Reports in ancient amphibians are limited to congenital (homeobox) phenomenon and isolated fractures. Other pathologies are rarely observed but have not been sufficiently described and analyzed for etiology to be confidently recognized.

Midline skull ossifications or atypical sutures (Table 1) were reported among nasals, frontals, parietals, and postparietals in 4–12% (Gubin and Novikov, 1999). The pineal foramen was absent in Thoosuchus yakovlevi. Frontals were laterally expanded in Thoosuchus yakovlevi and included in orbit borders in Platyoposaurus watsoni, Konzhukovia vetusta, Benthosuchus korobkovi, and Melosaurus platyrhinus.

Reported post-cranial anomalies among extinct amphibians have been limited to the axial skeleton. Sacral anomaly and fusion with adjacent vertebrae or urostyle (Figs. 3 and 4) were noted in Holocene frogs (Böhme 1982) and unilateral sacral wing enlargement, in Palaeobatrachus luedeckei and diluvianus (Špinar 1972). Witzmann (2007) reported a Middle Triassic temnospondyl with a hemivertebrae, restricted dorsal aspect of second pleurocentrum and larger alternate side intercentrum.

Reported femoral and tibial fractures affected Holocene Rana sp. and Bufo cf. bufo (Ippen and Heinrich 1977). The latter were infected (Fig. 5). Fractured, bowed fibulare was fused to tibiale in Palaeobatrachus (Špinar 1972). An exostosis which would have hosted a cartilaginous cap (osteochondroma) in a fossil frog is illustrated in Fig. 7.

Fractures of the lower jaw, rib, and leg are described in lizards and crocodiles (Figs. 8 and 9); vertebrae and ribs, of snakes (Abel 1935; Anthony and Serra 1951; Dämmrich 1985; Isenbügel and Frank 1985; Reichenbach-Klinke 1963; Rothschild 2008; Schlumberger 1958). Focal elevation of periosteum (Figs. 10–14) identifies hematoma secondary to trauma.

Bicephalism is the most commonly reported congenital pathology in snakes and has occasionally been noted in lizards (Acharji 1945; Amaral 1927; Cunningham 1937; Matz 1989; Payen 1991; Wallach 2004). Their congenital origin contrasts with tail duplications, which appear to be post-traumatic events (Blair 1960). Isolated reports of conjoined twins include the slow worm (Anguis fragilis), sand lizard (Lacerta agilis), and blue-tongued skink (Tiliqua scincoides) (Barten 1996; Bellairs 1965; Frye 1991; Hildebrand 1938). Other congenital anomalies (Figs. 11, 15–17) (Table 2) are usually reported as isolated phenomenon (Kälin 1937), but some (e.g., polymely, ectomely, and ectodactyly) have been attributed to environmental factors (Johnson et al. 2003; Ouellet et al. 1997; Rostand 1951, 1960).

Vertebral osteomyelitis is the most common infection in snakes (Ippen 1965; Isaza et al. 2000). Multifocal granulomatous spondylitis was noted in the hybrid Crotalus mitchellii/willardi (Frye and Kiel 1985). Infection, although less common, is often multifocal (Figs. 18–28) in other reptiles (e.g., Alligator mississippiensis, Caiman latirostris, and Crocodylus siamensis) (Brown 1971). Other isolated reports include an infected shoulder in Alligator mississippiensis (Frye 1991) and Erysipelothrix in Crocodylus acutus (Jacobson 2007).

Osteoarthritis is essentially, a disease of captivity (Fig. 29), and extremely rare in the wild (Frye 1991). Metabolic disease (Table 3) in reptiles presents as articular gout, pseudogout (calcium pyrophosphate deposition disease), and metabolic bone disease (Figs. 30 and 31). The latter, essentially limited to captive reptiles (Frye 1991), presents as pathologic fractures and folding fractures (Barten 1996; Frye 1973). Calcific overgrowths, noted in boa constrictors, rattlesnakes, a Burmese python (Python molurus bivittatus) (Frye 1991), and in a varanid (Figs. 32–39), are of unclear diagnosis. While they consist of wormian bone, the diagnosis of osteitis deformans or Paget’s disease has been discarded (Jacobson 2007).

Examination of a number of reports of exostoses in Iguana iguana (Chiodini and Nielsen 1983) or Paget’s disease in a boa constrictor, Bitis nasicornis, Crotalus, and southern copperheads (Isenbügel and Frank 1985) has revealed a new diagnosis of the inflammatory arthritis of the spondyloarthropathy variety (Rothschild 2009) and infection. Diffuse periosteal reaction may represent infection or hypertrophic osteoarthropathy (Figs. 40 and 41). A form of inflammatory arthritis associated with vertebral fusion and peripheral and axial joint erosions with reactive new bone and joint fusion (Figs. 42–53) has been documented in 2–20% of Varanus, dependent upon species (Rothschild 2009), representing the disease category termed spondyloarthropathy. A crystal arthritis, related to deposition of ­calcium, has been noted in varanids (Figs. 54–61) (Rothschild 2010).

Neoplasia has been directly observed in the form of benign growths such as enchondroma, osteoma (Fig. 63), osteochondroma (Figs. 9, 63–65), and chondro-osteofibromas and malignant growths (Fig. 66), as well as indirectly identified because of their induction of hypertrophic osteoarthropathy (Figs. 41 and 67) (Table 4).

Congenital anomalies are rarely reported. Witzmann (2007) reported a congenital hemivertebra was observed in a Jurassic Cimoliasaurus plicatus (Witzmann 2007), and Hopley (2001) reported Schmorl’s nodes (vertebral endplate holes) in a plesiosaur. MacGregor (1906) noted that the odontoid is fused with axis centrum in Phytosauria. Tooth malposition is present in Pseudosuchia (Fig. 68).

Injuries have been reported predominately as isolated observations. These include fractures and exostoses (Figs. 69–71). The latter are found especially on lower jaws, vertebrae (especially caudal), and paddles (especially digits). Williston (1898) reported distal caudal vertebral fractures with pseudoarthroses. The exception is Sawyer and Erickson’s 1998 study of Leidyosuchus formidabilis, which documented gastralia as the most common fracture site.

Decompression syndrome (bends) is universally recognized on the basis of linear patterns of bone loss or articular surface subsidence (Fig. 72) in Platecarpus, Tylosaurus, Mosasaurus, Plioplate­carpus, Prognathodon, Hainosaurus and in an Antarctic mosasaur, and invariably absent from Clidastes, Ectenosaurus, Globidens, Halisaurus, and Kolposaurus (Rothschild and Martin 1987, 2006). With the exception of the large percentage of the skeleton afflicted in Platecarpus, the frequencies of vertebral involvement in the other affected genera were indistinguishable (p < 0.02). Among the basal portion of the family Sauropterygia, avascular necrosis was found in only a single genus, Neusticosaurus (Rothschild and Storrs 2003). It is seen in both early and late Plesiosauridae, Elasmosauridae. Large intergeneric variation in frequency was noted among ­ichthyosaurs (Montani and Rothschild, 1999). Ophthalmosaurus, Ichthyosaurus, Temnodonto­saurus, and Platypterygius equally affected; Leptonectes, less so (chi-square = 5.36, p < 0.025) (Montani and Rothschild 1999), while Stenop­terygius was spared.

Infections are noted, predominantly as isolated phenomenon (Fig. 27). Auer (1909) suggested that changes in a Metriorhynchus cf. moreli femur represented fungal infection.

The only report of osteoarthritis in a fossil reptile was in the wrist and metacarpal phalangeal joints of pterodactyloid pterosaurs (Bennett 2003). Spondyloarthropathy has been observed in Dimetrodon, Diadectes, and Ctenorhachis (Figs. 73–75).

Moodie’s 1918 diagnosis of an osteoma in a mosasaur has been reassessed as another form of benign tumor, a hamartoma. The latter is actually overgrowth of normal tissue and not truly a neoplasia. Sawey and Erickson (1998) are credited with the first report of an actual osteoma and also described a probable chondroma in Eocene Crocodylus sp.

Vertebral fusion is well recognized in the fossil record. While the pathology in some mosasaurs is clearly related to the trauma of shark bites (Moodie 1917), other mosasaurs have vertebral bridging more characteristic of spondyloarthropathy (Figs. 76 and 77), as has been noted in contemporary varanids (Rothschild 2009). Ruffer’s 1917 description and illustrations of a Lower Miocene crocodile Tomistoma dowsoni and those of Sawyer and Erickson (1998) of Leidyosuchus formidabilis clearly document spondyloarthropathy. Pales’ 1930 description of anulus fibrosus ossification in a Pleistocene Cuban saurian further documents the antiquity of the problem.

Pathology in turtles (Reprinted from Rothschild BM, Schultze H-P, Pellegrini R. in press. Osseous and articular pathologies in turtles and abnormalities of mineral deposition. In: Morphology and Evolution of Turtles, D Brinkman, J Gardner, P Holroyd (eds.). New York: Springer):

It is difficult at times to determine whether anomalies observed in the embryo or neonate are the result of genetic alterations or of exposure to adverse environmental conditions, or to distinguish anomalies that have been inherited versus those occurring secondary to a new mutation. One does not necessarily need to invoke an environmental toxin. Environmental conditions may be just as important, either as a direct or indirect effect. Lynn and Ullrich (1950) examined turtle embryos from eggs exposed to partial drying during gestation interval days 35–50. Embryo pathologies ranged from “almost unrecognizable carapaces and plastrons, distorted limbs, and eyeless or jawless heads.” Newman (1923) suggested temperature effect, whereas Coker (1910) considered this as an effect of egg distension. Packard et al. (1977) noted that prolonged exposure to temperatures several degrees below the optimum produced developmental abnormalities. Incubation of the California desert tortoise, Gopherus agassizii, above the optimum temperature of 32 °C was associated with upper jaw foreshortening and lack of forelimbs (Frye 1991c), whereas incubation at 33.5°C was associated with anophthalmy, maxillofacial clefts, harelips, forelimb and partial hind limb agenesis, coccygeal hypoplasia and scute and shell plate duplication (Frye 1989, 1991c). However, organochlorine compounds (e.g., PCBs) induce missing claws and eyes, deformed carapaces, tails, limbs and crania, deformed upper and lower jaws in snapping turtles (Bishop et al. 1989). Greatest incidence of deformities was noted in Cranberry Marsh. Frequency in Lake Ontario was greater than in Lake Erie or Algonquin Park, correlated with organochlorine levels.

Whereas most studies represent isolated reports of deformities (e.g., Tables 5–9), several report statistical results. Bellairs (1981) and Yntema (1960) reported that 15% of the common snapping turtle, Chelydra serpentina, had abnormal tail, hind limb, or carapace. Carswell and Lewis (2003) reported 0.32% abnormalities in 14,361 loggerhead Caretta caretta turtle eggs in 1992 and 2001, manifest as small size, carapace deformities, folded or forshortened flippers, misshapened mouthparts and twinning. The most complex of the congenital anomalies in turtles is perhaps the Siamese, conjoined or parasitic twin (Anonymous 2007a; Kuvano 1902; Maddux 1996; Nakamura 1938). Most have been reported as isolated phenomena (Table 5). A variety of duplication patterns have been observed: plastron to plastron, side to side, or posterior to posterior. Noting Hildebrand’s (1938) tally of 27 cases, Table 5 suggests the rarity of this phenomenon. Only 45 cases appear to have been reported to date, and no epidemiologic studies are available. Complete or partial absence of a limb has been reported in isolated occurrences (Table 6). Not all are congenital. Jackson (1980) noted one instance in which a foreleg was gnawed off during hibernation by a rat, and Frye (1994) reported digit necrosis in red-eared slider turtle, Trachemys scripta elegans.