Ventral opisthostoma tear with exsanguination in a Brazilian salmon pink bird-eating tarantula (Lasiodora parahybana)

Sara Pagliarani, Heindrich Snyman

Department of Pathobiology, University of Guelph, Guelph, ON (Pagliarani), Animal Health Laboratory, University of Guelph, Guelph, ON (Snyman)

AHL Newsletter 2022;26(4):17.

An approximately 9-year-old Brazilian salmon pink bird-eating tarantula (Lasiodora parahybana) was noted to be having a difficult molt with leakage of hemolymph from the ventrum.  The animal was found moribund the following day, and was administered isofluorane and phenobarbital for euthanasia before being placed whole in formalin (Figs, 1, 2).

Histologically, there was a single ~ 5.0-6.0 mm wide full thickness defect within the integument along the ventral midline.  The exo- and endo-cuticle along the remaining edges of the integumentary defect were partially separated from each other and elevated from the underlying stroma, with irregular fragmentation and tattering of the edges.  The defect contained small amounts of fine granular to homogenous eosinophilic fluid with enmeshed fragmented yellow-brown plant substrate material (Fig. 3).  Moderate numbers of admixed hemocytes were also present, with hemocytes also extending along the lateral margins along the sub-epidermal connective tissue (Fig. 4).  No obvious bacteria were detected in the sections.

As was observed during clinical examination, this spider contained a regional integumentary defect along the ventral opisthosoma/abdomen.  These defects are considered one of the most common causes of captive spider mortality.  Gross lesions associated with this finding are usually those of epidermal discoloration, abrasion, and loss of surface structures to exoskeletal fractures.  While the cephalothorax and the limbs are considered solid and resilient structures, the opisthosoma, due to the absence of the more rigid chitinous exocuticle layer, is far more easily breached.  Any damage to the endo-cuticle, epidermis, or exoskeleton can result in loss of osmoregulatory capacity, hemolymph loss and shock (exsanguination), in addition to opportunistic infections and in many cases, death of the spider.

Whereas major injuries are usually detected promptly, small injuries may not be, and exsanguination then often goes unnoticed as the cause of deterioration and/or death.  While wounds over the dorsal opisthosoma are likely to cause more rapid hemolymph loss from the heart and surrounding pericardial sac, wounds at the base of appendages and the ventral opisthosoma seem to lose hemolymph slower and a spider may take several days to gradually exsanguinate, with little to no premonitory clinical signs.

Larger ruptures, such as in the current case, are easier to identify; however, quantification of fluid loss can still be difficult to estimate, especially considering that enclosure substrate will readily and rapidly absorb the relatively clear leaked fluid.  The defect in the current case contained proteinaceous fluid and hemocytes which probably suggests that this rupture/tear occurred before death.  Although foreign plant material (probably enclosure substrate) was embedded within the fluid, and there appeared to be some degree of hemocyte host inflammatory response, there was no obvious bacterial component.  Therefore, the deterioration and death of this spider was probably the result of hydrodynamic/hydrostatic derangement rather than secondary bacteremia and sepsis.  In most invertebrates, the first step towards wound healing is the formation of a hemolymph clot which rapidly prevents further hemolymph loss and entraps microbial pathogens before they can colonize other adjacent organs.

It is unclear whether or not the current case was the result of trauma during the actual shedding process or any other possible concurrent traumatic event (e.g. a fall).  There were no obvious accompanying degenerative or inflammatory changes described in the histologic sections; therefore this finding is considered to be an incidental event.   AHL

Figure 1. Full body, ventral view, Brazilian salmon pink bird-eating tarantula. Figure 2. Full body, dorsal view, Brazilian salmon pink bird-eating tarantula. Figure 3. Ventral opisthosoma, Brazilian salmon pink bird-eating tarantula. The opisthosoma contains a focal region of defect with eosinophilic material and embedded plant substrate fragments (*). H&E. Figure 4. Ventral opisthosoma, Brazilian salmon pink bird-eating tarantula. Hemocytes are also present within the opisthosomal defect (*), and extend along the lateral margins of the sub-epidermal connective tissue. H&E.

Figure 1. Full body, ventral view, Brazilian salmon pink bird-eating tarantula.
Figure 2. Full body, dorsal view, Brazilian salmon pink bird-eating tarantula.
Figure 3. Ventral opisthosoma, Brazilian salmon pink bird-eating tarantula. The opisthosoma contains a focal region of defect with eosinophilic material and embedded plant substrate fragments (*). H&E.
Figure 4. Ventral opisthosoma, Brazilian salmon pink bird-eating tarantula. Hemocytes are also present within the opisthosomal defect (*), and extend along the lateral margins of the sub-epidermal connective tissue. H&E.

References
1. Frey FL. Scorpions. In: Invertebrate Medicine. 2nd ed. Lewbart J, ed. Willey-Blackwell, 2012:223-234.
2. Newton AL, Smolowitz, R. Invertebrates. In: Pathology of Wildlife and Zoo Animals. Terio K, McAloose D, St. Leger J, eds. Academic Press, 2018:1019-1052.