Interpretation of the Findings
Table 16.1 is an incomplete listing of conditions causing sudden death. A more complete list can be found in the internet resource Consultant (White 2021). Approximately 160 conditions are listed and described, many of them toxicoses.
If the carcass is emaciated, refer first to the chapter on wasting diseases. Death may have been sudden, but a long-term problem often exists as the cause of death or predisposition to some terminal accident or infection.Most of these conditions are discussed elsewhere in this book and will not be repeated here. The situation of the kid found dead shortly after delivery deserves special comment. It is important to determine whether the kid was born alive and whether it breathed; if so, its lung tissue is inflated and floats. If the kid was stillborn, more consideration should be given to the long list of diseases causing abortion. It is critical to know whether the kid ever nursed (milk in the abomasum), as opposed to being too weak at birth to get up and nurse (because of in utero infection, swayback, congenital defects, prematurity, or nutritional muscular dystrophy), or having a dam with malnutrition, udder problems, or poor maternal behavior so that no milk could be obtained. Death from exposure is more common if the abomasum is empty, whereas other explanations should be sought if the kid has a full stomach. One should also evaluate body fat deposits on the pericardial sac and around the kidneys. These fat stores are normally light tan and extensive at birth, but quickly become dark red and reduced in volume with starvation. An ileal impression smear is helpful in diagnosing the cause of death of kids that lived long enough to die of enterotoxigenic Escherichia coli (packets of Gram-negative rods in microcolonies) or clostridial enterotoxemia (many large Gram-positive rods).
A complete necropsy can provide other information of use in the management of the herd, even if it does not directly pertain to the sudden death of the goat at hand.
A record of whether a doe is pregnant and the number of fetuses in the uterus is important for the differential diagnosis of pregnancy toxemia, but it is also needed for monitoring the reproductive efficiency of the herd. Joint diseases are not expected to cause sudden death, but necropsy is an
| Diagnosis | Comments |
All ages
| Trauma, including predation | Subcutaneous hemorrhage, broken bones, ruptured internal viscus. If the eyes are absent, postmortem damage to the carcass by birds is likely |
| Exposure Lightning strike, electrical shock Snake bite | Cold stress caused by exposure to rain and wind after shearing Subcutaneous hemorrhage, singe marks, often no lesions Fang marks in localized edematous swelling |
| Anesthesia overdose, idiosyncratic reaction Anaphylaxis | Verify dose actually given Death immediately after administration of penicillin, tetanus antitoxin, autogenous bacterins |
| Anthrax | bgcolor=white>Petechiae and ecchymoses throughout, large hemorrhagic lymph nodes. Bloody discharges from orifices or a greatly enlarged pulpy spleen, although common, are not always present|
| Clostridial wound infections | Crepitant (Clostridium chauvoei) or edematous (Clostridium septicum) tissues with odor of rancid butter (King et al. 2005); confirm by culture or fluorescent antibody |
| Enterotoxemia | Fluid and fibrin in pericardial sac, glucosuria; kidneys rot quickly; fresh ileal impression smear shows many Gram-positive rods |
| Polioencephalomalacia | Fluorescence of cerebral cortex under Wood's lamp suggestive, but may be absent if acute course |
| Encephalitis or meningitis | Impression smear of meninges if cloudy, to look for neutrophils or bacteria; evaluation and culture of cerebrospinal fluid |
| Tetanus | Limbs extended; diagnosis probably not possible if no clinical signs observed; history may include recent dehorning, dystocia, or other wound for entry of the organism |
| Pseudorabies | Fluorescent antibody test on liver and brain stem, viral isolation; history of exposure to pigs or syringe contaminated with live virus vaccine |
| Poisonous plants (see Table 19.7) | Examine rumen contents carefully; venous blood bright red with cyanide, dark with nitrates |
| Chemical poisoning, including insecticides and anthelmintics | Check history, package label |
| Rumensin toxicosis | Histologic myocardial damage; may not be visible grossly in acute case; access to improperly mixed feeds or cattle pellets |
| Urea toxicosis | Rumen pH >7.5; access to improperly mixed feeds, deicing products, or fertilizer |
| Rumen acidosis | Rumen fluid milky, pH otherwise suggestive of enterotoxemia. • Tracheal froth - agonal. May be significant if signs of pulmonary edema also present. • Endocardial, myocardial, epicardial hemorrhages - agonal. • Rumen mucosal sloughing - often an early autolytic change. • Postmortem abomasal rupture - along greater curvature, but lacks fibrin or hemorrhage. • Tiger striping in large intestine - terminal tenesmus. • Pseudomelanosis - blackening of tissues, especially adjacent to autolytic intestine. • Melanosis - normal black pigment in various organs.
Source:
Smith Mary C., Sherman David M.. Goat Medicine. 3rd edition. — Wiley-Blackwell,2023. — 976 p.. 2023
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