In the present systematic review and meta-analysis, we evaluated the effects of providing piglets with creep feed during lactation on piglet pre- and post-weaning performance. A total of 20 articles met the inclusion criteria. Creep feeding in lactation improved pre-weaning piglet performance in 46% of the studies selected, while 58% of the included studies reported that creep feeding in lactation improved piglet performance during the nursery phase. Creep feeding increased the average piglet body weight (creep = 7.23 ± 0.30, no creep = 6.96 ± 0.31; p = 0.03) and litter weight (creep = 81.2 ± 4.18, no creep = 76.4 ± 4.22; p < 0.001) at weaning. The average piglet body weight and litter weight were positively associated (p < 0.001 and p < 0.001, respectively) with total creep feed intake. Creep feeding of piglets for more than 14 days increased (p = 0.003) the litter weight at weaning compared to litters not provided or provided for shorter periods with creep feed. The present work strengthened the notion that creep feeding during lactation presents opportunities for improving weaning weights and post-weaning piglet performance compared to litters not provided or provided for shorter periods with creep feed.

A concurrent outbreak of infection with Yersinia pseudotuberculosis occurred in adult captive African lions (Panthera leo). Two 17-y-old male lions and one 14-y-old female lion developed respiratory distress, lethargy, ataxia, and hyporexia. Within 3–5 d of the onset of clinical signs, one male and the female lion died and were submitted for postmortem examination. Macroscopically, the liver and spleen had multifocal-to-coalescing, semi-firm, pale-tan nodules throughout the parenchyma. The lungs were non-collapsed and marked by petechiae. Histologic examination identified lytic, necrosuppurative foci in the liver, spleen, lungs, and kidney, with abundant intralesional gram-negative coccobacilli in the male lion. Similar findings were seen in the female lion in the liver, spleen, kidney, and mesenteric lymph node; however, the intralesional bacterial colonies were more pleomorphic, comprising rod and filamentous morphologies. Aerobic bacterial culture of the liver, spleen, and lung revealed Y. pseudotuberculosis growth. The source of infection is unknown, and an epidemiologic study was performed. Sources to be considered are from the predation of rodent and/or bird reservoirs, or contaminated soil or water. Mortality associated with Y. pseudotuberculosis has been described in an African lion cub, however, to our knowledge, Y. pseudotuberculosis has not been reported in adult African lions, and this is only the second report of Y. pseudotuberculosis with aberrant bacterial morphology observed histologically.

A concurrent outbreak of infection by canine parvovirus 2b (CPV-2b) and Clostridium difficile producing A and/or B toxins occurred in Asian small-clawed otters (Amblonyx cinereus). The 5 clinically affected otters were 6- to 24-mo-old intact females that had severe diarrhea, dehydration, were acutely comatose, and died 1–4 d after the onset of clinical signs. Postmortem examination was performed in 3 of 7 otters. Macroscopically, the small intestine was diffusely reddened and contained red-to-brown, malodorous, watery digesta without formed feces (3 of 3). Histologic examination identified loss of enterocytes and necrosis of crypt epithelial cells. Denuded villi were often covered by mixed bacterial colonies with a predominance of gram-positive cocci to short rods in addition to larger gram-positive and -negative rods. There was also splenic lymphoid follicle depletion (2 of 3). Immunofluorescence assay revealed CPV antigen in enterocytes (2 of 3), mesenteric lymph nodes (3 of 3), and spleen (1 of 3). Immunohistochemistry revealed CPV antigen in enterocytes, lymphocytes, and dendritic cells of the Peyer patches and spleen (3 of 3), and lingual epithelial cells (1 of 2). CPV was isolated from tissues from 2 of 3 otters, and DNA sequencing identified CPV-2b for the 1 isolate tested. C. difficile producing A and/or B toxins were identified in the intestinal content by ELISA (3 of 3). To our knowledge, an outbreak of CPV-2b infection and C. difficile with clinically significant gastrointestinal disease has not been described previously in otters. The source of the viral infections remains unknown; however, these agents should be considered in otters and other mesocarnivores with similar clinical and pathologic findings.

The giant anteater (Myrmecophaga tridactyla) is a vulnerable species from Central and South America, and is considered possibly extinct in Belize, Guatemala, El Salvador, and Uruguay. Due to the species’ conservation and reproductive importance, this research aimed to characterize the morphology, histochemical, immunohistochemical, and ultrastructural feature of the giant anteater prostate gland. For this, we collected 11 giant anteater prostate glands and performed macroscopic, morphological, histochemical, immunohistochemical, and ultrastructural analysis. Nine prostate glands from an adult subject and two from young subjects were studied. Grossly, the adult giant anteater prostate gland is divided in two distinct zones; the central zones (composed mainly of ducts) and the peripheral zones (of acini formed by secretory cells). The secretory cells showed positive periodic acid–Schiff staining. Furthermore, the immunohistochemical characterization revealed a similar human prostate pattern, with p63 staining basal cells, uroplakin III (UPIII) superficial cells of prostatic urethra, androgen receptor (AR) expressing nucleus of secretory and stromal cells, and prostatic specific antigen (PSA) staining prostatic epithelial cells. Overall, our research provided an in-depth morphological description of the giant anteater’s prostate gland, providing valuable information for futures studies focused on giant anteater conservation.

"Pathology in Practice" published on 21 Dec 2021 by American Veterinary Medical Association.

Heavy metal poisoning poses a challenge in diagnostic practices and environmental safety. This study describes the epidemiological, clinical, and pathological aspects of a chromium (Cr) poisoning outbreak in growing/finishing pigs housed in pens with bedding of pine wood shavings containing Cr. A visit to the affected farm was conducted. Epidemiological data were collected, and necropsy and histopathological examinations and heavy metal quantifications were performed. Up to 30% of the animals from the affected pens displayed clinical signs 48 h after housing, characterized by apathy, rigid gait, distended abdomen, pain to abdominal palpation, fever, vomiting, and skin cyanosis. The lethality rate reached 76.6%. Main postmortem findings consisted of ulcerative gastritis with perforation of the glandular stomach in all necropsied swine. Heavy metal analysis revealed a higher concentration of Cr in the bedding of the affected pens, along with elevated levels of Cr in the livers of the affected swine. Given that Cr is a known cause of poisoning in humans (with acute oral exposure resulting in corrosive lesions in the gastrointestinal tract), this study marks the first diagnosis of acute oral natural Cr poisoning in animals. This diagnosis was established through the association of epidemiological, pathological, and heavy metal quantification data.