Ecchymotic Hemorrhages Research Articles

Dual infection with attaching and effacing Escherichia coli and enterotoxigenic Escherichia coli in post-weaning pigs

Post-weaning diarrhoea in pigs occurred on two farms in Hokkaido, Japan, in 1994. Four piglets aged 35 or 45 days were examined after death. At necropsy, ecchymotic haemorrhages were seen on the mucosal surface of the caecum and colon. Histopathologically, numerous Gram-negative bacilli adhered to the brush border of the small intestines, but the brush border itself was intact. Typical attaching and effacing (AE) lesions were seen in the caecum and colon. Immunohistochemically, the bacilli which adhered to the brush border gave positive results with antisera against serogroup O149 of Escherichia coli; the bacilli which caused the AE lesions, however, belonged to serogroup O45. It was concluded that the disease resulted from dual infection with attaching and effacing E. coli (AEEC) and enterotoxigenic E. coli (ETEC).

Tissue-invasive Tritrichomonas foetus in four aborted bovine fetuses.

Bovine trichomoniasis is a venereally transmitted protozoal infection that is usually associated with infertility and occasionally causes pyometra and midto late-term abortions. Some cows can carry the infection throughout gestation and remain infected after parturition. Abortions caused by Tritrichomonas foetus are usually diagnosed by microscopic identification of trichomonads in placental fluids, uterine exudate, or fetal stomach contents or by culture. In addition, characteristic placental and fetal lung lesions have been described, and fluorescent antibody and immunohistochemica1 techniques have been used to identify T. foetus in tissue sections. The purpose of this report is to describe 4 cases of tissue-invasive T. foetus infection in aborted bovine fetuses. A male fetus (fetus 1) was aborted in the seventh month of gestation by an Angus-cross heifer and submitted to the Tulare Branch of the California Veterinary Diagnostic Laboratory System (CVDLS) for postmortem examination. At necropsy, spleen and liver were enlarged, and the lungs were firm with patchy, suffusive hemorrhages, interlobular edema, and pale tan areas. Multifocal mucosal necrosis ranging from 3 mm in diameter to 20 x 15 mm was present in the rumen, and focal mucosal hemorrhages were present in the rumen, omasum, and abomasum. Multifocal hemorrhages and segmental hyperemia were seen in the small intestine, and petechial hemorrhages were present in the meninges. A 7-month female fetus (fetus 2) and a 6-month male fetus (fetus 3) were aborted by Holstein cows from the same dairy and were submitted to CVDLS for necropsy and diagnostic tests. Necropsy of fetus 2 revealed 2 liters of cloudy, yellow, viscous fluid in the rumen and abomasum and rare fibrin flecks adherent to the surface of a mottled liver. Fetus 3 had firm, diffusely yellow lungs with interlobular edema and patchy, swollen, hemorrhagic areas in the cranial lobes. The lungs floated in formalin. The rumen was diffisely hemorrhagic with a granular mucosa and patchy to paintbrush serosal hemorrhages. The omasal wall was diffusely reddened and hemorrhagic. Numerous ecchymotic hemorrhages were visible from the serosal and mucosal surfaces of the small intestine. Mesenteric lymph nodes were mildly enlarged and contained focal hemorrhages. Rare hemorrhages were present in the spiral colon and capsule of the spleen. The liver was mottled and slightly yellow.

Hepatic Lipidosis in Turkeys

Two flocks of 14,000 twenty-week-old turkey hens each experienced increased mortality due to hepatic lipidosis. Some hens showed signs of dyspnea and cyanosis before death. Necropsy revealed dark muscles and enlarged livers with pale areas and numerous hemorrhages. Petechial and ecchymotic hemorrhages were also found on the abdominal fat and epicardium. Lung congestion and edema were prominent. In the heart and blood vessels, the blood was uncoagulated. Mortality was elevated for 12 days and resulted in the death of 0.7% of the turkey hens in one flock and 1.7% in the other. Vitamin E administered in water at a dose of 25 IU per hen appeared to reduce mortality. The nutritional and environmental factors that may contribute to the development of hepatic lipidosis in turkeys are discussed.

Pathology of Eastern Equine Encephalitis in Emus (Dromaius novaehollandiae)

Pathology of Eastern Equine Encephalitis in Emus (<i>Dromaius novaehollandiae</i>)

Bovine petechial fever (Ondiri disease)

Bovine petechial fever is a Rickettsial disease of cattle, which has been diagnosed, only in Kenya, East Africa. Other countries in the region share some of the biotopes in which the disease occurs, and may well have the infection. The disease is characterised by widespread petechial and ecchymotic haemorrhages on the mucosal surfaces, and throughout the serosal and subserosal surfaces of the body organs and cavities. It may be fatal in up to 50% of untreated cases. The causal organism may be demonstrated most readily in the cytoplasm of polymorphonuclear granulocytes of the peripheral blood, as well as other leucocytes, and has been classified as Cytoecetes ondirii, a member of the tribe Ehrlichiae. Circumstantial and other evidence suggests that the disease is transmitted by an arthropod vector, which has yet to be identified. The blood of a naturally infected wild ruminant, the bushbuck, Tragelaphus scriptus has been shown to remain infective for at least 2 years, and other species such as the African buffalo, Syncercus caffer for at least 5 weeks. These and possibly other species, may serve as the amplifying and reservoir hosts.

Pasteurella multocida septicaemia in fallow deer (Dama dama)

Thirteen of 100 fallow deer, aged between 6 months and 10 years, died over a 5 week period. The deaths occurred in 2 outbreaks 3 weeks apart. Both outbreaks were preceded by at least 3 days of cold wet and windy weather, and were associated with water-logged pastures. Affected animals were usually found dead, with a frothy blood-stained nasal discharge. In the 8 deer necropsied, gross lesions included widespread subserosal petechial haemorrhages, severe pulmonary congestion and oedema with froth-filled airways, and fibrinous pneumonia and pleurisy in 4 deer. Two deer, also, had extensive subcutaneous petechial and ecchymotic haemorrhages and oedema of skeletal musculature. Histologically, the most significant lesions were present in the lungs. Moderate to severe pulmonary congestion and oedema, with fibrinous exudation into alveoli and septal oedema, were present in all deer. In some deer these changes were accompanied by a diffuse infiltration with polymorphonuclear leucocytes. Pasteurella multocida was isolated from a range of tissues from 7 of 8 deer examined. The remaining animal had been treated with antibiotics 8 hours before death. The isolates had identical polyacrylamide gel electrophoresis patterns and were of the same antigenic type-Carter group A, Heddleston type 3,4.

Melioidosis in a koala

A 4-year-old female koala (Phascolarctos cinereus ) was seen on the ground about 40 hours after capture and release for routine survey purposes. It died shortly afterwards. A 5-month-old infant koala in its pouch was alive but died 36 hours later despite regular feeding with a milk supplement. PM examination of the adult revealed congestion and haemorrhage in lymph nodes, lungs, myocardium, kidneys and adrenal glands as well as ecchymotic haemorrhages on most serosal surfaces. Histological changes included necrotic foci in liver and spleen. A brown pigment which is a feature of normal koala liver was present in hepatocytes generally. Distinctive eosinophilic intranuclear hepatocyte inclusions were present which were unrelated to necrotic foci. Occasional bacterial colonies were associated with the necrotic foci. Gram negative bacteria were seen in liver, spleen and lung sections. Escherichia coli and Pseudomonas pseudomallei were isolated from liver and kidney samples. Enterobacter cloacae was isolated from the liver and P. putida and Streptococcus sp. from the lung. The adult koala was serologically negative for melioidosis using the complement fixation test but 8 (16%) of 50 free-living koalas in the same colony were positive, although apparently healthy. Histological examination of the infant koala liver revealed small foci of necrosis; no bacteria were visible and no bacteria were cultured.

Severe thrombocytopenia in young calves experimentally infected with noncytopathic bovine viral diarrhea virus

Seven calves between 1 week and 2 months of age were infected with a noncytopathic field isolate of bovine viral diarrhea virus (BDV) in order to evaluate the effect of BDV infection on the concentration of circulating platelets in the blood. All calves were determined to be free of BDV and neutralizing antibodies to BDV before infection. Platelet counts were performed on a daily basis over a 30-day period beginning at the time of infection. By 2 weeks postinfection, all calves showed a significant drop in the number of circulating platelets and a marked hyperplasia of megakaryocytes in the bone marrow. In three of the seven calves, thrombocytopenia was severe (less than or equal to 5,000/microliters) for 1 to 6 days. In two of these three animals, extensive petechial and ecchymotic hemorrhages were observed on all mucosal surfaces and on various internal organs during the period of severe thrombocytopenia. BDV was consistently isolated from the platelets during the early phases of the infection, and viral antigen was occasionally detected on platelets by a fluorescent-antibody assay. The results demonstrate that BDV infection is associated with decreases in platelet numbers and suggest that platelets may serve as carriers of circulating virus.

Haemorrhagic lesions resulting from Trypanosoma vivax infection in ayrshire cattle

Infection of Ayrshire cattle with a stock of Trypanosoma vivax from the Galana Ranch, Kenya, resulted in an acute disease characterised by profound anaemia and haemorrhage, which reached maximum severity between 3 and 5 weeks after infection. Bleeding from the ears, nose and rectum occured. At necropsy, petechial and ecchymotic haemorrhages were widespread, but were particularly severe in the gastrointestinal tract. In confirmation of the gross findings, congestion, haemorrhage and degenerative changes in most tissues and organs were found histologically. Thrombi were seen in the lymphatic vessels and clots of fibrin were present in the ventricles of the brain. The anaemia was a consequence of frank blood loss through haemorrhaging, exacerbated by erythrophagocytosis of deformed red blood cells, whose occurrence was indicative of microangiopathic changes. Animals were euthanisedbetween 23 and 36 days after infection when they became recumbent with PCV values as low as 9%. There is no doubt that animals affected by this syndrome in the field would die within a few weeks of infection, if left untreated.

The effects of the calcium entry blockers, nilvadipine and nitrendipine, on endotoxin-induced disseminated intravascular coagulation

We previously reported that calcium entry blockers (CEBS) protected against endotoxin-induced mortality in rats. In this investigation, the i.v. injection of endotoxin (ETX) in control awake male Wistar rats was found to produce pathophysiological changes indicative of disseminated intravascular coagulation (DIC). The latter included increased serum fibrin (ogen) degradation products (FDP), decreased plasma fibrinogen, reduced blood platelet count as well as microscopic findings of fibrin microthrombi in small blood vessels of visceral organs. Gross pathological examination revealed pronounced hemorrhagic congestion of the gastrointestinal tract and petechial and ecchymotic hemorrhages in other visceral organs. Pretreatment with the CEBs, nilvadipine (FR 34235) and nitrendipine, inhibited the elevation in serum FDP and decrease in plasma fibrinogen but did not prevent the thrombocytopenia produced by ETX. The gross pathological manifestations of DIC were also inhibited by pretreatment with the CEBs. The results suggest that the protective effect of CEBs against endotoxin-induced mortality in rats may be related to inhibition of DIC caused by the lipopolysaccharide.

Septicemic pasteurellosis in elk (Cervus elaphus) on the United States National Elk Refuge, Wyoming.

Septicemic pasteurellosis caused by Pasteurella multocida is believed responsible for the deaths of 48 elk (Cervus elaphus) on the National Elk Refuge near Jackson, Wyoming (USA) during 1986 and 1987. Clinical signs included depression and salivation; necropsy findings included congestion and petechial and ecchymotic hemorrhages in lymph nodes, diaphragm, lungs and endocardium. Pasteurella multocida was isolated from femur marrow of eight carcasses and a variety of tissues from eight others.

Quantitative Platelet Disorders

Thrombocytopenia may be caused by abnormal platelet production, accelerated removal owing to immunologic or nonimmunologic reasons, or sequestration of platelets in the spleen. Bleeding associated with thrombocytopenia usually presents as petechial or ecchymotic hemorrhages or epistaxis. Immunologic and nonimmunologic cases of thrombocytopenia may be diagnosed with routine hematology, bone marrow cytology, and platelet specific tests. Thrombocythemia may also be associated with platelet functional abnormalities, contrasting the normal platelet function noted in reactive thrombocytosis.

Omental response to long-term implantation of diffusion chambers containing allogeneic and xenogeneic bone marrow

Diffusion chambers were filled with bone marrow from 2-4 weeks old rabbits and dogs, and implanted into the peritoneal cavity of adult animals for 28-45 days. The diffusion chambers were encapsulated by omentum in both dogs and rabbits, and the character of the omental response was influenced by the chamber contents. Empty chambers were enveloped by omentum composed principally of fibrous-fatty tissues, with a thin fibrous layer adherent to the chamber walls. Chambers containing allogeneic marrow evoked a marked cellular and angiogenic response in the adherent omentum. In rabbits, lymphocytes were the predominant cell type. In dogs, large ecchymotic haemorrhages were found immediately adjacent to the chambers, with aggregations of lymphocytes in the surrounding dense fibrous tissue. Diffusion chambers containing xenogeneic marrow were surrounded by a thick fibrous tissue capsule, without any adhesion of the omental tissues to the chambers. The internal layer of the omental capsule was necrotic and chambers were bathed in serosanguinous fluid. It was concluded that antigens on fragments of marrow cells escaping from the diffusion chambers had evoked the various omental responses which were observed.

A coccolithophorid algal dermatitis of the spiny dogfish, Squalus acanthias L.

Abstract. Skin diseases of sharks and algal diseases of animals are reviewed. A specific progressive skin disease of wild, laboratory‐maintained and display‐aquaria populations of spiny dogfish, Squalus acanthias L., observed during a 2.5‐year period at Woods Hole, Massachusetts, is described. Skin lesions, from 1mm to over 1cm in diameter, developed in the following sequence: petechial and ecchymotic haemorrhages; dome‐shaped vesicles; larger lesions with central ulceration; and hyperpigmented granulations in the final repair stage. A coccolithophorid algal agent could be demonstrated in skin lesions and is described. Since both sharks and coccolithophorid algae are primitive organisms, the possible evolutionary implications of algal symbionts modified to become pathogens are discussed.

Blue wing disease of chickens: Signs, pathology and natural transmission

A new peracute disease of chickens is described. The disease is called blue wing disease (BWD) and has occurred frequently in all parts of Sweden since the first outbreak in 1972. Most of the outbreaks have affected broilers at the age of 2 to 4 weeks with a mortality rate of 1 to 60%. BWD is characterised by skin lesions in the form of ecchymotic haemorrhages, most frequently on the wings. These lesions are often infected secondarily by bacteria, leading to a gangrenous dermatitis. Infectious bursal disease, inclusion body hepatitis and infectious aplastic anaemia, which also have been associated with gangrenous dermatitis, are not found in the outbreaks of BWD. BWD is closely related to certain parent flocks, which suggests that the disease is transmitted vertically. The parent flocks which transmit the disease do not show any signs of disease themselves.

CLINICO‐PATHOLOGICAL EFFECT OF BLUETONGUE VIRUS SEROTYPE 20 IN SHEEP

Fifty-four Merino crossbred sheep were inoculated with bluetongue virus serotype 20 (BTV-20) by the intravenous, subcutaneous and intradermal routes. BTV-20 was successfully transmitted by Culicoides (Avaritia) spp. No. 5 to two additional sheep. Clinical and pathological effects were studied. In the artificially infected sheep, clinical signs were observed after an incubation period of 6 to 10 days and consisted of pyrexia, oral and subcutaneous hyperaemia mild oedema of the ears, face and lips, and coronitis. The major internal pathological changes were petechial and ecchymotic haemorrhages in the tunica media of the pulmonary artery near its junction with the heart and mild haemorrhage and mild oedema in the intestines, coronet, lips, cheeks and ears. Viraemia was detected between day 2 and day 14 post inoculation. The two sheep infected by insect transmission were mildly affected and became viraemic between 16 and 19 days after transmission. No deaths occurred and under experimental conditions BTV-20 caused only mild disease in housed sheep. To date there has been no reported outbreak of natural bluetongue infection in Australia. Compared to other serotypes BTV-20 appears to be of low pathogenicity in sheep.

AN EPORNITIC OF DUCK PLAGUE ON A WISCONSIN GAME FARM

In April, 1973, an acute disease with a high rate of mortality appeared in a flock of 233 ducks and geese at a private game farm. Most of the flock (220) were black ducks (Anas rubripes) and mortality was restricted to them. In May, the remaining live birds were placed in isolation but mortality continued in black ducks and occurred in other species. The overall rate of mortality for black ducks was 93% and the case fatality rate was 97%. No hemorrhaging from either the bill or vent was observed. The most commonly observed gross lesions were extensive fibrino-necrotic plaques covering the mucosal surface of the esophagus, posterior colon and cloaca. Petechial and ecchymotic hemorrhages on visceral organs, particularly the heart, were also common. Virus isolation was attempted from tissues of three black ducks. Duck plague virus was isolated from liver, kidney, spleen and intestine of each. Sixteen black ducks survived the outbreak. Seven of these birds had significant levels of neutralizing antibody to duck plague virus.

Brugia pahangi Infections in Mongolian Jirds and Dogs Following the Ocular Inoculation of Infective Larvae

Infective larvae of Brugia pahangi collected from mosquitoes readily infected Mongolian jirds or dogs when placed on the intact eyeball. Histological studies in jirds showed that the larvae quickly penetrated into the orbital tissues. Further study in jirds showed that the larvae migrated rapidly via the veins or lymphatic vessels to the lungs, produced pulmonary ecchymotic hemorrhages within 5 min, and then accumulated in the pleural cavity where they induced a profuse pleural exudate. A considerable number of larvae persisted in the heart or pulmonary artery of jirds. Some of the larvae migrated to the cervical, iliolumbar, and renal lymphatics of jirds and a few larvae traveled to the peritoneal cavity. Thus, ocular inoculation of infective 3rd-stage larvae in jirds produced an infection predominantly of the heart, lungs, and pleural cavity. Third-stage larvae that had developed for 2 days in the peritoneal cavity of jirds were not infective for this host by ocular inoculation. Although inoculation of infective 3rd-stage larvae regularly induced patent infections in both jirds and dogs, the numbers of circulating microfilariae were low. Experimental infections of Brugia pahangi, a lymphatic-dwelling filaria, are usually achieved by the introduction of the infective thirdstage larvae by either the bite of infected mosquitoes or surgical methods such as syringe injection or inoculation onto artificial puncture wounds (Ewert and Singh, 1969). The subcutaneous route of larval inoculation by syringe is most commonly used for establishing infection. By this route, infections have been induced by injecting infective larvae in man (Buckley, 1958), lower primates, dogs, cats, and rodents (cf. reviews by Nelson, 1969; Ash and Riley, 1970). Successful infections were also produced in Mongolian jirds by intraperitoneal (McCall et al., 1973) and oral (Gwadz and Chernin, 1972) routes of infection. This paper presents evidence indicating that infective third-stage larvae of B. pahangi placed upon the corneal surface of the eye penetrate the conjunctival epithelium of jirds and dogs and subsequently produce patent infections Received for publication 29 May 1973. * Published as paper 1043, University of Georgia Institute of Comparative Medicine. This work was supported in part by the U. S.Japan Cooperative Medical Science Program, administered by the Geographic Medicine Branch, NIAID, Contract 69-92; Grant AI 09280 from NIAID, NIH; and in part by NIH-General Support Grant 3-R01-AM14901. t Department of Biology, Millersville State College, Millersville, Pa. $ Deceased. with microfilaremia. Observations on the migratory behavior and pathways of the early developing stages of the parasite are also presented. MATERIALS AND METHODS The animals used in this work were juvenile jirds (Meriones unguiculatus) procured from commercial sources and laboratory-reared mongrel dogs (Males, approximately 4 months old). Infective third-stage larvae of Brugia pahangi were obtained from Aedes aegypti (Liverpool strain) 10 days after the infective blood meals, by procedures previously described (Ah and Thompson, 1973). Inocula were prepared in Hanks' balanced salt solution (HBSS) by placing thoroughly washed infective larvae in 1-ml syringes. To permit prompt settling of larvae at the tip of the syringe barrel, the syringes containing the suspension were placed upright in the test tube rack. The larvae concentrated at the bottom of syringes were placed on the surface of the right eyeball of jirds by expelling a minute amount of HBSS. In dogs, drops of larval suspension were instilled onto the eyeball. Inoculations were done without anesthesia. Microfilarial counts were made by examining Giemsa-stained thick films of 20-mm3 samples of blood. At necropsy, all jirds were examined with the aid of a dissecting microscope. Generally, the protocol was as follows: (1) examination of all major lymphatic vessels and nodes, based upon prior studies of their location using Evans blue (Ah and Thompson, 1973); (2) examinations of heart blood, heart, lungs, and washings of pleural and peritoneal cavities; and (3) search of the subcutaneous tissues and removed skin, directly and by soaking. Recovery of the larvae from heart

Case Report: Isolation and Identification of Infectious Bursal Disease Virus in Lebanon

On the 3rd week of May 1973, a pathological condition in chickens similar to infectious bursal disease (IBD) occurred, for the first time, in the Bekaa Valley, East of Lebanon. The disease appeared suddenly in an enzootic form. The major clinical signs were: anorexia, depression, ruffled feathers, severe prostration. Morbidity was 90%o of the affected flocks. Mortality (18-32%) occurred 5-7 days after the onset of clinical signs. In general the affected flocks were 5 to 7 weeks old. Postmortem examination revealed the following gross lesions: dehydration, darkened discoloration of the pectoral and thigh muscles with frequent hemorrhages, enlargement of the kidneys, enlargement of the bursa with edema and hyperemia. The bursae were cream-colored instead of the normal white color, and some showed petechial or ecchymotic hemorrhages on the mucosal surface. Hemorrhages were very frequent on the mucosa at the juncture of the proventriculus and gizzard. The histopathology of the affected bursa showed degeneration of the follicles with interfollicular edema mixed with phagocytic cells.

Copper deficiency and the central nervous system. Myelination in the rat: morphological and biochemical studies.

Less histologically demonstrable myelin was present in the central nervous system of newborn rats having a mean brain copper concentration only 20% that of normal. Tremor, spontaneous tail elevation and a loss of aggressive character were consistent features. Significant decreases in typical myelin lipids, sulfatide, and especially galactocerebroside were found in agreement with the histological deficit. The composition of gangliosides and phospholipids were unaltered except for a slight enrichment in phosphatidylcholine. Galactosylation of ceramide, in vitro, was depressed in copper-deficient brain and the relevance of this finding is discussed. Swayback, a non-febrile, ataxic disorder of newborn and young lambs, was first reported by Bennetts in Western Australia (4, 5). The disease is associated with low levels of copper in tissue of both ewes and affected lambs (6) due to low copper content in pastures. Supplementation with copper of either the ewe during pregnancy, or the lamb directly, prevents manifestations of the disease (7, 15). Although a well known entity in sheep, a condition resembling swayback also has been reported in copper-deficient goats (26, 37, 41) and pigs (33, 50). The common pathological features of swayback include symmetrical demyelination with subsequent cavitation of the cerebral white matter and degeneration of descending tracts in the spinal cord (28, 42, 43); however, myelin aplasia has also been observed (27). Similar changes have been induced in lambs (31) and guinea pigs (16) born to mothers fed experimental diets deficient in copper, but myelin changes have not been reported in the copper-deficient rat. Demyelination and amyelination accompanying swayback disease in sheep are associated with a depletion of typical myelin lipids such as cerebroside (27). The decrease in lipids may be involved in the pathogenesis of the disease in the nervous system, but the basic defect that results in decreased myelin lipid is not known. Recently, DiPaolo and Newberne (13) observed a variety of clinical and morphological abnormalities in copper-deficient newborn rats which include a high mortality, retarded growth, petechial and ecchymotic hemorrhages in brain, muscle and subcutaneous tissue, focal necrosis in the brain associated with neonatal incoordination of the hind limbs, hemorrhagic necrosis of the liver, cardiac hemorrhage, and severe, widespread vascular dilation in cardiac walls and septae. We also observed behavioral changes in rats having a mean brain copper concentration about 20% of normal. The purpose of this report is to describe further these changes, present the histological myelin anomalies observed in these animals, and correlate this morphological observation with quantitation of brain lipids and the in vitro synthesis of galactocerebroside.