ABSTRACT
The increased risk of food allergy in infants with atopic dermatitis (AD) has long been recognized; an epidemiologic phenomenon termed "the atopic march." Current literature supports the hypothesis that food antigen exposure through the disrupted skin barrier in AD leads to food antigen-specific immunoglobulin E production and food sensitization. However, there is growing evidence that inflammation in the skin drives intestinal remodeling via circulating inflammatory signals, microbiome alterations, metabolites, and the nervous system. We explore how this skin-gut axis helps to explain the link between AD and food allergy beyond sensitization.
ABSTRACT
In collaboration with the American College of Veterinary Pathologists.
Subject(s)
Pathology, Veterinary , Veterinarians , Animals , Humans , United StatesABSTRACT
Malakoplakia in humans most often affects the urinary bladder and is characterized by inflammation with von Hansemann-type macrophages, with or without Michaelis-Gutmann bodies, and is frequently associated with Escherichia coli infection. We describe the microscopic features of malakoplakia in the urinary bladder of 4 puppies. In all cases, the lamina propria of the urinary bladder was markedly expanded by sheets of large, round to polygonal macrophages with intracytoplasmic, periodic acid-Schiff-positive granules and granular inclusions, and rare Prussian blue-positive inclusions. Macrophages were positive for CD18 and Iba1. In 2 cases, Michaelis-Gutmann bodies were detected with hematoxylin and eosin stain and were best demonstrated with von Kossa stain. E. coli infection was confirmed in 2 cases with bacterial culture or polymerase chain reaction (PCR) and sequencing of the bacterial 16S ribosomal RNA gene. Transmission electron microscopy of one case demonstrated macrophages with abundant lysosomes, phagolysosomes, and rod-shaped bacteria. Microscopic features were similar to human cases of malakoplakia. In dogs, the light microscopic characteristics of malakoplakia closely resemble granular cell tumors and histiocytic ulcerative colitis.
Subject(s)
Dog Diseases , Malacoplakia , Animals , Dog Diseases/diagnosis , Dogs , Escherichia coli , Inclusion Bodies , Macrophages , Malacoplakia/diagnosis , Malacoplakia/veterinary , Urinary BladderABSTRACT
Canine collagen type III glomerulopathy (Col3GP) is a rare juvenile nephropathy in which irregular type III collagen fibrils and fibronectin accumulate in glomerular capillary walls and the mesangium. Necropsy findings were reviewed from 5 puppies diagnosed with Col3GP at 6 to 18 weeks of age. Histologically, with hematoxylin and eosin stain, the glomerular capillary walls and mesangium were diffusely and globally expanded by homogeneous pale eosinophilic material. Ultrastructurally, the subendothelial zone and mesangium were expanded by fibronectin and cross-banded collagen type III fibrils, diagnostic of Col3GP. Two additional stains were employed to identify the material within glomeruli as fibrillar collagen using light microscopy. In all 5 cases, the material was red with picrosirius red and birefringent under polarized light, and was blue with periodic acid-Schiff/hematoxylin/trichrome (PASH/TRI), thereby identifying it as fibrillar collagen. Based on these unique staining characteristics with picrosirius red and PASH/TRI, Col3GP may be reliably diagnosed with light microscopy alone.
Subject(s)
Dog Diseases/diagnosis , Kidney Diseases/veterinary , Animals , Azo Compounds , Collagen Type III/metabolism , Dog Diseases/pathology , Dogs , Eosine Yellowish-(YS) , Female , Glomerular Mesangium/pathology , Hematoxylin , Kidney Diseases/diagnosis , Kidney Diseases/pathology , Kidney Glomerulus/pathology , Male , Methyl Green , Staining and Labeling/veterinary , Urinary Tract/pathologyABSTRACT
Streptococcus spp. are a source of morbidity and mortality in captive nonhuman primate populations. However, little is known about the lesions associated with naturally occurring streptococcal infections in baboons (Papio spp.). The pathology database of the Southwest National Primate Research Center was searched for all baboon autopsies from 1988 to 2018 in which Streptococcus spp. were cultured. Baboons on experimental protocol were excluded. The gross autopsy and histopathology reports were reviewed. Archived specimens were retrieved and reviewed as needed for confirmation or clarification. Fifty-six cultures were positive for Streptococcus spp. in 54 baboons with evidence of bacterial infection. Associated gross lesions included purulent exudate, fibrinous to fibrous adhesions, hemorrhage, mucosal thickening, organomegaly, and abscessation. Histologic lesions included suppurative inflammation, abscessation, necrosis, hemorrhage, fibrin accumulation, and thrombosis. Lungs and pleura (n = 31) were the most commonly infected organ followed by the central nervous system (n = 16), spleen (n = 15), soft tissues (n = 12), air sacs, liver, peritoneum, adrenal glands, heart, lymph nodes, uterus, kidneys, biliary system, bones, ears, umbilical structures, mammary glands, pancreas, placenta, and salivary glands. Infections by non-ß-hemolytic Streptococcus spp. predominated in the lungs and air sacs; the most common isolate was Streptococcus pneumoniae. Infections by ß-hemolytic Streptococcus spp. predominated in the soft tissues and reproductive tract. Naturally occurring ß-hemolytic and non-ß-hemolytic Streptococcus spp. infections cause morbidity and mortality in captive baboon populations. The lesions associated with streptococcal infection are similar to those reported in human infection. Thus, the baboon may represent an underutilized model for studying Streptococcus spp. as pathogens.
