search.noResults

search.searching

note.createNoteMessage

search.noResults

search.searching

orderForm.title

orderForm.productCode
orderForm.description
orderForm.quantity
orderForm.itemPrice
orderForm.price
orderForm.totalPrice
orderForm.deliveryDetails.billingAddress
orderForm.deliveryDetails.deliveryAddress
orderForm.noItems
Zonneveld et al.—Bored turtle shell


ectoparasites (Ryan and Lambert, 2005; McCoy et al., 2007; Readel et al., 2008). Seasonality plays a strong role in the presence of leeches on aerial baskers in temperate settings wherein the turtles may spend more time out of, and away from, water during warmer months (Koffler et al., 1978). Although leeches need only a single blood meal per year to survive, they require more for growth and reproduction (Sawyer, 1986). Concomitantly leeches will commonly remain attached to individual turtles for long intervals (i.e., through multiple feedings) and will commonly remain attached to an individual hibernating turtle throughout the winter (Graham et al., 1997). Although leeches most commonly occur on the soft


integument of the areas around the head and neck (Esch and Gibbons, 1967; McAucliffe, 1977; MacCulloch, 1981), in some populations leeches may be common on the carapace and plastron (Hulse, 1976; Brooks et al., 1990; Siddall and Gaffney, 2004; Bielecki et al., 2012). The leeches feed on blood sinuses within bones of the plastron and carapace with attachment sites most commonly occurring at, although not excluded to, the sulci between epidermal scutes (Siddall and Gaffney, 2004). This feeding activity was interpreted as a possible explanation for the pitting observed on some fossil turtles by Hutchison and Frye (2001). Siddall and Gaffney (2004) argued that the complex salivary secretions of the leech Placobdella ornata is capable of bone decalcification and digestion of connective tissue matrix although this has not be demonstrated in the laboratory and pits attributable to leeches have not been illustrated. Freshwater turtles are also prone to numerous


internal parasites including flukes (Martin, 1972; Flynn, 1973). Although most are non-pathogenic, spirorchid liver flukes cause a variety of ailments including ulcerative lesions on the carapace (Johnson et al., 1998). Spirorchid liver flukes occur in a large proportion of wild aquatic turtle populations in North America (Flynn, 1973); however, pitted ulcerations in the shell have been reported by only a few authors (Flynn, 1973; Johnson et al., 1998; Johnson, 2004). These shell imperfections are noted primarily in veterinary journals (Johnson et al., 1998; Johnson, 2004). Because the parasitic infection, if treated, does not result in death, shell damage caused by spirorchid liver flukes has not been illustrated.


Shell disease in terrestrial and aquatic turtles.—Freshwater turtles may be affected by a variety of shell-degrading bacterial infections including NSD (necrotizing scute disease), USD (ulcerative shell disease), and SCUD (septicemic cutaneous ulcerative disease). NSD is primarily a disease of the epidermal lamellae (i.e., scutes) but may also affect the underlying dermal bone (Rose et al., 2001). NSD is caused by a fungal infection (identified as Fusarium semitectum) and is only active while the host animal is alive suggesting that the fungus utilizes some substance other than the keratin (Rose et al., 2001). This disease has been reported primarily in terrestrial turtles and tortoises and appears to have only a surficial effect on the dermal bone (Jacobson et al., 2000; Rose et al., 2001). USD is a chronic condition in many wild populations and is


considered endemic in areas where environmental conditions have become degraded, either through anthropogenic or natural means (Wallach, 1975; Johnson, 2004; Bishop et al., 2007). USD has been attributed to the bacterium Baneckea chitinovora


817


(Wallach, 1975; Johnson, 2004). Pitting and erosion of turtle shell are a common effect of USD, allowing invasion of other bacteria as well as macroparasites such as trematodes (Lovich et al., 1996, Garner et al., 1997; Johnson, 2004). SCUD, also known as ‘shell rot’ is a common form that can


result in extensive degradation of the carapace and plastron (Kaplan, 1957). SCUD is caused by the bacterium Citrobacter freundii, which occurs naturally in soil and water (Raphael, 2003). Turtles become infected through skin abrasions and exposure (Raphael, 2003; Johnson, 2004). Pitting and extensive erosion of the shell are common effects ofSCUD in free-ranging turtle populations (Raphael, 2003; Johnson, 2004). SCUD commonly results in the death of the host organism. Although both USD and SCUD result in pitting and erosion of the dermal bone of both the plastron and carapace, SCUD degradation is commonly more extensive and more typically results in the death of the turtle (Johnson, 2004). All three of these diseases, but particularly USD and


SCUD, can result in extensive shell damage to freshwater turtles. However, the amorphous, typically extensive, etching and bone dissolution that characterize these diseases differs significantly from the discrete holes and pits that characterize the South Pass material.


Macroparasites in modern terrestrial turtles.—Neotropical ter- restrial turtles play host to a variety of parasites, primarily ixodid arachnids (i.e., ticks) (Ernst and Ernst, 1977). Although in many cases ticks occur on soft tissue in the area around the limbs and head, ticks are also common on the carapace and plastron (Fair- child, 1943; Ernst and Ernst, 1977). A behavior and ecological study of the brown wood turtle (Rhinoclemys annulata) on Barro Colorado Island in Panama revealed that all specimens analyzed possessed ticks (Mittermeier, 1971). An investigation of five species of the emydid genus Callopsis from Central and South America revealed similar levels of tick infestation (Ernst and Ernst, 1977). In the Callopsis study, it was noted that the ticks (four species of genus Ambylomma) preferentially attached to the shell (78.5%) as opposed to the skin (Ernst and Ernst, 1977). Although most of the ticks attached to the carapace, some were also observed attached to the plastron (Ernst and Ernst, 1977). The ticks on the shell occurmost commonly, although not exclusively, at epidermal scute boundaries (Ernst and Ernst, 1977). Most notably, in both Callopsis and Rhinoclemys, ticks


occupy pits within the carapace and plastron (Schmidt, 1946; Mittermeier, 1971; Ernst and Ernst, 1977). These pits are roughly circular, up to 6mm in diameter and up to 4mm deep (Mittermeier, 1971; Ernst and Ernst, 1977). It is unknown how the ticks bore through the epidermal scute and into the dermal bone of the carapace and plastron; however, it is thought that this is accomplished using either a histolytic secretion or through the activity of a microorganism that attacks the shell at the site of the attachment wound (Mittermeier, 1971; Ernst and Ernst, 1977). We believe that the former hypothesis is most likely since the pits do not expand significantly beyond the size of the tick and, when removed from the pits, a milk white fluid was observed in the holes (Mittermeier, 1971). To date, we are unaware of any confirmed reports of


tick-generated pits or holes in temperate taxa; however, similar pits have been observed on the carapace of North American box


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76  |  Page 77  |  Page 78  |  Page 79  |  Page 80  |  Page 81  |  Page 82  |  Page 83  |  Page 84  |  Page 85  |  Page 86  |  Page 87  |  Page 88  |  Page 89  |  Page 90  |  Page 91  |  Page 92  |  Page 93  |  Page 94  |  Page 95  |  Page 96  |  Page 97  |  Page 98  |  Page 99  |  Page 100  |  Page 101  |  Page 102  |  Page 103  |  Page 104  |  Page 105  |  Page 106  |  Page 107  |  Page 108  |  Page 109  |  Page 110  |  Page 111  |  Page 112  |  Page 113  |  Page 114  |  Page 115  |  Page 116  |  Page 117  |  Page 118  |  Page 119  |  Page 120  |  Page 121  |  Page 122  |  Page 123  |  Page 124  |  Page 125  |  Page 126  |  Page 127  |  Page 128  |  Page 129  |  Page 130  |  Page 131  |  Page 132  |  Page 133  |  Page 134  |  Page 135  |  Page 136  |  Page 137  |  Page 138  |  Page 139  |  Page 140  |  Page 141  |  Page 142  |  Page 143  |  Page 144  |  Page 145  |  Page 146  |  Page 147  |  Page 148  |  Page 149  |  Page 150  |  Page 151  |  Page 152  |  Page 153  |  Page 154  |  Page 155  |  Page 156  |  Page 157  |  Page 158  |  Page 159  |  Page 160  |  Page 161  |  Page 162  |  Page 163  |  Page 164  |  Page 165  |  Page 166  |  Page 167  |  Page 168  |  Page 169  |  Page 170  |  Page 171  |  Page 172  |  Page 173  |  Page 174  |  Page 175  |  Page 176  |  Page 177  |  Page 178  |  Page 179  |  Page 180  |  Page 181  |  Page 182  |  Page 183  |  Page 184  |  Page 185  |  Page 186  |  Page 187  |  Page 188  |  Page 189  |  Page 190  |  Page 191  |  Page 192  |  Page 193  |  Page 194  |  Page 195  |  Page 196  |  Page 197  |  Page 198  |  Page 199  |  Page 200  |  Page 201  |  Page 202  |  Page 203  |  Page 204  |  Page 205  |  Page 206  |  Page 207  |  Page 208  |  Page 209  |  Page 210  |  Page 211  |  Page 212