Histiocytic Inflammation Research Articles

BUBBLES IN THE BOX: RECURRENT PNEUMOTHORAX FROM BRONCHOPLEURAL FISTULA IN A PATIENT WITH RHEUMATOID ARTHRITIS

SESSION TITLE: Medical Student/Resident Pulmonary Manifestations of Systemic Disease 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: When considering Rheumatoid Arthritis (RA)-associated pulmonary diseases, formation of bronchopleural fistula (BPF) represents an extremely rare complication; and is often associated with peripheral pulmonary nodules that burst into the pleural cavity. We are presenting a case of BPF secondary to RA in the absence of underlying pulmonary nodules. CASE PRESENTATION: A 79-year-old Caucasian female with long-standing RA presented with progressive shortness of breath and chest tightness for 2 days. No reported cough, fever, or night sweats. No recent trauma; history of smoking, or drug abuse; and no past surgeries. Current RA medications are methotrexate, hydroxychloroquine, and prednisone. Chest exam revealed bilateral coarse crackles, decreased breath sounds and hyper-resonant percussion note over the right side. Labs showed neutrophilic leukocytosis (28,000, 95% Neutrophils) and normal chemistry panel. Chest X-ray revealed right-sided pneumothorax with right lung collapse and mediastinal shift to the left. Patient had acute hypoxic respiratory failure secondary to spontaneous right side tension pneumothorax and surgical chest tube was emergently placed. Computed Tomography of the chest (Figure 1) showed right pneumothorax, bilateral pulmonary fibrosis and no discrete pulmonary nodules were identified. After removing the surgical chest tube, air continued to build in the right pleural space and she became hypoxic. Pigtail drain was placed into the right pleural space; afterwards, O2 sats rose above 95%. Air leak and bubbling continued from the pigtail chest tube for 5 days and she did not tolerate chest tube clamping. BPF was considered and cardio-thoracic surgery team was consulted. An open thoracotomy (Figure 2) revealed BPF at the apical segment of the right lower lobe, which was sutured and reinforced by parietal pleura. Pathological exam of the lung biopsy revealed fibrosing pleuritis with acute and chronic histiocytic inflammation and sub-pleural septal fibrosis, which was correlated to her long-standing RA and methotrexate therapy. DISCUSSION: Interstitial lung disease and pleural disease are the most common RA-associated pulmonary manifestations while spontaneous pneumothorax and BPF are among the extremely rare ones. Up to the best of our knowledge, all the previously reported cases of RA-associated BPFs were attributed to peripherally-located pulmonary nodules that necrotize and open into the pleural cavity. However, our patient had spontaneous pneumothorax and BPF with no evidence of pulmonary nodules in chest imaging or in pathology. CONCLUSIONS: Formation of BPF is a rare RA-associated pulmonary disease and is often associated with peripheral pulmonary nodules, which open into the pleural cavity and lead to the fistula formation. However, as demonstrated in our case, BPF in RA patients can form even in the absence of underlying rheumatic pulmonary nodules. Reference #1: Rueth N, Andrade R, Groth S, et al. Pleuropulmonary complications of rheumatoid arthritis: a thoracic surgeon's challenge. Ann Thorac Surg 2009; 88:e20.Rueth N, Andrade R, Groth S, et al. Pleuropulmonary complications of rheumatoid arthritis: a thoracic surgeon's challenge. Ann Thorac Surg 2009; 88:e20. Reference #2: Nishida C, Yatera K, Kunimoto M, et al. [A case of rheumatoid arthritis with pneumothorax due to subpleural pulmonary rheumatoid nodules]. Nihon Kokyuki Gakkai Zasshi 2008; 46:934. DISCLOSURES: No relevant relationships by Masoud AlZeerah, source=Admin input No relevant relationships by ASM ISLAM, source=Web Response No relevant relationships by Lusine Nahapetyan, source=Web Response No relevant relationships by AHMED TAHA, source=Web Response

Pathology and Case Definition of Severe Perkinsea Infection of Frogs.

Severe Perkinsea infection (SPI) is an emerging disease of frogs responsible for mass mortalities of tadpoles across the United States. It is caused by protozoa belonging to the phylum Perkinsozoa that form a distinct group referred to as the Pathogenic Perkinsea Clade of frogs. In this work, we provide detailed description of gross and histologic lesions from 178 naturally infected tadpoles, including 10 species from 22 mortality events and 6 amphibian health monitoring studies from diverse geographic areas. On external examination, we observed abdominal distension (10, 5.6%), cutaneous erythema and petechia (3, 1.7%), subcutaneous edema (3, 1.7%), and areas of white skin discoloration (3, 1.7%). On macroscopic examination of internal organs, we found hepatomegaly (68, 38.2%), splenomegaly (51, 28.7%), nephromegaly (47, 26.4%), ascites (15, 8.4%), segmental irregular thickening and white discoloration of the intestine (8, 4.5%), pancreatomegaly (4, 2.2%), and pancreatic petechia (1, 0.6%). Histologically, over 60% of the liver (148/165, 89.7%), kidney (113/147, 76.9%), spleen (96/97, 99%), and pancreas (46/68, 67.6%) were invaded by myriad intracellular and extracellular Perkinsea hypnospore-like and trophozoite-like organisms. Numerous other tissues were affected to a lesser extent. Mild histiocytic inflammation with fewer lymphocytes or eosinophils was commonly observed in areas of infection that were not obscured by lympho-granulocytic hematopoietic tissue. In light of these observations, we suggest a logical pathogenesis sequence. Finally, we propose a "case definition" for SPI to promote standardized communication of results and prevent misdiagnosis with epidemiological and pathologically overlapping diseases such as ranavirosis.

Subconjunctival Exposure to Carbopol Causes Chronic Histiocytic Inflammatory Response in Rabbits.

PurposeWe recently reported a clinical association between surgical exposure to the ophthalmic lubricant GenTeal gel and postoperative subconjunctival necrotizing granulomatous inflammation. We used a rabbit model to test our hypothesis that subconjunctival exposure to the carbopol 980 component is responsible for inciting chronic inflammation.MethodsOf eight adult wild-type Dutch belted rabbits, 16 eyes received subconjunctival injections of the following: hydroxypropyl methylcellulose (HPMC) 0.3% with carbopol 980 (GenTeal gel, n = 4), HPMC 0.3% (GenTeal tears, n = 3), 0.1% carbopol 980 in sterile water (n = 3), HPMC 1.7% (ImproVue, n = 3), and balanced salt solution (BSS, negative control, n = 3). Rabbits were examined weekly for clinical evidence of inflammation, and biopsies were taken for final pathology 10 weeks postinjection.ResultsAll seven eyes exposed to subconjunctival carbopol 980 (HPMC 0.3% with carbopol 980 or 0.1% carbopol 980) demonstrated conjunctival injection and edema at 4 weeks followed by yellow subconjunctival lesions with scattered pigmentation at 10 weeks. Each of these eyes demonstrated chronic histiocytic inflammation on pathology. No eyes treated with HPMC 0.3%, HPMC 1.7%, or BSS (noncarbopol-containing agents) developed clinical abnormalities or histiocytic inflammation (Fisher's exact test P < 0.0001).ConclusionsSubconjunctival exposure to ophthalmic lubricants containing carbopol 980 stimulates a chronic histiocytic inflammatory response. HPMC-based lubricants lacking carbopol 980 are well tolerated in the subconjunctival space.Translational RelevanceOphthalmic lubricants containing carbopol polymers should be avoided during surgical procedures that may result in subconjunctival exposure. Caution should be exercised when considering surgical use of biomedical products containing highly cross linked, high molecular weight acrylic acid polymers.

Minimal Risk Level Derivation for Cadmium: Acute and Intermediate Duration Exposures

The Agency for Toxic Substances and Disease Registry (ATSDR) lists cadmium as one of its priority hazardous substances. The agency conducted a comprehensive literature review of cadmium and used the information to develop a toxicological profile that identified the full range of health effects associated with exposure to cadmium. It included an assessment that identified screening levels, termed health guidance values or minimal risk levels (MRLs), below which adverse health effects are not expected. In this paper, we describe how MRLs for cadmium are derived. For the acute inhalation MRL, the traditional no observed adverse effect level or lowest observed adverse effect level (NOAEL/LOAEL) approach is used; for the oral intermediate MRL, the benchmark dose (BMD) approach is used. MRLs were developed for the most sensitive route-specific end points, other than mortality and cancer that were sufficiently supported and justified by the data. These included an acute duration (1-14 day exposure) inhalation MRL of 0.03 µg Cd/m3 for alveolar histiocytic infiltration and focal inflammation in alveolar septa and an intermediate duration (15-365 day exposure) oral MRL of 0.5 µg Cd/kg/day for decreased bone mineral density.

Granulomatous diseases: Kids are not just little people

Granulomatous diseases represent a heterogeneous group of conditions characterized by histiocytic inflammation that affect patients of any age. These diseases differ widely in their pathogenesis and include infectious and noninfectious conditions. This review focuses on noninfectious granulomatous conditions, with particular emphasis on age-related differences in the onset, epidemiology, clinical manifestations, prognosis, and age-specific management of specific granulomatous disorders. Knowledge of age-specific aspects of granulomatous conditions in adults and children improves both the extent of the diagnostic workup and the management of these patients.

Pathological Findings in Wild Rats (Rattus rattus) Captured at Guafo Island, Northern Chilean Patagonia

The black rat (Rattus rattus) is an invasive species and potential reservoir of significant pathogens of man, domestic animals and wildlife. During the 2012-2014 austral summers, 201 black rats were captured and examined on the uninhabited Guafo Island, in Northern Chilean Patagonia (43.593029°S, 74.713481°W). The mite Ornithonyssus bacoti caused lymphoplasmacytic and eosinophilic dermatitis in all infected rats (105/210, 52%), but no skin lesions were observed in rats infected with Nosopsyllus spp. and Plocopsylla spp. fleas. Eighty-eight rats (44%) had mild lymphoplasmacytic and eosinophilic enterocolitis and 61 of these rats were infected with the nematode Heterakis spumosa. In the liver, 63 animals (31%) had areas of necrosis with histiocytic and eosinophilic inflammation associated with multiple Calodium hepaticum eggs, and in 15 cases there was co-infection with several Taenia taeniaeformis strobilocerci. Mild interstitial lymphoplasmacytic sialadenitis with intranuclear inclusion bodies, suggesting cytomegalovirus infection, was observed in 28 rats (15%). In the lung, alveolar histiocytosis (69 rats, 34%) and perivascular lymphocytic infiltrates (46 rats, 23%) were the most common findings. There was mild to moderate lymphoplasmacytic interstitial nephritis in 52 rats (26%) and in 15% of these cases Leptospira spp. antigen was detected in the distal renal tubules. Some of the diseases of black rats on Guafo Island are likely to play a role in rat population dynamics. The endemic Guafo Island long-clawed mole mouse (Geoxus lafkenche), sea lions and fur seals may be at risk for infection by some of these rat pathogens.

Identification and pathological characterization of persistent asymptomatic Ebola virus infection in rhesus monkeys.

Ebola virus (EBOV) persistence in asymptomatic humans and Ebola virus disease (EVD) sequelae have emerged as significant public health concerns since the 2013-2016 EVD outbreak in Western Africa. Until now, studying how EBOV disseminates into and persists in immune-privileged sites was impossible due to the absence of a suitable animal model. Here, we detect persistent EBOV replication coinciding with systematic inflammatory responses in otherwise asymptomatic rhesus monkeys that had survived infection in the absence of or after treatment with candidate medical countermeasures. We document progressive EBOV dissemination into the eyes, brain and testes through vascular structures, similar to observations in humans. We identify CD68+ cells (macrophages/monocytes) as the cryptic EBOV reservoir cells in the vitreous humour and its immediately adjacent tissue, in the tubular lumina of the epididymides, and in foci of histiocytic inflammation in the brain, but not in organs typically affected during acute infection. In conclusion, our data suggest that persistent EBOV infection in rhesus monkeys could serve as a model for persistent EBOV infection in humans, and we demonstrate that promising candidate medical countermeasures may not completely clear EBOV infection. A rhesus monkey model may lay the foundation to study EVD sequelae and to develop therapies to abolish EBOV persistence.

The Natural History of Pneumonic Tularemia in Female Fischer 344 Rats after Inhalational Exposure to Aerosolized Francisella tularensis Subspecies tularensis Strain SCHU S4

The inbred Fischer 344 rat is being evaluated for testing novel vaccines and therapeutics against pneumonic tularemia. Although primary pneumonic tularemia in humans typically occurs by inhalation of aerosolized bacteria, the rat model has relied on intratracheal inoculation of organisms because of safety and equipment issues. We now report the natural history of pneumonic tularemia in female Fischer 344 rats after nose-only inhalational exposure to lethal doses of aerosolized Francisella tularensis subspecies tularensis, strain SCHU S4. Our results are consistent with initial uptake of aerosolized SCHU S4 from the nasal cavity, lungs, and possibly the gastrointestinal tract. Bacteremia with hematogenous dissemination was first detected 2 days after exposure. Shortly thereafter, the infected rats exhibited fever, tachypnea, and hypertension that persisted for 24 to 36 hours and then rapidly decreased as animals succumbed to infection between days 5 and 8 after exposure. Tachycardia was observed briefly, but only after the core body temperature and blood pressure began to decrease as the animals were near death. Initial neutrophilic and histiocytic inflammation in affected tissues became progressively more fibrinous and necrotizing over time. At death, as many as 1010 colony-forming units were found in the lungs, spleen, and liver. Death was attributed to sepsis and disseminated intravascular coagulation. Overall, the pathogenesis of pneumonic tularemia in the female F344 rat model appears to replicate the disease in humans.

Subkutane Taenia-crassiceps-Zystizerkose bei einem Hund mit Cushing-Syndrom

A male, 12-year-old Cairn terrier suffering from Cushing's syndrome with two therapy-resistant inflammatory subcutaneous lesions was examined pathomorphologically and parasitologically. Within the subcutaneous tissue, there was a suppurative to necrotizing and histiocytic inflammation present with the formation of caverns. Intralesional whitish-grey cysts with a diameter of 1-4 mm were detected. Molecular investigations of the cysts confirmed the preliminary morphological identification as Cysticercus longicollis. The adenohypophysis showed an infiltrative growing carcinoma. Cysticercus longicollis is the metacestode of Taenia (T.) crassiceps, a tapeworm of foxes and coyotes. Small rodents are typical intermediate hosts, in which the metacestode develops within the body cavities as well as in the subcutis. Subcutaneous cysticercosis after infection with eggs of T. crassiceps is also described in different domestic animal species and in humans, who represent aberrant intermediate hosts. Immunosuppression due to Cushing's syndrome, probably caused by the tumor of the adenohypophysis, may have played a role in the pathogenesis of the present case.

Endolymphatic Sac Carcinoma In Situ in a Tokay Gecko (Gekko gecko)

Abstract An 11-year-old female tokay gecko (Gekko gecko) was presented for bilateral asymmetric swellings of the cervical region. Baseline hematologic and plasma biochemical analyses demonstrated anemia, hypercalcemia, hyperphosphatemia, and hypoalbuminemia. Whole-body radiographs revealed a mass effect and irregular mineralization in the region of the left endolymphatic sac. Fine needle aspiration of this region revealed many elongated calcium-based crystals with pointed ends, histiocytic inflammation, and clusters of epithelial cells, consistent with hyperplasia or neoplasia of the epithelium of the endolymphatic sac. The crystals were shown to be calcium carbonate by infrared crystallography. Given the advanced state of disease and inability to completely excise the mass due to the intimate association between the meninges and endolymphatic sac, the gecko was euthanized. Gross necropsy and histopathologic evaluation revealed carcinoma in situ of the left endolymphatic sac. To our knowledge, this is the...

Lymphocytic colitis with giant cells and granulomatous inflammation

Introduction Several variants of microscopic colitis (MC) have been described. These include MC with giant cells and MC with granulomatous inflammation, amongst others. Aim We present a case of lymphocytic colitis with both giant cells and pericryptal granulomatous inflammation, which to our knowledge has not previously been described in combination. Methods A 63-year-old female with chronic bloodless diarrhoea and no specific endoscopic findings had random colon biopsies performed. Results Microscopically, the left sided biopsies revealed classic lymphocytic colitis. The right sided biopsies showed CD3 positive intraepithelial lymphocytosis with CD68 positive subepithelial multinucleated giant cells and superficial non-necrotising pericryptal granulomas. No fungal organisms or acid fast bacilli were seen with special stains. No foreign bodies or vasculitis was identified. No clinical or histological features of inflammatory bowel disease were present. Discussion This case demonstrates combined features of two rare atypical forms of MC previously described as separate variants. It is possible these three appearances may represent a spectrum of MC with associated histiocytic inflammation. Though uncommon, recognition of the atypical variants as MC is of importance to avoid confusion with other entities.

Disseminated histoplasmosis in two juvenile raccoons (Procyon lotor) from a nonendemic region of the United States

Two 6-month-old raccoon kits, which had been rescued and fostered in preparation for return to the wild, became acutely ill and died 3 weeks before scheduled release. At necropsy, the kits had grossly enlarged livers and spleens, diffusely consolidated lungs, and generalized lymphadenopathy. Histologically, extensive infiltrates of macrophages containing yeast organisms were identified in lung, liver, kidney, spleen, lymph nodes, intestinal tissues, brain, adrenal gland, bone marrow, and thymus of both animals. Histiocytic inflammation with accompanying fibrosis was widespread, with necrotic foci evident in lungs, spleen, and intestinal sections. Fungal organisms were observed on sheep blood agar plates; however, repeated subcultures to fungal media designed to induce conidial structures for fungal identification were unsuccessful. Partial DNA sequencing of the 28S ribosomal RNA gene of the blood agar isolate identified 100% homology with Ajellomyces capsulatus (anamorphic name Histoplasma capsulatum). The kits were rescued and fostered in the San Francisco Bay area and it is likely that the exposure to H. capsulatum occurred in this area. Histoplasma sp. infection in wild mammal species is often used as an indication of spore contamination of a geographic region. Northern California is not known to be an endemic region for H. capsulatum, which is not a reportable disease in this state. The presence of severe, disseminated disease and the need for molecular identification associated with the isolate from a nonendemic region identified in the present report may indicate genetic adaptation and altered characteristics of this agent and may warrant further investigation.

Circovirus in Tissues of Dogs with Vasculitis and Hemorrhage

We characterized the complete genome of a novel dog circovirus (DogCV) from the liver of a dog with severe hemorrhagic gastroenteritis, vasculitis, and granulomatous lymphadenitis. DogCV was detected by PCR in fecal samples from 19/168 (11.3%) dogs with diarrhea and 14/204 (6.9%) healthy dogs and in blood from 19/409 (3.3%) of dogs with thrombocytopenia and neutropenia, fever of unknown origin, or past tick bite. Co-infection with other canine pathogens was detected for 13/19 (68%) DogCV-positive dogs with diarrhea. DogCV capsid proteins from different dogs varied by up to 8%. In situ hybridization and transmission electron microscopy detected DogCV in the lymph nodes and spleens of 4 dogs with vascular compromise and histiocytic inflammation. The detection of a circovirus in tissues of dogs expands the known tropism of these viruses to a second mammalian host. Our results indicate that circovirus, alone or in co-infection with other pathogens, might contribute to illness and death in dogs.

Histiocytic inflammation induced by granulocyte-macrophage colony–stimulating factors

Histiocytic inflammation induced by granulocyte-macrophage colony–stimulating factors

Falciform ligament abscess from left sided portal pyaemia following malignant obstructive cholangitis

Abscess formation of the falciform ligament is incredibly rare and perplexing when encountered for the first time. It is reported to occur in the setting of cholecystitis and cholangitis, but the pathophysiology is poorly understood.In this case report, we present a 73-year-old man with falciform ligament abscess following cholangitis from an obstructive ampullary carcinoma. The patient was referred to the Royal Adelaide Hospital from a country hospital, with progressive jaundice, anorexia and nausea. Prior to transfer, he deteriorated with cholangitis, dehydration and renal failure. On arrival, his abdomen was exquisitely tender along the course of the falciform ligament. His blood tests revealed an elevated white cell count of 14.9 x 103/μl, bilirubin of 291μmol/l and creatinine of 347 μmol/l. His CA 19-9 was markedly elevated at 35,000 kU/l. A non-contrast computed tomography (CT) demonstrated gross biliary dilatation and a collection tracking along the path of the falciform ligament to the umbilicus.The patient was commenced on intravenous antibiotics and underwent an urgent endoscopic retrograde cholangiopancreatogram (ERCP) with sphincterotomy and biliary stent drainage. Cholangiogram revealed a grossly dilated biliary tree, with abrupt transition at the ampulla, which on biopsy confirmed an obstructing ampullary carcinoma. Following ERCP, his jaundice and abdominal tenderness resolved. He was optimized over 4 weeks for an elective pancreaticoduodenectomy.At operation, we found abscess transformation of the falciform ligament. Copious amounts of pus and necrotic material was drained. Part of the round ligament was resected along the undersurface of the liver. Histology showed that there was prominent histiocytic inflammation with granular acellular eosinophilic components. The patient recovered slowly but uneventfully.A contrast CT scan undertaken 2 weeks post-operatively (approximately 7 weeks after the initial CT) revealed left portal venous thrombosis, which was likely to be a delayed discovery and was managed conservatively.We present this patient’s operative images and radiographic findings, which may explain the pathophysiology behind this rare complication. We hypothesize that cholangitis, with secondary portal pyaemia and tracking via the paraumbilical veins, can cause infectious seeding of the falciform ligament, with consequent abscess formation.

Gastrointestinal involvement in langerhans cell histiocytosis: consider treatment as for multi-system disease

Aims Langerhans cell histiocytosis (LCH) is a rare disorder characterised by abnormal proliferation of the Langerhans cell.1 While single system disease has a good prognosis, multisystem disease often requires intensive combination chemotherapy.23 Gastrointestinal (GI) involvement in LCH remains rare4 and its presence alone does not fit criteria for such treatment.3 The clinical picture can vary but most often consists of bloody diarrhoea, non bloody diarrhoea or constipation, protein losing enteropathy, hypoproteinaemia and anaemia.45 It almost exclusively affects children below two years of age and it has been noted that over half of patients with LCH and GI involvement die within one and a half years of diagnosis.45 Here we describe the case of a young female who required combination chemotherapy to control her GI disease. Methods A six month old female infant initially presented with a non-blanching erythematous rash involving the abdomen and groin, later developing bloody diarrhoea, intermittent bilious vomiting and failure to thrive. She was pale, wasted and developmentally delayed with a painless cystic lump on the occiput. There was lymphadenopathy and an enlarged spleen. Investigations revealed anaemia, thrombocytosis, elevated fibrinogen, a raised ESR and hypoalbuminaemia. Florid histiocytic inflammation of the small bowel was identified at endoscopy and a barium swallow showed narrowing of the distal duodenum and proximal jejunum without obstruction. Gut biopsies and skin samples confirmed the diagnosis of LCH. Results Dual therapy consisting of vinblastine and prednisolone was commenced with quick regression of her bone and skin disease. The addition of mercaptopurine and methotrexate was eventually required to control her GI disease. Almost three years post diagnosis she remains on this quadruple regimen as maintenance therapy. Her current disease status is that of regressing disease although her symptoms return towards the end of treatment intervals. Discussion The prevalence of GI involvement may be underestimated given its presentation; mild cases could be overlooked without endoscopic examination and biopsies. We may see a rise in recorded cases with increased availability of endoscopy. From our experience of this case we recommend that combination therapy is considered for cases of LCH with GI involvement.

Diffuse Alveolar Damage of the Lungs in Forensic Autopsies: Assessment of Histopathological Stages and Causes of Death

Introduction. Diffuse alveolar damage (DAD) is a morphological prototype of acute interstitial pneumonia. Hospital autopsies or open-lung biopsies are used to monitor common alveolar damage and hyaline membrane (HM) development histopathologically. The aim of this study was to detect histopathological profiles and frequency of DAD and HM in adult forensic autopsies. Materials and Methods. In total, 6813 reports with histopathological samples in 12,504 cases on which an autopsy was performed between 2006 and 2008 were investigated. Sixty-six individuals >18 years of age who were diagnosed with DAD were included. Hematoxylin- and eosin-stained lung preparations were reexamined in line with the 2002 American Thoracic Society/European Respiratory Society idiopathic interstitial pneumonia consensus criteria. Results. Histopathological examination revealed that 50 cases (75.7%) were in the exudative phase and 16 (24.2%) were in the proliferative phase. Only the rate of alveolar exudate/oedema in exudative phase cases (P = 0.003); those of alveolar histiocytic desquamation (P = 0.037), alveolar fibrosis (P = 0.017), chronic inflammation (P = 0.02), and alveolar fibrin (P = 0.001) in proliferative cases were significantly higher. The presence of alveolar fibrin was the only independent variable in favour of proliferative cases (P = 0.016). Conclusion. The detection of all DAD morphological criteria with the same intensity is not always possible in each case. Forensic autopsies may provide a favourable means for expanding our knowledge about acute lung damage, DAD, and interstitial lung disease.

Ocular lesions following suspected lightning injury in a horse

To describe the gross and histopathological ocular findings in a horse following suspected lightning injury. The eyes of a 2-year-old thoroughbred gelding were clinically and histopathologically evaluated following a severe lightning storm following euthanasia because of visual impairment. Severe corneal edema and hydrops were noted clinically oculus dexter. Indirect ophthalmoscopy revealed bilateral symmetrical raised hyporeflective peripapillary geographic lesions. Histopathologic evaluation revealed corneal edema in the right eye with normal corneal endothelium. Posterior segment evaluation revealed localized, pericentral choroidal lesions characterized by the presence of hemorrhage, early fibrosis, and minimal lymphoplasmacytic, neutrophilic, and histiocytic inflammation with spindle cell proliferation. The retinas overlying the choroidal lesions were necrotic and mostly absent. Peripheral to the focal lesion, the retina abruptly returned to normal architecture peripheral to a zone of apoptotic photoreceptors. Centrally, swollen axons extended into the optic disc. There have been few descriptions of ocular lesions in animals following suspected lightning injury. We believe these findings to be unique because of the type of thermal injury that may be characteristic of lightening injury. We do not know whether these lesions would have progressed over time.

Mycobacterium fortuitum prosthetic valve endocarditis: a case for the pathogenetic role of biofilms

Prosthetic valve endocarditis presents unique challenges for both diagnosis and treatment. A potential role of biofilm has been hypothesized in the pathogenesis of these infections. A patient with infective endocarditis involving a stentless (Freestyle) porcine prosthetic aortic valve with annular abscess and paravalvular leak 8 months after implantation is reported. The infected valve did not show vegetations or perforations, but histiocytic inflammation was seen along the endocardial surfaces of the valve. Auramine-rhodamine staining revealed many acid-fast organisms associated with the inflammation. There was also an acellular matrix material with ultrastructural features of biofilm. Blood cultures grew Mycobacterium fortuitum, a biofilm-associated microbe. The role of biofilm in prosthetic valve endocarditis is discussed. The importance of microscopy for prosthetic valves, even when no vegetations are present, is highlighted along with correlation of pathologic findings with culture results.

Epizootic Myocarditis Associated With Encephalomyocarditis Virus in a Group of Rhesus Macaques (Macaca mulatta)

Six cases of fatal myocarditis associated with encephalomyocarditis virus occurred over a 14-month period in a group of outdoor-housed juvenile rhesus macaques. All animals were younger than 3 years of age and died or were euthanized following acute onset of dyspnea or pulmonary effusion (3 of 6) or were found dead without premonitory signs (3 of 6). Gross findings included pulmonary congestion (6 of 6), variable degrees of pleural effusion (4 of 6), multifocal pale tan foci throughout the myocardium (3 of 6), hepatomegaly and hepatic congestion (3 of 6), and pericardial effusion (1 of 6). Histologically, affected myocardium was infiltrated multifocally by lymphoplasmacytic and histiocytic inflammation admixed with necrotic and degenerate myofibers and infrequent mineralization (6 of 6). Pulmonary edema was present in all animals. Encephalomyocarditis virus was confirmed in 6 of 6 hearts by immunohistochemistry, and virus was isolated from one case by polymerase chain reaction. Sequencing of virus isolated from 1 affected animal indicated infection with a novel encephalomyocarditis virus. Encephalomyocarditis virus should be considered as a differential etiology in outbreaks of myocarditis and pulmonary edema in juvenile primates.