thiadiazolyl, 1,2,3- oxadiazolyl, 1,2,4-triazolyl, 1,2,4-thiadiazolyl, 1,2,4-oxadiazolyl, 1,3,4-triazolyl, 1,3,4-thiadiazolyl, and 1,3,4-oxadiazolyl. A six-membered heteroaryl ring is a heteroaryl with a ring having six ring atoms wherein one or more (e.g., 1, 2, or 3) ring atoms are independently selected from N, O, and S. Exemplary six-membered ring heteroaryls are pyridyl, pyrazinyl, pyrimidinyl, triazinyl and pyridazinyl. As used herein, “heterocycloalkyl” refers to non-aromatic monocyclic or polycyclic heterocycles having one or more ring-forming heteroatoms selected from O, N, or S. Included in heterocycloalkyl are monocyclic 4-, 5-, 6-, 7-, 8-, 9- or 10- membered heterocycloalkyl groups. Heterocycloalkyl groups can also include spirocycles. Example heterocycloalkyl groups include pyrrolidin-2-one, 1,3- isoxazolidin-2-one, pyranyl, tetrahydropuran, oxetanyl, azetidinyl, morpholino, thiomorpholino, piperazinyl, tetrahydrofuranyl, tetrahydrothienyl, piperidinyl, pyrrolidinyl, isoxazolidinyl, isothiazolidinyl, pyrazolidinyl, oxazolidinyl, thiazolidinyl, imidazolidinyl, azepanyl, benzazapene, and the like. Ring-forming carbon atoms and heteroatoms of a heterocycloalkyl group can be optionally substituted by 1 or 2 independently selected oxo or sulfido groups (e.g., C(O), S(O), C(S), or S(O)2, etc.). The heterocycloalkyl group can be attached through a ring- forming carbon atom or a ring-forming heteroatom. In some embodiments, the heterocycloalkyl group contains 0 to 3 double bonds. In some embodiments, the heterocycloalkyl group contains 0 to 2 double bonds. Also included in the definition of heterocycloalkyl are moieties that have one or more aromatic rings fused (i.e., having a bond in common with) to the cycloalkyl ring, for example, benzo or thienyl derivatives of piperidine, morpholine, azepine, etc. A heterocycloalkyl group containing a fused aromatic ring can be attached through any ring-forming atom including a ring-forming atom of the fused aromatic ring. In some embodiments, the heterocycloalkyl is a monocyclic 4-6 membered heterocycloalkyl having 1 or 2 heteroatoms independently selected from nitrogen, oxygen, or sulfur and having one or more oxidized ring members. In some embodiments, the heterocycloalkyl is a monocyclic or bicyclic 4-10 membered heterocycloalkyl having 1, 2, 3, or 4 heteroatoms independently selected from nitrogen, oxygen, or sulfur and having one or more oxidized ring members. At certain places, the definitions or embodiments refer to specific rings (e.g., an azetidine ring, a pyridine ring, etc.). Unless otherwise indicated, these rings can be attached to any ring member provided that the valency of the atom is not exceeded. For example, an azetidine ring may be attached at any position of the ring, whereas a pyridin-3-yl ring is attached at the 3-position. The term “compound” as used herein is meant to include all stereoisomers, geometric isomers, tautomers, and isotopes of the structures depicted. Compounds herein identified by name or structure as one particular tautomeric form are intended to include other tautomeric forms unless otherwise specified. The compounds described herein can be asymmetric (e.g., having one or more stereocenters). All stereoisomers, such as enantiomers and diastereomers, are intended unless otherwise indicated. Compounds of the present invention that contain asymmetrically substituted carbon atoms can be isolated in optically active or racemic forms. Methods on how to prepare optically active forms from optically inactive starting materials are known in the art, such as by resolution of racemic mixtures or by stereoselective synthesis. Many geometric isomers of olefins, C=N double bonds, N=N double bonds, and the like can also be present in the compounds described herein, and all such stable isomers are contemplated in the present invention. Cis and trans geometric isomers of the compounds of the present invention are described and may be isolated as a mixture of isomers or as separated isomeric forms. In some embodiments, the compound has the (R)-configuration. In some embodiments, the compound has the (S)-configuration. Compounds provided herein also include tautomeric forms. Tautomeric forms result from the swapping of a single bond with an adjacent double bond together with the concomitant migration of a proton. Tautomeric forms include prototropic tautomers which are isomeric protonation states having the same empirical formula and total charge. Example prototropic tautomers include ketone – enol pairs, amide - imidic acid pairs, lactam – lactim pairs, enamine – imine pairs, and annular forms where a proton can occupy two or more positions of a heterocyclic system, for example, 1H- and 3H-imidazole, 1H-, 2H- and 4H- 1,2,4-triazole, 1H- and 2H- isoindole, and 1H- and 2H-pyrazole. Tautomeric forms can be in equilibrium or sterically locked into one form by appropriate substitution. As used herein, the term “cell” is meant to refer to a cell that is in vitro, ex vivo or in vivo. In some embodiments, an ex vivo cell can be part of a tissue sample excised from an organism such as a mammal. In some embodiments, an in vitro cell can be a cell in a cell culture. In some embodiments, an in vivo cell is a cell living in an organism such as a mammal. As used herein, the term “contacting” refers to the bringing together of indicated moieties in an in vitro system or an in vivo system. For example, “contacting” a cell with a compound of the invention includes the administration of a compound of the present invention to an individual or patient, such as a human, having the cell, as well as, for example, introducing a compound of the invention into a sample containing a cellular or purified preparation containing the cell. As used herein, the term “individual”, “patient”, or “subject” used interchangeably, refers to any animal, including mammals, preferably mice, rats, other rodents, rabbits, dogs, cats, swine, cattle, sheep, horses, or primates, and most preferably humans. As used herein, the phrase “effective amount” or “therapeutically effective amount” refers to the amount of active compound or pharmaceutical agent that elicits the biological or medicinal response in a tissue, system, animal, individual or human that is being sought by a researcher, veterinarian, medical doctor or other clinician. As used herein, the term “radioisotope” refers to an atom having an atomic mass or mass number different from the atomic mass or mass number typically found in nature (i.e., naturally occurring). As used herein, the term “isotopic enrichment factor” refers to the ratio between the isotopic abundance and the natural abundance of a specified isotope. “ ¹⁸ F” refers to the radioisotope of fluorine having 9 protons and 9 neutrons. “F” refers to the stable isotope of fluorine having 9 protons and 10 neutrons (i.e., the “ ¹⁹ F isotope”). A compound of the present disclosure has an isotopic enrichment factor for each designated ¹⁸ F atom of at least 3500 (52.5% ¹⁸ F incorporation at each designated ¹⁸ F atom), at least 4000 (60% ¹⁸ F incorporation), at least 4500 (67.5% ¹⁸ F incorporation), at least 5000 (75% ¹⁸ F), at least 5500 (82.5% ¹⁸ F incorporation), at least 6000 (90% ¹⁸ F incorporation), at least 6333.3 (95% ¹⁸ F incorporation), at least 6466.7 (97% ¹⁸ F incorporation), at least 6600 (99% ¹⁸ F incorporation), or at least 6633.3 (99.5% ¹⁸ F incorporation). “ ¹¹ C” refers to the radioisotope of carbon having 6 protons and 5 neutrons. “C” refers to the stable isotope of carbon having 6 protons and 6 neutrons (i.e., the “ ¹² C isotope”). A compound of the present disclosure has an isotopic enrichment factor for each designated ¹¹ C atom of at least 3500 (52.5% ¹¹ C incorporation at each designated ¹¹ C atom), at least 4000 (60% ¹¹ C incorporation), at least 4500 (67.5% ¹¹ C incorporation), at least 5000 (75% ¹¹ C), at least 5500 (82.5% ¹¹ C incorporation), at least 6000 (90% ¹¹ C incorporation), at least 6333.3 (95% ¹¹ C incorporation), at least 6466.7 (97% ¹¹ C incorporation), at least 6600 (99% ¹¹ C incorporation), or at least 6633.3 (99.5% ¹¹ C incorporation). As used herein the term “treating” or “treatment” refers to 1) inhibiting the disease; for example, inhibiting a disease, condition or disorder in an individual who is experiencing or displaying the pathology or symptomatology of the disease, condition or disorder (i.e., arresting further development of the pathology and/or symptomatology), or 2) ameliorating the disease; for example, ameliorating a disease, condition or disorder in an individual who is experiencing or displaying the pathology or symptomatology of the disease, condition or disorder (i.e., reversing the pathology and/or symptomatology). EXAMPLES Materials and methods Study design: the studies were designed to develop PET/MRI imaging probes for bacterial endocarditis. Initial optical and nuclear imaging in mice was followed by validation in a cohort of piglets subjected to either right- or left-sided endocarditis. The rationale was to improve imaging tools for monitoring host-pathogen interactions. Formal power estimations were not performed, however the number of mice included per study (n=6) was based on prior endocarditis imaging in mice. Mice were randomly assigned to disease and treatment groups. Investigators were not blinded to group allocation. Wherever possible, studies were repeated at least once. The number of animals used and experimental replicates performed are stated for each experiment in the figure legends. Bacteria: Xen29 and Xen36 are both bioluminescent strains of coagulase- positive methicillin-susceptible Staphylococcus aureus (MSSA). Xen 43 is S. epidermidis strain. All Xen strains were purchased from PerkinElmer Inc.. S. aureus ^RFP+ is a fluorescence version of methicillin-resistant S. aureus USA 300, NE1260R JE2 pckA::rfp that was obtained from Dr. J. Bose of the University of Kansas Medical Center. Briefly, strains were cultured in liquid brain heart infusion broth under constant shaking at 150-200 rpm at 37 °C. For injecting the animals, overnight cultures were diluted 20-fold in sterile Dulbecco’s phosphate buffer saline without calcium or magnesium (PBS, Lonza). The injections’ approximate CFU counts were assessed by light scattering at 600 nm using a Shimadzu UV-2101PC spectrophotometer according to the manufacturer’s guidelines. Prior to injection, bioluminescence production was confirmed using a bioluminescence imager (FujiFilm LAS-1000) set to 10 min integration time. Post injection, true CFU numbers were verified by serial plating on 5% sheep blood agar (Hardy Diagnostics) and expression of either the bioluminescent or fluorescent reporter gene was confirmed by imaging the agar plates. To maximize microbe pathogenicity for the porcine models, the Xen strain with strongest bioluminescence in the piglets was selected after a limited screen, and the porcine-passaged strain was cultured from a port abscess. All piglet experiments use this porcine-primed Xen36 strain. Mouse endocarditis: to induce mouse endocarditis, protocols for artery isolation surgery were followed, 4.0 suture material insertion and S. aureus infection as previously reported. A 4-0 suture was advanced through the surgically exposed right carotid artery into the left ventricular outflow tract and fixed in place. After a 24 hour recovery period, 1×10 ⁶ CFU S. aureus in 100 μL PBS were injected through the tail vein. Continual endothelial damage to the aortic valve caused by the indwelling suture allowed the bacteria to attach and form vegetations. All animal experimentation and cohort size determination were approved in advance by the Massachusetts General Hospital’s Subcommittee on Research Animal Care. Mouse renal infection: mice (n=14 mice) were anesthetized with isoflurane (1- 3% / 2 L O2) and received 6×10 ⁷ CFU of S. aureus Xen 36 in 50 µl sterile phosphate buffered saline by intravenous injection. Mice were imaged for bioluminescence signal in the region of the kidneys starting at 48 hrs post infection. Mice (n=8) showing apparent kidney infection were separated and half of those animals received the DAB-VT680XL (10 nmol) by intravenous injection. All mice were imaged at 24 hrs after probe injection, when unbound DAB-VT680XL was excreted, and compared to non-infected control animals that only received the DAB-VT680XL injection (n=3). Imaging entailed collection of both bioluminescence (300 s exposure time) and fluorescence (675 nm excitation and 720 nm emission filters) using an IVIS Lumina XRMS system (PerkinElmer Inc.). Mice were euthanized and confirmatory in situ and ex vivo images were also collected. All experimentation was approved by the Institutional Animal Care and Use Committee for Auburn University. Piglet endocarditis: a total of 36 newly weaned piglets (16-20 days old, weighing 10-15 lb) were purchased from the Swine Research and Education Center at Auburn University for use in model development (bioluminescence imaging (BLI) only), fluorescence probe co-localization, and clinical PET/MRI studies. The animals were acclimated for 5-7 days prior to central-line implantation surgery. Piglets were sedated with dexmedetomidine (Dexdomitor; Zoetis) and butorphanol. An intravenous catheter was placed and anesthesia was induced using a combination of ketamine (10 mg/kg; Ketaset; Zoetis), dexmedetomidine (20 mcg/kg) and butorphanol (0.4 mg/kg). A line block of 0.5 % lidocaine (Xylocaine-MPF; Fresenius Kabi USA) was placed prior to making a 3-4 cm incision just lateral to the midline. A combination of sharp and blunt dissection was used to identify and isolate the left jugular vein and then to create a subcutaneous pocket for the vascular access port (VAP; 5Fr ClearPort; Access Technologies). The vascular port consisted of a titanium outlet with a silicone septum and catheter. A small jugular venotomy was made and a 0.025 guide-wire was introduced into the vascular lumen. The polyurethane VAP catheter was placed over the guide wire and advanced into the right ventricle under fluoroscopic guidance. Correct positioning of the catheter was confirmed using multiple injections of radiopaque contrast under fluoroscopic observation. Ports were implanted in the front right region of the neck. Once the desired catheter positioning was confirmed, the VAP catheter was secured within the jugular vein with several circumferential sutures of 3-0 polypropylene (Prolene; Ethicon). The catheter tubing was cut to an appropriate length and connected to the VAP that was then secured within the subcutaneous pocket with multiple polypropylene sutures. The surgical site was lavaged with saline and closed with 3-0 poliglecaprone 25 (Monocryl; Ethicon) in the subcutaneous and intra-dermal layers. A 22-gauge Posi-grip Huber point needle was placed into the VAP, continued patency was confirmed and the VAP was heparin- locked. The VAP site was marked with a permanent skin marker for ease of injection. The piglets then recovered from anesthesia. Analgesia was provided with carprofen (2.2 mg/kg per os every 12 hrs; Rimadyl; Zoetis) and butorphanol (0.2-0.4 mg/kg, intramuscularly every 4-6 hrs). At 6-8 hours following surgery, piglets were injected with 4-8×10 ⁸ CFU of S. aureus Xen 36 (PerkinElmer Inc.) through the VAP using a Huber needle. Thereafter the port was flushed with 5 mL sterile PBS. For aortic valve endocarditis, piglets were similarly prepared but the aorta was accessed via the left carotid artery. Aortic valve damage was induced by repeated passing of a 2.5 mm diameter cytology brush (Endoscopy Support Services) through the valve. The brush was positioned under fluoroscopy guidance aided by repeated contrast injection. A venous leg catheter was used to administer anesthesia and the S. aureus Xen 36 inoculum (5-8 × 10 ⁸ CFU) followed by a bolus 60 mL sterile saline flush. For optical studies, piglets were injected with 0.4 µmol DAB-VT680XL in 2 mL sterile PBS via the ear vein using a 25-gauge butterfly. Animals were euthanized 10-12 hours later and BLI and fluorescence reflectance imaging (FRI) performed immediately following necropsy using an IVIS Lumina XRMS imaging system (PerkinElmer). For PET/MRI, piglets were transferred to Mt. Sinai Hospital. All experimentation and the transport were approved by the Institutional Animal Care and Use Committee for Auburn University under protocol AU# 2016-2860. Synthesizing fluorescent and fluorine-18 labeled dabigatran: the fluorescent and nuclear thrombin-specific imaging agents are derived from the FDA-approved thrombin inhibitor dabigatran. Synthesizing both agents requires converting the parent compound’s carboxylic acid functionality to an amine, which can be further modified with either a fluorochrome or ¹⁸ F-prosthetic group. Thrombin activity assay: to confirm that modification did not inhibit binding activity, VT680XL and ¹⁹ F-labeled dabigatran were examined with the SensoLyte AFC Thrombin Assay Kit (AnaSpec). Thrombin cleaves the substrate, releasing 7- amido-4-trifluoromethylcoumarin, which was monitored at excitation/emission = 380/500 nm. 1 ⁸ F-DAB blood half-life: To determine the blood half-life of the fluorine-18 ( ¹⁸ F)-labeled imaging agent derived from the thrombin inhibitor dabigatran ( ¹⁸ F- DAB), blood from ¹⁸ F-DAB-injected mice was collected by retro-orbital bleeding and sampled with gamma-counting. Under isoflurane (1.5-3 %) anesthesia, ¹⁸ F-DAB was injected via tail vein (approximately 250 µCi in 100 µl PBS) in 12-week-old 6 C57BL/6 mice. Mice were kept on a heated stage (37 °C) under isoflurane anesthesia and bled 20 µl 1-2, 5, 10, 15, 30, 60 and 120 minutes after probe injection. Blood samples were weighed and residual radioactivity in the samples was measured using a gamma-counter and the percent injected dose per gram blood (%IDGB) was computed. Blood half-life was derived from fitting %IDGB to the one compartment pharmacokinetic equation C ( t) = C ( o ) e ^{− kt} whereas C(t) is %IDGB at time t and k is the rate constant. Half-life is denoted as Intravital microscopy of thrombi in the femoral artery: intravital microscopy was used to visualize DAB-VT680XL binding to freshly formed thrombi. Arterial thrombosis was induced by applying ferric chloride solution (500 mM concentration; Sigma) on the exposed femoral artery of mice. Fluorescently conjugated anti-CD41 mAb (Biolegend) was injected via tail vein to label platelets in vivo before thrombosis induction. DAB-VT680XL and control fluorochrome VT680XL were injected intravenously 5 min after thrombosis induction. Images were acquired with IVM (Olympus) in vivo. Intravital microscopy of vegetation in the femoral artery: a 12-0 Ethicon suture material was inserted into the saphenous artery, advanced into the femoral artery and fixed in position while maintaining sufficient blood flow. Mice were allowed to recover for 6 hours before injection of 10 ⁶ CFU S. aureus ^RFP+ bacteria in 100 µl PBS.6 hours after bacteria administration, SC- and vWBp-neutralizing mAb (GMA-2105 and GMA-2510, Green Mountain Antibodies) or isotype IgG-control antibodies were injected.90 minutes before imaging, neutrophils were labeled by injecting 15 µg fluorescein isothiocyanate (FITC) anti-mouse Ly-6G antibody (Clone 1A8, BioLegend) and the vegetation was stained by injecting 2 nmol DAB- VT680XL. All injections were done via tail vein. Intravital microscopy was performed 24 hours after bacteria injection. Mice were anesthetized using 1-2 % isoflurane, then placed on a heated (37 °C) stage for imaging, and the wound was reopened. Imaging was done using an Olympus (IV100) microscope with a water- immersion objective (UMPlanFL N 20× NA 0.50, Olympus). Three channels were recorded (Ly-6G FITC, 488 nm excitation; RFP, 561 nm excitation; DAB-VT680XL, 647 nm excitation) to generate z-stacks at 2 µm steps. Image post-processing was performed using ImageJ software. FMT/CT: on day 3 after suture insertion and 48 hours after injection of either 1×10 ⁶ CFU S. aureus Xen29 in 100 µl PBS or PBS only for the sham group, FMT/CT imaging was performed. To this end, mice were injected with 2 nmol of the fluorescent imaging probe and imaged 2 hours later using an FMT-2500 LX Quantitative Tomography Imaging System (PerkinElmer). After excitation at 680 nm and emission collection at 700 nm, a three-dimensional dataset containing fluorescence concentration per voxel was reconstructed. FMT imaging was accompanied by hybrid X-ray CT angiography (Inveon PET-CT, Siemens). Image fusion was achieved using Osirix software and fiducial markers on a dedicated multimodal imaging cassette frame, as described previously. During CT acquisition, IsoVue 370 was infused at 50 μl/min through a tail vein catheter. The CT was reconstructed using a modified Feldkamp cone beam reconstruction algorithm (COBRA, Exxim Inc.), bilinear interpolation and a Shepp-Logan reconstruction filter. Voxels were scaled to Hounsfield units. The isotropic spatial resolution was 110 μm for CT and 1 mm for FMT. Fused data sets were used to place regions of interest in the left ventricular outflow tract and the aortic valve region. After FMT/CT, underwent ex vivo fluorescence imaging of excised aortas on an OV-110 epifluorescence microscope (Olympus). The same setup was used to evaluate the effects of SC und vWBp-neutralizing mAb treatment. Six hours after bacteria injection, either SC und vWBp-neutralizing mAb or unspecific IgG-control antibodies were injected. Fluorescence reflectance imaging and histology: excised aortas were imaged side-by-side with controls using epifluorescence microscope (OV-110, Olympus). The tissue was then fixed in 4 % paraformaldehyde (PFA) for at least 12 hours, embedded in optimal-cutting-temperature compound and flash-frozen in an isopentane / dry ice bath. Hematoxylin and eosin (H&E), Gram staining (Sigma-Aldrich) and immunofluorescence staining for CD11b were performed to verify the presence of S. aureus bacteria and myeloid cells on the aortic valve. Fluorescence microscopy (Eclipse 80i, Nikon) was performed to investigate microscopic DAB-VT680XL localization in the vegetation, and bright field images were scanned and analyzed using a Nanozoomer 2.0RS (Hamamatsu). PET/CT imaging in mice: on day 3 post surgery, animals were injected with 250 µCi of ¹⁸ F-DAB and imaged by PET-CT 1.5 hours later. We used an Inveon small animal PET-CT scanner (Siemens), a three-dimensional ordered subsets maximum likelihood with maximum a posteriori (OSEM3D/MAP) algorithm with 2 OSEM and 18 MAP iterations to reconstruct into three-dimensional images. The CT was performed prior to the PET scan. The PET voxel size was 0.796 × 0.861 × 0.861 mm, for a total of 128 × 128 × 159 voxels. Standard uptake values (SUV) were obtained from manually drawn regions of interest in the invent research workplace software environment. Following PET/CT imaging, the aortic root was excised, counted on a Wallac wizard 3 gamma counter to obtain percent injected dose per gram tissue (%IDGT) and imaged for bioluminescent signal. This was followed by overnight exposure on an autoradiography cassette. Plates were read on a Typhoon 9400 Variable Mode Imager (GE Healthcare). Target to background of both the bioluminescent signal and autoradiography were quantified using manual ROI’s of the aorta and background in Amira software (ThermoFisher Scientific). Generating monoclonal antibodies that neutralize SC and vWBp: the murine monoclonal antibodies against synthetic peptides corresponded to the N-terminal residues 1 through 10 of either SC or vWBp from S. aureus Newman D2 Tager 104 strain. Corresponding peptides were synthesized with an additional C-terminal cysteine that conjugated to keyhole limpet hemocyanin (KLH) and ovalbumin (OA) using m-maleimidobenzoyl-N-hydroxysuccinimide ester. To generate these monoclonal antibodies, mice were injected on day 1 with KLH-peptide conjugate (100 µg) in complete Freund’s adjuvant. On days 17, 27 and 42, mice were injected with KLH-peptide conjugate (50 µg) in incomplete Freund’s adjuvant. Serum titers from each mouse were determined by solid-phase ELISA, and spleen cells from the mouse with the highest serum titer were fused to NS1 myeloma cells on day 162, as described using polyethylene glycol. Hybridoma were selected using hypoxanthine, azaserine and thymidine. Fusion clones were screened by solid-phase ELISA with peptide-OA coated microtiter plates. Selected clones showing signal above ~2×- background were expanded, re-screened, sub-cloned three times by limiting dilution and stored in liquid nitrogen. SC-specific antibodies were designated GMA-2105 and others specific for vWBp were designated GMA-2510. Hybridoma cells were grown in Hybridoma-SFM media (Gibco) and antibodies purified by protein G affinity chromatography. Purified antibody was sterile-filtered and stored at 4 ºC. Antibody aggregation was ruled out by size exclusion chromatography on an S-300 column and dynamic light scattering with a Zetasizer Nano-S instrument (Malvern Panalytical). The isotype of each respective antibody was independently verified using/via goat anti-mouse isotype-specific antibody (Bethyl Laboratories) using a MagPix (Luminex). Antibody specificity for SC and vWBp: Western blot confirmed specificity of prothrombin activation-specific monoclonal antibodies. Previously characterized recombinant proteins were subjected to SDS gel electrophoresis with lanes corresponding to (1) vWBp-(1-263), (2) vWBp-(1-474), (3) SC-(1-325),(4) SC-(1- 660) and (5) protein standards with indicated molecular weights. The elaborated proteins were transferred to PVDF membrane for western blot analysis to probe the specificity and cross-reactivity of the monoclonal antibodies targeting the critical N- termini of either SC or vWBp. The same blot was probed with either the anti-vWBp monoclonal antibody (GMA-2510) (5 µg/mL) or the anti-SC (GMA-2105) (10 µg/mL) for 1 hour at 4 °C. Following primary antibody treatment, blots were washed and probed with horseradish peroxidase-labeled rabbit anti-mouse IgG that lacked the constant region and then imaged for chemiluminescence substrate oxidation using a Fuji-Films LAS1000. The blot was stripped between primary antibody challenges. Finally, since the antibodies were intended to be used together, it was verified that GMA-2510 and GMA-2105 would have additive functions in recognizing these S. aureus virulence factors. To accomplish this, the blot was probed with both SC and vWBp neutralizing antibodies and then stained for total mouse IgG content using an anti-mouse IgG (H+L)-FITC polyclonal antibody. The blot was imaged for fluorescence using a Fuji-films FLA5100 with the 473 laser and LBP channel. Fibrinogen turbidity assays: cleavage of fibrinogen by either prothrombin●vWBp-(1-263) or prothrombin●SC-(1-325) complexes was monitored from the increase in turbidity at 450 nm at 25 °C in 50 mM Hepes, 110 mM NaCl, 5 mM CaCl2, 1 mg/mL polyethylene glycol (PEG) 8000 (pH 7.4) buffer by using a SpectraMax 340 PC 384 plate reader (Molecular Devices Inc.). Individual reaction conditions were tested to determine the effect of the respective antibodies on the ability of either vWBp or SC to activate prothrombin and subsequently cleave of fibrinogen. GMA-2510 (anti-vWBp Ab) was incubated with vWBp-(1-263) and GMA-2105 (anti-SC Ab) was incubated with SC-(1-325) for 25 minutes at 25 °C prior to addition of prothrombin. The 3 components were then incubated together for an additional 25 minutes at 25 °C prior sub-sampling into the turbidity assay. The vWBp assays had final concentrations of 75 nM prothrombin●vWBp(1-263) complex with either 0 nM, 300 nM or 1.5 µM anti-vWBp ab. The SC assays had 15 nM prothrombin●SC(1-325) complex with either 0 nM, 50 nM, or 300 nM anti-SC ab. Fibrinogen (1.5 mg/mL) was added simultaneously to initiate all reactions. Progress curves were collected over time ranges necessary to observe total substrate depletion under the positive control conditions. Survival study: to determine the potentially beneficial impact of eliminating prothrombin activation by bacteria, we simultaneously administered either both GMA-2105 and 2510 mAbs or an isotype control mAb (Green Mountain Antibodies, Burlington, VT). Endocarditis was induced in 30 mice, which were randomized to treatment groups. Six hours post surgery, the mice received GMA-2105, GMA-2510 or isotype-labeled mAbs by intraperitoneal injection. Mice were kept under normal husbandry without further treatment except for pain management with buprenorphine as needed until death occurred, humane endpoints were reached or up to day 7 after injection of the 1×10 ⁶ CFU S. aureus. MRI of piglets: left ventricular ejection fraction was quantified from retrospectively gated short-axis cardiac cine MR images (Siemens 3T Biograph mMR). Acquisition parameters for cine short axis stacks were as follows: repetition time (TR) 56.24 ms, echo time (TE) 3.32 ms, number of averages 2, 24 or 30 slices, 25 cardiac frames, 3 mm slice thickness, no interslice gap, flip angle 12, spatial resolution 0.94×0.94 mm ² . Retrospective electrocardiogram (ECG) gating was used to acquire the images. Regions of interest (ROIs) were manually segmented with Osirix MD v 9.5.1 and exported using the ‘Export ROIs’ Osirix plugin. The cine acquisition contains a total of 600 or 750 images from 24 slices with 25 cardiac frames per slice. Right ventricle vegetations were quantified from an ECG triggered axial T2 weighted turbo spin echo (TSE) stack using the following acquisition parameters: TR 1125- 1485 ms, TE 76 ms, number of averages 4, 11-24 slices, 3 mm slice thickness, no interslice gap, spatial resolution 0.94x0.94 mm ² . ROIs were manually segmented with Osirix MD v 9.5.1. ROIs were exported using the ‘Export ROIs’ Osirix plugin. Vegetations were segmented as high intensity areas within the right ventricle while excluding the catheter whenever possible. PET/MRI of piglets: eight piglets underwent imaging with a clinical PET/MR system (Siemens 3T Biograph mMR). The piglets received an intravenous injection of ¹⁸ F-DAB (51.8 and 25 MBq, respectively) 90 minutes before PET acquisition. Piglets were intubated and placed on the scanner bed under isoflurane anesthesia at 1.5-2 % by inhalation, and were oxygenated throughout the PET/MR imaging experiment. Vital parameters were monitored. A 6-channel body matrix product coil was used for signal reception. Following scout scans, a static thoracic PET was performed for 60 minutes while simultaneously acquiring cardiac and T2 weighted TSE anatomical MR images as detailed above. Attenuation correction of PET images was performed by using a vendor-built-in Dixon MR-based attenuation map (MR-AC) with 4 tissue compartments (soft tissue, fat, lung and air). Images were reconstructed using a three dimensional ordinary Poisson ordered subsets expectation maximization (OP-OSEM) algorithm with point-spread-function (PSF) resolution modeling, using 3 iterations and 21 subsets and filtered with a 4 mm Gaussian filter. Autoradiography of piglet samples: after euthanasia, animals were perfused and heart samples were excised. To determine radiotracer distribution, digital autoradiography was performed by placing tissue samples in a film cassette against a phosphorimaging plate (BASMS-2325, Fujifilm) for 12.5 hours at –20 °C. Phosphorimaging plates were read at a pixel resolution of 25 μm with a Typhoon 7000IP plate reader (GE Healthcare). Quantification was carried out using ImageJ software. Statistical analysis: results are reported as mean ± standard error of mean (SEM). Statistical analysis was performed using GraphPad Prism 7 software (GraphPad Software, Inc.). Normal distribution of variables was tested using the Kolmogorov-Smirnov-test or the D’Agostino-Pearson omnibus normality test. Data were analyzed by parametric tests if normal distribution was detected. An unpaired student t-test was applied for two-group comparisons and data presented as mean ± s.e.m. with significance indicated by *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.001. If more than two groups were compared, one-way analysis of variance (ANOVA) analysis and Bartlett’s test for equal variances was used. If data were non- normally distributed, differences were evaluated using an unpaired, nonparametric Mann-Whitney test. A log-rank test was applied in the survival study. Significance level in all tests was 0.05. Raw data are provided in data file S1. Example 1 - Synthesizing imaging agents ¹⁸ F-DAB and DAB-VT680XL Thrombin activation through S. aureus virulence factors is a key bacterial defense mechanism downstream of potential drug targets. A targeted imaging agent thus has the potential to aid first preclinical discovery and later therapeutic trials. Provided herein is an imaging agent based on the Food and Drug Administration (FDA)-approved thrombin inhibitor dabigatran (DAB), capitalizing on the high affinity and specificity of this small molecule inhibitor. Both fluorescent and radioactively labeled versions were prepared in two steps (Fig.1A). First, dabigatran was derivatized with an amino group. The DAB-amino intermediate was then used to attach either the radioisotope 18-Fluorine ( ¹⁸ F), to yield the PET imaging agent ¹⁸ F- DAB, or the fluorochrome VivoTag 680XL (VT680XL), to synthesize the near infrared imaging agent DAB-VT680XL, which can be used for intravital microscopy and fluorescence molecular tomography. Mass spectrometry after liquid chromatography confirmed the identities of DAB-VT680XL (Fig.1B) and the non- radioactive standard ¹⁹ F-DAB (Fig.1C). Note that ¹⁸ F-DAB has a specific collection window (Fig.1D) to obtain the imaging agent with high radiochemical purity (Fig.1, E and 1F). Synthesizing dabigatran-NH2: dabigatran (50 mg, 106 μmol) was suspended in dimethylformamide (DMF, 4.0 mL) in a 20-mL vial with a magnetic stir-bar, to which N-Boc- 2,2′-(ethylenedioxy)diethylamine (105 mg, 424 μmol) and EDC (265 mg, 1.38 mmol) were then added. After stirring for 3 h, the reaction mixture was concentrated to dryness, re-dissolved in DMSO:H2O (2.0:0.1 mL) and subjected to reverse phase chromatography, resulting in 50 mg for a 67.2 % isolated yield of Dabigatran-NH-Boc. LC-ESI-MS(+) m/z = 702.5 [M+H+]+. Dabigatran-NH-Boc was dissolved in H2O:MeCN (1:1, 400 μL), and then HCl (4 M) in dioxane (1 mL) was added. The homogeneous solution was stirred at room temperature for 30 min and the reaction was concentrated by rotovap to give 41 mg, a 95.6 % yield, of Dabigatran- NH2 as a colorless solid. LC-ESI-MS(+) m/z = 602.4 [M+H+]+; LC-ESI-MS(-) m/z = 600.4 [M-H+]-. Synthesizing DAB-VT680XL: dabigatran-NH ² (0.5 mg, 0.7 μmol) was dissolved in DMF (12 μL) in a 1.5-mL centrifuge tube and added to VivoTag680 XL- NHS ester (1.0 mg, 0.7 μmol) in DMF (100 μL). After 3 h, this mixture was concentrated to dryness then redissolved in H2O/MeCN (10:1, 110 µL) and subjected to C18 reverse-phase HPLC purification. The combined HPLC collections were concentrated to give 1.1 mg of product, a 75.6 % yield. LC-ESI-MS(-) m/z = 917.4 ([M-2H+]/2)-, m/z = 611.2 ([M-3H+]/3)-. Synthesizing ¹⁹ F-DAB: dabigatran-NH2 (4 mg, 6.7 μmol) was dissolved in DMF (100 μL) and triethylamine (3 μL) in a 1.5-mL centrifuge tube and treated with N-succinimidyl-4-fluorobenoate (3 mg, 12.5 μmol) in DMF (50 μL). After 4 h the mixture was concentrated by rotary evaporation and subjected to HPLC purification resulting in 4.1 mg of ¹⁹ F-Dabigatran, a 68% yield. LC-ESI-MS(+) m/z = 724.6 [M+H+]+, 746.6 [M+Na+]+. Synthesizing ¹⁸ F-DAB: the prosthetic group N-succinimidyl-4-[ ¹⁸ F]- fluorobenzoate ( ¹⁸ F-FSB) was synthesized following the automated procedure of Scott and Shao, adapted for a Synthra RN Plus automated synthesizer (Synthra GmbH) operated by SynthraView software. Starting with [ ¹⁸ F]-F-, n.c.a., (~1772 MBq, 50 ± 4 mCi), ¹⁸ F-SFB was prepared in 25.0 % isolated yield in 100 min. Dabigatran-NH2 (4 mg, 6.7 μmol) dissolved in acetonitrile (500 μL) and triethylamine (4 μL) was reacted with ¹⁸ F-SFB (447 MBq, 12 ± 3 mCi) at 65 °C for 5 min, cooled and subjected to C18 reverse-phase HPLC using a Machery-Nagel Nucleodur C18 Pyramid 250×10 mm Vario-Prep column eluted with 75:25 water-acetonitrile (100 mM ammonium formate) at 5.5 mL/min and a 254 nm UV detector and radiodetector connected in series. ¹⁸ F-Dabigatran was synthesized in 10.7 % isolated yield (189 MBq, 5.1 ± 0.2 mCi) and at 99 ± 0.9 % radiochemical purity. 1 ⁸ F-Dabigatran for piglet imaging was produced using a GE FX2N automated synthesizer (GE Healthcare). A QMA cartridge containing cyclotron-produced [ ¹⁸ F]fluoride (~30 GBq, 0.81 ± 0.05 Ci) was eluted with a solution containing 9 mg 4,7,13,16,21,24-hexaoxa-1,10 diazabicyclo[8.8.8]hexacosane (Kryptofix [2.2.2]); 0.08 mL 0.15 M K2CO3 and 1.92 mL acetonitrile into a 5 mL reaction vial. Solvents were removed azeotropically at 110 °C under a slight flow of helium. Then, N- succinimidyl-4-[ ¹⁸ F]-fluorobenzoate ( ¹⁸ F-SFB) was synthesized in 30 % isolated yield (as described in previous section) and reacted with dabigatran-NH2 (4 mg, 6.7 μmol) dissolved in acetonitrile (500 μL) and triethylamine (4 μL) at 65 °C for 5 min. The reaction mixture was purified by HPLC using a C-18 semi-preparative column (Luna C-18, 250 × 10 mm, 5 µm - Phenomenex) and isocratic elution with 90:10 water (75 mM ammonium formate)/ethanol at 5 mL/min and a 254 nm UV detector. ¹⁸ F- dabigatran was synthesized in 8 ± 1.2% decay corrected radiochemical yield (2.3 ± 1.1 GBq, 0.06 ± 0.03 Ci, at room temperature (RT) for 32 min) and at > 98 % radiochemical purity. Purity was assessed via Radio-HPLC using a C-18 analytical column (Atlantis T3, 100Å, 250 x 4.6 mm, 5 µm - Waters, Milford, MA, USA, RT = 9.8 min). Summary: as expected, ¹⁹ F-DAB’s affinity for thrombin was less than the drugs argatroban and dabigatran (Fig.1G); however, it remained sufficient for use as a sensitive imaging agent. Serial blood sampling after intravenous ¹⁸ F-DAB injection into mice yielded a short blood half-life of 2.0±0.6 minutes, which is typical for small molecule imaging agents that are rapidly renally eliminated (Fig.1H). Such fast clearance is advantageous for imaging endocarditis vegetations, which are surrounded by blood. Bio-distribution studies of ¹⁸ F-DAB in mice documented low uptake in the normal heart and vasculature (Fig.1I). Example 2 - DAB-VT680XL binds to endocarditic vegetations After establishing the chemical and kinetic properties of the two dabigatran- based imaging agents, we next investigated the in vivo binding of DAB-VT680XL to arterial thrombi. We induced thrombosis in the femoral artery of mice by placing a ferric chloride-soaked filter paper on the exposed artery. Using intravital microscopy and platelet visualization by injecting a fluorescently labeled antibody binding CD41, we detected DAB-VT680XL in the thrombus (Fig.2A), whereas a control VT680XL compound (Gly-VT680XL) did not show any binding (Fig.2B). To test if DAB-VT680XL binds to vegetations, we induced S. aureus endocarditis in mice using a combination of suture insertion and intravenous injection of bacteria, as described previously, and injected 2 nmol of DAB-VT680XL 90 minutes prior to euthanasia. Vegetations and valve involvement were accessed by Gram staining (Fig.3, A and B). On an adjacent tissue section, DAB-VT680XL visualized the typically fibrin-rich wall that surrounds bacterial vegetation (Fig.3, C to G). Co-staining for CD11b ⁺ innate immune cells indicates that the DAB- VT680XL-positive vegetation barrier shields bacteria from the host immune response, as myeloid cells assembled in the vascular wall in front of this barrier but were unable to cross it into the bacterial colony (Fig.3, D and G). Example 3 - Noninvasively imaging S. aureus endocarditis in mice Due to light waves’ poor penetration depth in tissue, optical imaging is unsuitable for imaging deep tissues. Companion fluorescent and PET imaging agents were therefore developed and deployed for fluorescence molecular (DAB-VT680XL, Fig.4, A to E) and positron emission tomography ( ¹⁸ F-DAB, Fig.4, F to J), respectively. Fluorescence molecular tomography/ X-ray computed tomography (FMT/CT) data demonstrated high DAB-VT680XL concentration in the aortic roots of mice with endocarditis (Fig.4, A and B), while some signal was also observed in more distal vasculature along the suture inserted to induce endocarditis, likely due to bacteria colonizing the foreign material. Ex vivo fluorescence imaging of the excised aorta co-localized DAB-VT680XL signal with bioluminescent signal from Xen29 S. aureus (Fig.4C). In sham-operated control mice that were also injected with DAB- VT680XL, fluorescent background was much lower than in mice with endocarditis (Fig.4D), while bioluminescence signal was absent (Fig.4E). A blocking experiment with 100-fold excess intravenous injection of dabigatran preceding injection of the imaging probe DAB-VT680XL confirmed specificity of binding (fig.8). No DAB- VT680XL enrichment was observed in FMT/CT imaging of mice with myocardial infarction, a setting of sterile inflammation (fig.9). If endocarditis was induced with S. epidermidis Xen43, the FMT/CT signal obtained from lesions was lower than with S. aureus Xen29 (fig.10). PET/CT imaging after ¹⁸ F-DAB injection indicated binding of the PET isotope-labeled imaging agent to endocarditis vegetations (Fig.4, F and G). Ex vivo scintillation counting of aortas confirmed high ¹⁸ F-DAB uptake (Fig.4H), which co-localized on autoradiography with bacteria-derived bioluminescent signal (Fig.4, I and J). To explore the utility of this imaging approach in other sites of infection, mice was imaged that developed renal S. aureus lesions. Twenty-four hours after injection, DAB-VT680XL accumulation as observed in infected kidneys (fig.11). Example 4 - S. aureus endocarditis in piglets Ideally, molecular imaging probes that show satisfactory performance in mice are next tested in a large animal model. This step enables testing the approach using clinical imaging equipment. Perhaps even more importantly, host defense processes differ considerably between mice and large animals or humans. We employed two piglet models of acute S. aureus endocarditis: one affecting the tricuspid and the other the aortic valve. To mimic the typical pathogenesis of right heart endocarditis in patients, we subcutaneously implanted a vascular port into newly weaned piglets, inserting the central line into the right external jugular vein. The central line was then advanced via the superior vena cava into the right ventricle under fluoroscopy guidance. Six hours after implantation, 4-8×10 ⁸ colony forming units (CFU) bioluminescent S. aureus were injected into the port. Over the course of 10 days, piglets developed typical clinical signs of endocarditis, including fever (103.5-106.5 °F) and heart murmurs. Bacteria presence on the porcine tricuspid valve was verified by hematoxylin and eosin staining (Fig.5A) and staphylococcal cells were identified by Gram staining (Fig.5B). This S. aureus endocarditis piglet model was subsequently characterized by clinical cardiac MRI on a 3 Tesla human scanner. The development of two to four differently sized tricuspid endocarditis lesions were observed in the right ventricles of piglets on days 10-11 after bacterial injection (Fig.5C). Autopsy confirmed endocarditis vegetations, the morphology of which were reminiscent of those typically found in patients (Fig.5D). Further, administering fluorescent DAB- VT680XL into the piglets’ ear veins allowed visualization of endocarditis vegetations, as the probe’s fluorescent signal co-localized with bacterial bioluminescence (Fig.5, E to H). For induction of left-sided endocarditis, the aortic valve was damaged with a cytology brush after gaining vascular access via the carotid artery, followed by intravenous injection of 5-8×10 ⁸ CFU bioluminescent S. aureus. Piglets with left- sided endocarditis deteriorated clinically faster than piglets with right-sided endocarditis. They were imaged on day 7 after disease induction. Cardiac MRI revealed development of aortic valve lesions (Fig.5, I and J). Volumetric assessment of piglet hearts with right- and left-sided endocarditis indicated that the right ventricular ejection fraction was lower in piglets with tricuspid disease (Fig.5K). Ex vivo bioluminescence signal co-localized with lesions on autopsy, which enriched DAB-VT680XL after intravenous injection (Fig.5, L to P). Encouraged by the PET data obtained in mice and optical DAB-VT680XL signal in piglets with endocarditis, a proof-of-concept PET/MR imaging study was initiated, a step typically taken if a molecular imaging probe performs as desired in small animals. To that aim, an integrated PET/MR cardiac imaging protocol was developed on a clinical scanner to simultaneously acquire high-resolution morphological information and radiotracer distribution in piglet hearts. The PET imaging probe ¹⁸ F-DAB was injected into three piglets with left- or right-sided endocarditis, respectively. PET/MRI revealed focal enrichment of the PET imaging agent in the aortic (Fig.6, A and B) and tricuspid valves (Fig.6, C and D). Autoradiographic ¹⁸ F-DAB signal co-localized with bacterial bioluminescence arising from vegetations (Fig.6, E to G). Taken together, these data indicate that combining molecular PET imaging with cardiac MRI's soft tissue contrast, anatomic detail and functional capabilities may provide complementary diagnostic information to monitor and manage endocarditis. The fluorescence in aortic versus tricuspid vegetations of piglets injected with DAB-VT680XL were further compared. We found that the target-to-background ratio was higher in aortic valve vegetations when compared to tricuspid disease (fig.12A), which was matched by the higher bioluminescence signal in aortic lesions (fig.12B). This difference in imaging signal may relate to bacterial load, supported by a positive correlation between bacterial bioluminescence signal and DAB-VT680XL binding across vegetations examined in both valves (fig.12C). These differences may have been caused by the faster clinical disease progression and the earlier imaging time point in piglets with left-sided endocarditis. E ^{xample 5 - Antibody immunotherapy disrupts vegetation anatomy and} improves mouse survival Staphylocoagulase (SC) and von Willebrand factor-binding protein (vWBp) are virulence factors that S. aureus employs to activate the clotting cascade. The resulting fibrin wall protects bacterial colonies from the host’s immune system. It was thus hypothesized that combined antibody-mediated inhibition of these two factors would disrupt S. aureus’ ability to form fortified vegetations. Monoclonal antibodies raised against NH2-terminal peptides of SC (GMA-2105) and vWBp (GMA-2150), which were engineered in mice, were tested for specificity by immunoblotting. The western blot data indicate excellent specificity and no cross-reactivity of the GMA- 2105 antibody with vWBp or cross-reactivity of GMA-2510 with SC (Fig.7, A to C). Clotting assays demonstrated that targeted antibodies reduce fibrinogen conversion to fibrin in a concentration-dependent manner for both anti-SC and anti-vWBp therapies (Fig.7, D and E). Treating mice with these monoclonal antibodies led to reduced DAB-VT680XL signal in FMT/CT imaging (Fig.7, F and G), thereby indicating that therapeutically inhibiting SC and vWBp reduces active thrombin in bacterial colonies. Injecting neutralizing antibodies improved the survival of mice with endocarditis (Fig.7H). To explore how this treatment acts mechanistically, vegetations were imaged using DAB-VT680XL and intravital microscopy. The heart valves in living mice are difficult to approach with a microscope objective. S. aureus vegetations were established in the femoral artery by inserting a suture and then intravenously injecting S. aureus expressing red fluorescent protein (RFP). This formed femoral artery vegetations that were comparable to the anatomy observed in the aortic valves of mice (Fig.7, I and J). Specifically, a central RFP ⁺ bacterial colony surrounded by DAB- VT680XL signal were observed, highlighting a thrombin-rich layer (Fig.7J). Staining neutrophils with intravenously injected fluorescent antibody targeting Ly6g indicated that neutrophils were unable to penetrate the capsule around RFP ⁺ bacteria. Treatment with antibodies neutralizing SC and vWBp disrupted the DAB-VT680XL-stained capsule around RFP ⁺ bacteria, thereby granting neutrophils access to invade the S. aureus colony (Fig.7I). Discussion of Examples 1-5 PET is the most sensitive and translatable molecular imaging modality, as demonstrated by its clinical track record. The limitations of PET imaging include relatively low spatial resolution and high costs. Co-developing a fluorescent agent with the same affinity ligand provides cellular resolution data for molecular targets imaged by PET. In conjunction with fluorescence molecular tomography, a quantitative imaging method available for non-invasive mouse studies, DAB-VT680XL compound of the present examples proved useful in a preclinical neutralizing antibody trial in mice. A lower imaging signal in endocarditis vegetations echoed therapy-induced survival benefits, suggesting this imaging biomarker may predict survival. In a clinical scenario, PET imaging with ¹⁸ F-DAB would track therapeutic efficiency in a trial of candidate drugs similar to the SC- and vWBp-neutralizing antibodies that we tested in mice. PET imaging with ¹⁸ F-DAB would identify patients in need of therapy or monitor therapeutic effects. The PET/MRI data in piglets with endocarditis indicate that combining molecular PET with MRI is particularly informative, as MRI provides outstanding soft tissue contrast and sufficient temporal and spatial information to visualize S. aureus vegetations. Given its capacity for bedside use, facile Doppler assessment of valve function and lower cost, echocardiography will remain a mainstay for serially monitoring acute endocarditis. However, molecular PET/MRI, using either ¹⁸ F-DAB or other radioactive probes previously reported by others, has the potential to improve antibiotic selection and guide timing and extent of surgical interventions during key disease stages. In contrast to other endocarditis imaging agents, ¹⁸ F-DAB and DAB- VT680XL of the present disclosure do not directly bind bacteria but rather report on S. aureus’ interaction with the host’s clotting system, which contributes to biofilm formation. This fibrin-rich wall protects the bacterial colony against host immunity and — in combination with exopolysaccharides, extracellular DNA and other factors — hinders penetration of antibiotics. Our data indicate that ¹⁸ F-DAB and DAB- VT680XL avidly bind to this critical vegetation component. Using DAB-VT680XL in intravital microscopy visualized innate immune cells’ inability to penetrate the wall, swarm into the vegetation and kill S. aureus. Treatment with antibodies against SC and vWBp decreased DAB-VT680XL uptake, and myeloid cells were able to enter the vegetations. Prior work has demonstrated a similar trend for dabigatran therapy in vitro; however, our microscopy data provide in vivo evidence of such host-pathogen interactions. In addition to helping test therapeutics and imaging approaches in a human- like setting, the piglet model could be useful for research on surgical management, a potentially life-saving treatment still in need of optimization and standardization. As pig hearts are similar to humans’ in size and anatomy, experiments in pigs with endocarditis could address questions such as when and how to best replace an infected valve or remove a vegetation and explore minimally invasive, catheter-based strategies. S. aureus’s co-evolution with the human immune system endowed the bacteria with several efficient countermeasures against host defenses. These include bacterial factors that kill cells, inhibit the complement system, impede neutrophil and macrophage migration, evade phagocytosis and facilitate bacterial survival after phagocytosis. Some virulence factors promote colonization of indwelling catheters by generating a biofilm. Typically, S. aureus endocarditis vegetations activate the host’s clotting system to anchor the colony and surround it with a protective fibrin mesh. Upstream interventions that curtail bacterial virulence rather than host clotting factors could ultimately be a safer alternative. Indeed, decreased thrombin was detected in mouse endocarditis vegetations after treatment with antibodies that neutralize SC and vWBp. In line with studies using knock-out bacteria, vegetations still evolved and mice succumbed eventually; nevertheless, antibody treatment prolonged survival while DAB-VT680XL signal decreased in the lesions and innate immune cells invaded bacterial colonies. OTHER EMBODIMENTS It is to be understood that while the present application has been described in conjunction with the detailed description thereof, the foregoing description is intended to illustrate and not limit the scope of the present application, which is defined by the scope of the appended claims. Other aspects, advantages, and modifications are within the scope of the following claims.