Air sacculitis is an important clinical condition in non-human primates.
We evaluated 37 baboons and 7 chimpanzees with spontaneous air sacculitis submitted to pathology over a 20 year period.
Air sacculitis was observed almost exclusively in males. Common reported signs were halitosis, coughing, nasal discharges, depression, anorexia, and weight loss. Gross lesions included thickened air sacs and suppurative exudate lining the walls. Microscopic lesions included marked epithelial hyperplasia or hypertrophy, necrosis, fibrosis, cellular infiltrates, and bacterial colonies. Mixed bacterial infections were more common than infections by single species of bacteria. Streptococcus sp. was the most frequent bacteria isolated in both baboons and chimpanzees.
This is the first report describing the gross and microscopic lesions of air sacculitis in chimpanzees. The preponderance of males suggests a male sex predilection in baboons.
Air sac; Airsacculitis; Pan; Papio; Non-human primate
Chewing of regurgitated food with rumination elicits, gastroesophageal reflux (GER) in baboons. Protracted reflux transforms the distal multilayered squamous cell-lined epithelium into columnar-lined mucosa, with mucus-producing glands having interspersed oxyntic glands. In humans, this histological constellation is called Barrett's mucosa type 2 (BMT2).
Materials and Methods
The distal esophagus together with the proximal stomach was removed en bloc, at autopsy, from 35 adult baboons. Longitudinal sections were stained with toluidine blue, a stain that permits easy discrimination between parietal and chief gastric glands. Using a calibrated ocular scale, the length of the BMT2 was assessed in all 35 baboons.
The mean length of the BMT2 was 9.80 mm (range 1.0 mm–40.2 mm).
BMT2 in baboons is an integrated part of the natural phenomenon of mucosal adaptation to daily regurgitation of gastric acid into the distal esophagus (natural GER), whereas BMT2 in humans might reflect an evolutionary atavism in the esophagus, triggered by a non-physiological disorder (pathological GER). The baboon offers a suitable model to monitor the series of histological events that take place in the distal esophagus under the influence of protracted GER.
Barrett's mucosa; esophagus; baboon; reflux; mucus; metaplasia
Erratic regulation of glucose metabolism including hyperglycemia is a common condition of premature infants and is associated with increased morbidity and mortality.
To examine histological and ultra-structural differences in the endocrine pancreas in fetal (throughout gestation) and neonatal baboons.
Twelve fetal baboons were delivered at 125 days (d) gestational age (GA), 140dGA, or 175dGA. Eight animals were delivered at term (185dGA); half were fed for 5d. Seventy-three non-diabetic adult baboons were used for comparison. Pancreatic tissue was studied utilizing light microscopy, confocal imaging and electron microscopy.
The fetal and neonatal endocrine pancreas islet architecture became more organized as GA advanced. The percent areas of α-β-δ-cell type were similar within each fetal and newborn GA (NS), but were higher than the adults (P<0.05) regardless of GA. The ratio of β-cells within the islet (whole and core) increased with gestation (P<0.01). Neonatal baboons who survived for 5 days (feeding), had a 2.5-fold increase in pancreas weight compared to their counterparts euthanized at birth (P=0.01). Endocrine cells were found amongst exocrine ductal and acinar cells in 125,140 and 175dGA fetuses. Subpopulation of cells that co-expressed trypsin and glucagon/insulin show the presence of cells with mixed endo-exocrine lineage in fetuses.
The fetal endocrine pancreas has no prevalence of a of α-β-δ-cell type with larger endocrine cell percent areas than adults. Cells with mixed endocrine/exocrine phenotype occur during fetal development. Developmental differences may play a role in glucose homeostasis during the neonatal period and may have long term implications.
Insulin; glucagon; fetus; islet cells; primates
Nonhuman primates have been a common animal model to evaluate experimentally-induced malformations. Reports on spontaneous malformations are important in determining the background incidence of congenital anomalies in specific species and in evaluating experimental results. Here we report on a stillborn cynomolgus monkey (Macaca fascicularis) with multiple congenital anomalies from the colony maintained at the Southwest National Primate Research Center at the Southwest Foundation for Biomedical Research, San Antonio, Texas. Physical findings included low birth weight, craniorachischisis, facial abnormalities, omphalocele, malrotation of the gut with areas of atresia and intussusception, a Meckel diverticulum, arthrogryposis, patent ductus arteriosus, and patent foramen ovale. The macaque had normal male external genitalia, but undescended testes. Gestational age was unknown but was estimated from measurements of the limbs and other developmental criteria. Although cytogenetic analysis was not possible due to the tissues being in an advanced state of decomposition, array Comparative Genomic Hybridization analysis using human bacterial artificial chromosome clones was successful in effectively eliminating aneuploidy or any copy number changes greater than approximately 3–5 Mb as a cause of the malformations. Further evaluation of the animal included extensive imaging of the skeletal and neural tissue defects. The animal’s congenital anomalies are discussed in relation to the current hypotheses attempting to explain the frequent association of neural tube defects with other abnormalities.
neural tube defects; schisis association; macaque; cynomolgus monkey; non-human primate; congenital defects; malformations
Adenoviruses (AdVs) are DNA viruses that infect many vertebrate hosts, including humans and nonhuman primates. Here we identify a novel AdV species, provisionally named “simian adenovirus C (SAdV-C),” associated with a 1997 outbreak of acute respiratory illness in captive baboons (4 of 9) at a primate research facility in Texas. None of the six AdVs recovered from baboons (BaAdVs) during the outbreak, including the two baboons who died from pneumonia, were typeable. Since clinical samples from the two fatal cases were not available, whole-genome sequencing of nasal isolates from one sick baboon and three asymptomatic baboons during the outbreak was performed. Three AdVs were members of species SAdV-C (BaAdV-2 and BaAdV-4 were genetically identical, and BaAdV-3), while one (BaAdV-1) was a member of the recently described SAdV-B species. BaAdV-3 was the only AdV among the 4 isolated from a sick baboon, and thus was deemed to be the cause of the outbreak. Significant divergence (<58% amino acid identity) was found in one of the fiber proteins of BaAdV-3 relative to BaAdV-2 and -4, suggesting that BaAdV-3 may be a rare SAdV-C recombinant. Neutralizing antibodies to the other 3 AdVs, but not BaAdV-3, were detected in healthy baboons from 1996 to 2003 and staff personnel from 1997. These results implicate a novel adenovirus species (SAdV-C) in an acute respiratory outbreak in a baboon colony and underscore the potential for cross-species transmission of AdVs between humans and nonhuman primates.
Adenoviruses (AdVs) are DNA viruses that infect many animals, including humans and monkeys. In 1997, an outbreak of acute respiratory illness from AdVs occurred in a baboon colony in Texas. Here we use whole-genome sequencing and antibody testing to investigate new AdVs in baboons (BaAdVs) during the outbreak, one of which, BaAdV-3, came from a sick animal. By sequence analysis, BaAdV-3 may be a recombinant strain that arose from a related BaAdV found in baboons nearby in the colony (who were not sick) and yet another unknown AdV. We also found antibodies to these new BaAdVs in baboons and staff personnel at the facility. Taken together, our findings of a new AdV species as the cause of an acute respiratory outbreak in a baboon colony underscore the ongoing threat from emerging viruses that may carry the potential for cross-species transmission between monkeys and humans.
An inverse relationship between serum prostate specific antigen (PSA) levels and body mass index (BMI) has been reported in men but not in any animal model.
Serum PSA in a colony of cynomolgus monkeys was assayed and correlated to body weight, prostate weight and age. In addition 15 animals were selected and fed a high sugar high fat (HSHF) diet for 49 weeks to increase their BMI and correlate it to PSA
Serum PSA levels were positively correlated to prostate weight (r=0.515, p=0.025) and age (r=0.548, p=0.00072) but was not significantly correlated to body weight (r=−0.032, p=0.419). For the animals on the HSHF diet, body weight, lean mass, fat mass and BMI were significantly higher at 49 weeks than at baseline (p<0.01). PSA was not significantly correlated to body weight and insulin at both baseline and 49 weeks. PSA was negatively correlated to BMI and insulin resistance (HOMA-IR) at 49 weeks but not at baseline. In addition we observed hepatic steatosis and increases in serum liver enzymes.
Increases in BMI in cynomolgus monkeys as a result of consuming a HSHF diet resulted in PSA changes similar to those in humans with increased BMI. Cynomolgus monkeys are a useful model for investigating the relationship between obesity, diabetes and PSA changes resulting from prostate gland pathology.
Diabetes; insulin resistance; BMI
Marmosets and tamarins are increasingly used in research, but their pathology remains poorly defined compared to old world primates.
Necropsy records of 129 marmosets and 52 tamarins were reviewed; none were used experimentally.
The most common marmoset lesions were dehydration, emaciation, nephritis, colitis and inanition. The most common tamarin lesions were dehydration, ascites, emaciation and congestive heart failure. Colitis and heart disease were the most common cause of death in marmosets and tamarins, respectively. Immature marmoset and tamarin deaths often occurred within the first month of life. Immature marmosets usually died from inanition, stillbirth and colitis; immature tamarins from atelectasis, stillbirth, heart failure and colitis. Lymphoma was the most common neoplasm for both marmosets and tamarins.
The findings were similar to prior reports with differences in frequency and severity. We report the first case of endometriosis in a marmoset.
nonhuman primate; Callitrichidae; disease; epidemiology; cancer
In baboons, Papio sp. neoplasms tend to affect the hematopoietic system most commonly, with rare documentation of myxomatous neoplasms. In contrast, women can develop myxomatous masses within deep peripelvic tissues with some frequency during their reproductive years.
We have identified and examined, retrospectively, myxomatous perineal masses in twelve female baboons within one research facility and compared their histopathologic, immunohistochemical and electron microscopic features to their human variants.
Our results indicate that these myxomatous neoplasms, in humans and non-human primates, share common features.
Further research, particularly molecular genetic analysis, may be needed to identify the baboon as a true animal model for myxomatous perineal neoplasms.
Aggressive angiomyxoma; angiomyofibroblastoma; cdk4; estrogen receptor; MDM2; progesterone receptor
Squamous cell carcinoma (SCC) is a neoplastic proliferation of epithelial cells undergoing squamous differentiation and represents a diagnostic challenge in nonhuman primates (NHP), especially in baboons with perineal SCC.
Fourteen SCC (13 baboons, 1 spider monkey) were identified over a 20-year period. A literature search identified 86 additional published cases of spontaneous NHP SCC.
SCC was most commonly reported in macaques, baboons, marmosets, and squirrel monkeys. Metastasis occurred in 23%, of NHP. The most frequently reported primary locations were the oral cavity, integument, esophagus, and cervix-uterus. Perineal SCC occurred mainly in baboons. All reported SCC in marmosets occurred in the head. Nasal cavity SCC was only reported in male marmosets. All reported pulmonary SCC occurred in males, mostly in tree shrews.
SCC is a common neoplasm in NHP and exhibits species differences. NHPs may provide a useful SCC animal model.
Cancer; neoplasm; Papio; skin; oral cavity; esophagus
Colonic amyloidosis has been previously reported in animals, however its prevalence rate has not yet been explored. The aim of the present work was to assess the prevalence of colonic amyloidosis at the Southwest National Primate Research Center since 1986.
Materials and Methods
Colonic amyloidosis was sought in autopsy material from baboons collected under the diagnosis of systemic amyloidosis.
Between 1986 and 2007, a mean of 3,315 baboons per year (range 2,578–3,931) were housed at the Southwest National Primate Research Center. After examination, colonic amyloidosis was detected in 6 (6.8% ) of the 88 baboons with systemic amyloidosis, yielding a prevalence rate of 0.27 cases per year since 1986. Colonic amyloid deposits were found in the interstitial aspect of the lamina propria, often replacing normal mucosal crypts of Lieberkuhn.
It was observed that only 6.8% of animals with systemic amyloidosis examined between 1986 and 2007 developed colonic amyloidosis. The apparent natural resistance to colonic amyloidosis in baboons presenting systemic amyloidosis deserves to be further investigated.
Amyloidosis; colon; baboon
For anatomists, the cardia is a portion of the stomach. However, at the histological level, the cardiac mucosa, described as columnar-lined with mucus-producing glands (CLMMG), is for some pathologists part of the stomach (already present at birth) and for others a metaplastic change of the esophagus induced by gastro-esophageal reflux (GER).
Materials and Methods
The distal esophagus and the proximal stomach of 5 adult male baboons were removed en bloc at autopsy. The distance between the most distal part of the squamous epithelium of the esophagus and the first oxyntic fundic gastric gland (representing the entire CLMMG) was assessed using an ocular microscale.
The length of the CLMMG varied from 1.2 mm to 12.4 mm. The CLMMG had replaced the squamous epithelium of the distal esophagus in all 5 baboons.
Regurgitation with rumination is a natural physiological, daily, recurrent process in baboons that leads to GER. The luminal cytoplasmic vacuoles with neutral mucins contained in the columnar cells and the neutral mucins produced by the mucin glands buffer the low pH of the gastric juices that reflux into the distal esophagus. This protective action against the acid refluxate cannot be achieved by the squamous epithelium.
The results of this preliminary investigation suggest that in baboons, CLMMG is an adaptation process of the esophageal mucosal to the low pH microenvironment conveyed by protracted GER.
Metaplasia; esophagus; reflux; baboons
Chagas disease (CD) or American trypanosomiasis is caused by a hemoflagellate protozoan, Trypanosoma cruzi (TC). This organism has been isolated from more than 100 mammalian species and several insect vectors demonstrating a wide host distribution and low host specificity.
A 23 year old male chimpanzee died acutely and a complete necropsy was performed to evaluate gross and microscopic pathologic changes. After observation of trypanosomal amastigotes in the myocardium, PCR and immunohistochemistry was employed to confirm the diagnosis of TC.
Gross findings were consistent with mild congestive heart failure. Microscopic findings included multifocal myocardial necrosis associated with severe lymphocytic to mixed inflammatory infiltrates, edema, and mild chronic interstitial fibrosis. Multifocal intracytoplasmic amastigotes morphologically consistent with TC were observed in cardiac myofibers. TC was confirmed by PCR and immunohistochemistry.
We report, to the best of our knowledge, the first fatal spontaneous case of TC infection in a chimpanzee.
Ape; nonhuman primate; protozoa; fatal case; Trypanosoma cruzi
Systemic amyloidosis, caused by abnormal tissue accretion of plasma proteins, affects several organs of the gastrointestinal (GI) tract. Gastric amyloidosis, rare in humans, has only been reported once in animals.
Materials and Methods
Gastric amyloidosis was sought for in baboons with systemic amyloidosis.
During the past 22 years (between January 1986 and January 2007) a mean of 3,315 baboons/year (range 2,578–3,931) were housed at the Southwest National Primate Research Center. Gastric amyloidosis was found in 9 (10.2%) of the 88 baboons having a diagnosis of systemic amyloidosis. Consequently, the prevalence of gastric amyloidosis occurring since 1986 at this facility was 0.41 baboons/year. Gastric amyloid deposits were found in the interstitial aspect of the lamina propria, replacing normal mucosal structures, in the submucosal stroma along the interface with the muscularis mucosae and in the interstitial tissue of submucosal lymphoid aggregates. In one of the animals, lumps of amyloid deposits with giant cells were found in the gastric mucosa.
Baboons with systemic amyloidosis usually show increasing frequency of amyloid deposits in the liver, large intestine, lymph nodes, spleen and the small intestine. We now demonstrate that it may also involve the stomach. Why certain organs of the GI tract in baboons are more susceptible than others to be affected by the process of systemic amyloidosis remains unexplained. The apparent natural resistance of the stomach of baboons to be affected by systemic amyloidosis deserves further investigation. The review of the literature indicates that this is only the second report on gastric amyloidosis in baboons.
Amyloidosis; stomach; baboons
The frequency of histological changes mimicking those described for reflux esophagitis in humans was assessed in a cohort of non-human primates (NHP).
Materials and Methods
A total of 121 consecutive esophagi (from 103 baboons and 18 macaques) were classified according to Ismail-Beiji for reflux esophagitis in humans into grade 1, grade 2 and grade 3 esophagitis.
Histological features compatible with reflux esophagitis were found in 28.2% of the baboons and in 22.2% of the macaques. Esophagitis grade 1 was more common in baboons (24%) than in macaques (6%), while esophagitis grade 2 was more common in macaques (17%) than in baboons (2%).
Although the prevalence of reflux esophagitis in man is at least 2%, only a fraction of patients demonstrate histological features consistent with grades 1, 2 or 3 esophagitis. Hence, the finding that 27% of a cohort of consecutive, unselected NHP had grades 1, 2 or 3 esophagitis at histology is remarkable. The possible causes for the difference between species, such as the oblique position often adopted by NHP during the gastric phase of digestion, the diet, regurgitation and subsequent re-ingestion, as well as the stress of NHP when kept in captivity, are reviewed.
Esophagitis; reflux; non-human primates indent
In humans and in baboons, protracted gastro-esophageal reflux (GER) transforms the squamous-lined esophagus into columnar-lined (that is Barrett's mucosa, BM). Alcian blue stain (AB) is used to evidence sialomucin-producing goblet cells in human BM.
To assess the frequency and distribution of sialomucin-producing cells in BM in baboons.
Materials and Methods
Sections from 137 consecutive baboon esophagi were alternatively stained with hematoxylin-eosin (H&E) and with AB (pH 2.5), without counterstain.
Out of 137 baboons, 131 (95.6%) had BM. Columnar and intramucosal glandular cells produced sialomucin in all 131 of these animals. Many BM cells were ballooned and filled with sialomucins, despite goblet cells not being found in H&E sections.
In humans, protracted GER is a disease requiring medication that may lead to BM; AB stains mainly goblet cells and occasional columnar cells in BM. In baboons, in contrast, BM is a natural postnatal process of adaptation to GER, triggered by regurgitation and rumination. AB stains all columnar and intra-mucosal glandular cells. Sialomucin-overstuffed cells were more frequent and larger in baboons than in humans. The extra load of sialomucin in BM might be an integrated part of the postnatal life-long process of adaptation to regurgitation and rumination in baboons.
Esophagus; baboons; glandular metaplasia; sialomucins
Gastric parietal cells in a baboon were recently found to be auto-fluorescent. Aim: To study gastric sections with a fluorescent microscope in a cohort of baboons.
Material and Methods
Gastric sections from 38 baboons were stained with hematoxylin-eosin (H&E) and examined in a fluorescence microscope (FLM). The thickness of the parietal cell population was assessed at ×10 magnification.
H&E stained all mucosal cells: fovelar, parietal and chief cells. When the same sections were analyzed with an FLM, only parietal cells were auto-fluorescent, whereas fovelar and chief cells remained non-fluorescent. Parietal cells formed a distinct, continuous auto-fluorescent band. The ratio of the auto-fluorescent parietal cell band/total mucosa ranged between 0.20 and 0.30.
Gastric parietal cells became auto-fluorescent when H&E-stained sections from baboon stomachs were observed with an FLM. Eosin was the stain responsible for this optical phenomenon.
Gastric mucosa; parietal cells; auto-fluorescence; identification
Gastrointestinal stromal tumors (GISTs) are believed to originate from the intestinal pacemaker cells (interstitial cells of Cajal) or their progenitor cells. Spontaneous tumors have been reported in dogs, horses, rhesus, and a chimpanzee and they have been produced experimentally in mice and rats. GISTs represent a diagnostic challenge because they cannot be differentiated from nonlymphoid mesenchymal tumors without using human c-kit (CD117) immunohistochemistry.
Three neoplasms were incidental findings at necropsy in the stomachs of a baboon and a spider monkey and in the rectum of a chimpanzee.
The GISTs were initially diagnosed grossly and histologically with hematoxylin and eosin as leiomyomas. Immunohistochemical analysis revealed all three were c-kit (CD117) positive.
These are the first reports of GISTs in the baboon and spider monkey and the second in a chimpanzee. The occurrence of GISTs in nonhuman primates may provide a unique opportunity to study these tumors.
Cancer; neoplasm; nonhuman primate; Papio anubis; Ateles paniscus; Pan troglodytes; interstitial cells of Cajal
Chagas disease is common in Central and South America and the southern United States. The causative agent is Trypanosoma cruzi (T cruzi, Order Kinetoplastida, Family Trypanosomatidae), a kinetoplastid protozoan parasite of humans and other vertebrates. It is a serious public health issue and the leading cause of heart disease and cardiovascular death in Central and South America. In 1984 a colony baboon was discovered to be infected with T cruzi.
Since the initial diagnosis was made by microscopic observation of the amastigote forms of T. cruzi in myocardial fibers, T. cruzi amastigotes have been identified in three additional baboons.
The primary findings were similar in all four baboons and were congestive heart failure with edema of dependent areas, hydrothorax, hydropericardium, and multifocal to diffuse lymphoplasmacytic myocarditis.
A baboon animal model of Chagas disease could contribute significantly to the development of therapies for the disease in humans.
nonhuman primate; protozoa; animal model; heart; Trypanosoma cruzi
A comprehensive survey of the prevalence of congenital anomalies in baboons has not been previously reported. We report the congenital anomalies observed over a 26-year period in a large captive baboon colony.
A computer search was performed for all baboon congenital anomalies identified at necropsy and recorded on necropsy submissions.
We identified 198 congenital anomalies in 166 baboons from 9,972 necropsies (1.66% of total necropsies). The nervous, urogenital, musculoskeletal, and cardiovascular systems were most commonly affected. The most common organs affected were the brain, bone, heart, testicle, kidney, penis, aorta, and skeletal muscle. The most frequent congenital anomalies were blindness, seizures, and hydrocephalus.
The baboon has an overall frequency of congenital anomalies similar to humans and other nonhuman primates. Although the most frequently affected systems are similar, congenital anomalies involving the digestive system appear to be less common in the baboon.
nonhuman primate; pathology; spontaneous disease; natural
The metabolic syndrome is common in populations exposed to a typical Western diet. There is a lack of an animal model that mimics this condition.
We fed 15 cynomolgus monkeys ad libitum a high sugar high fat (HSHF) diet for 33 weeks. Body weight, body composition, serum lipids and insulin were measured at baseline and at 33 weeks.
The animals tolerated the HSHF diet very well. In the intervention group, total serum cholesterol and LDL-C were 3- and 5-fold higher, respectively, at 33 weeks as compared to their baseline levels. Serum HDL-C and triglycerides were not significantly affected. Dual-energy X-ray absorptiometry (DXA) analysis of the intervention group indicated that the trunk fat mass increased by 187% during this period.
Cynomolgus monkeys should be a useful model for investigating the interactions of diet and other factors such as genetics in the development of the metabolic syndrome.
Dual X-ray absorptiometry; LDL-cholesterol; triglyceride; insulin
Primary neuroendocrine carcinomas of the liver have rarely been reported in humans and domestic animals, but not in non-human primates.
We describe the morphologic and immunohistochemical features of a primary hepatic neuroendocrine carcinoma found in a 29-year-old female baboon.
Results and conclusions
The neoplasm was characterized by multiple solid nodules that were multifocally distributed in the liver. Metastases were not observed. Histologically, the neoplasm was composed of cords and nests of epithelial cells arranged in a neuroendocrine pattern, occasionally forming glandular and rosette-like structures. On immunohistochemical evaluation, the neoplastic cells were immunopositive for pancytokeratin, chromogranin A, neuron-specific endolase, and synaptophysin and were negative for vimentin, S100 protein, glucagon, and insulin.
Endocrine; liver; non-human primate; tumor
Glands with glassy cells (GGCs) were recently found in 1.8% of patients showing Barrett’s mucosa in esophageal biopsies. Similar GGCs were more recently detected in a baboon having glandulo-metaplastic esophageal mucosa (GMEM). The aim was to assess the frequency of baboons with GMEM having GGCs.
Materials and Methods
GGCs were searched for in 68 consecutive baboons having GMEM. Sections were stained with H&E and with alcian blue (pH 2.5), to detect sialomucins in goblet cells (a marker of Barrett’s mucosa in GMEM).
Two out of the 68 baboons with Barrett’s mucosa (2.9%) showed GGCs.
In similarity to humans, the Barrett’s mucosa in baboons may show GGCs. Although the significance of GGCs in baboons (and in humans) remains poorly understood, their presence might not be a fortuitous event but linked to the molecular events leading to the development of intestinal metaplasia in Barrett’s mucosa, a known pre-neoplastic mucosal change in the distal esophagus in humans.
Nonhuman primate; pathology; disease; intestinal metaplasia
Baboons are useful animal models for biomedical research, but the natural pathology of the baboon is not as well defined as other non-human primates.
A computer search for all morphologic diagnoses from baboon necropsies at the Southwest National Primate Research Center was performed and included all the natural deaths and animals euthanized for natural causes.
A total of 10,883 macroscopic or microscopic morphologic diagnoses in 4297 baboons were documented and are presented by total incidence, relative incidence by sex and age-group, and mean age of occurrence. The most common diagnoses in descending order of occurrence were hemorrhage, stillborn, amyloidosis, colitis, spondylosis, and pneumonia. The systems with the most diagnoses were the digestive, urogenital, musculoskeletal, and respiratory.
This extensive evaluation of the natural pathology of the baboon should be an invaluable biomedical research resource.
diseases; monkey; non-human primates; pathology; spontaneous; survey
Congenital transmission of Trypanosoma cruzi has been described in humans and experimental work has been conducted with mice, but not with non-human primates (NHPs).
We conducted a retrospective study of female baboons (Papio hamadryas spp.) naturally seropositive or seronegative for T. cruzi with history of fetal loss, and we report a stillbirth in a cynomolgus macaque (Macaca fascicularis) with placental T. cruzi amastigotes.
There were no differences in menstrual cycle parameters and the number of fetal losses between seropositive and seronegative baboons with history of fetal loss. The amount of parasite DNA detected using quantitative polymerase chain reaction (Q-PCR) in M. fascicularis placenta was within the range detected in infected baboon tissues.
There is no evidence that chronic maternal T. cruzi infection causes fetal loss in baboons. Q-PCR is a useful diagnostic tool to study archived NHP placentas.
Baboon; macaque; placental lesions; reproductive performance; serology; trypanosomiasis
Maternal obesity is present in 20–34% of pregnant women and has been associated with both intrauterine growth restriction and large-for-gestational age fetuses. While fetal and placental functions have been extensively studied in the baboon, no data are available on the effect of maternal obesity on placental structure and function in this species. We hypothesize that maternal obesity in the baboon is associated with a maternal inflammatory state and induces structural and functional changes in the placenta. The major findings of this study were 1) decreased placental syncytiotrophoblast amplification factor, intact syncytiotrophoblast endoplasmic reticulum structure and decreased system A placental amino acid transport in obese animals; 2) fetal serum amino acid composition and mononuclear cells (PBMC) transcriptome were different in fetuses from obese compared with non-obese animals 3) maternal obesity in humans and baboons is similar in regard of increased placental and adipose tissue macrophage infiltration, increased CD14 expression in maternal PBMC and maternal hyperleptinemia. In summary, these data demonstrate that in obese baboons in the absence of increased fetal weight, placental and fetal phenotype are consistent with those described for large- for-gestational age human fetuses.