Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental Lassa virus infections of squirrel monkeys, guinea-pigs, and the African multimammate rat, Mastomys natalensis, were studied virologically and pathologically. In the monkeys, early viral lymphoreticulotropism, hepatotropism, nephrotropism, and viraemia were noted. At the time of death, viral titres in nearly all target organs were associated with necrotic changes: splenic lymphoid necrosis, renal tubular necrosis, myocarditis, arteritis, and hepatocytic regeneration. In convalescent monkeys, organ titres diminished slowly, and viraemia persisted at 28 days. At this time, renal and splenic regeneration was occurring and a new lesion, choriomeningitis, was present.Guinea-pigs infected with Lassa virus developed respiratory insufficiency with pulmonary oedema, alveolar hyaline membranes, myocarditis, and focal calcification of myocardial fibres and hepatocytes. Dying animals contained Lassa virus in virtually every organ tested, whereas survivors at 56 days were free of virus and had high complement-fixing antibody titres.Infection of neonatal Mastomys did not cause any clinical disease or pathological lesions despite the presence of virus in the blood, lymph nodes, liver, spleen, lung, brain, urine, and throat secretions throughout the 74-day study. Infected adult Mastomys also remained normal but had virus in many organs. In one animal, virus persisted until the termination of the study at 103 days. Several animals developed a mild meningoencephalitis. The pattern of infection and virus shedding in M. natalensis is ideal for maintenance of the virus in nature; together with the epidemiological field data this emphasizes the incidental nature of the exposure and infection of man.
 ...
PMID:Comparative pathology of Lassa virus infection in monkeys, guinea-pigs, and Mastomys natalensis. 82 25

Three South African patients with severe Rickettsia conorii infection had complicated courses of illness with 2 fatal cases and 1 with gangrene of multiple digits. Immunofluorescent organisms of R. conorii were demonstrated in vascular endothelium of brain, leptomeninges, renal glomerular arterioles and capillaries, renal arteries and veins, myocardial capillaries and arteries, pulmonary alveolar capillaries, pancreatic septa, splenic arterioles, and dermis. Rickettsiae were also observed in hepatic sinusoidal lining cells, splenic and lymph node macrophages, and the blood vessels of the partially viable zone of the amputated digits. Pathologic lesions included cerebral and cerebellar perivascular mononuclear leukocytes, mild mononuclear leptomeningitis, glomerular arteriolitis, vascular and perivascular mononuclear cell-rich inflammatory foci in the kidney, pancreas, skin, and myocardium, hepatocellular necrosis, and pulmonary edema. The sites of lesions and rickettsiae showed strong topographical correlation. Thrombi and hemorrhage occurred in a minority of the sites of vascular injury. Rickettsiae were the apparent direct cause of meningoencephalitis, peripheral gangrene, and other foci of vascular injury. Fatal R. conorii infection with disseminated organ involvement emphasizes the pathogenic potential of this disease.
 ...
PMID:Correlation of the distribution of Rickettsia conorii, microscopic lesions, and clinical features in South African tick bite fever. 388 74

Rocky Mountain spotted fever occurs during seasonal tick activity. A history of exposure to tick-containing habitats within the 3- to 12-day incubation period is a key epidemiological factor. The signs of fever, headache, myalgia, nausea, vomiting, and anorexia at onset of infection are difficult to distinguish from those of self-limited viral infections. Rash usually appears later and, if present, progresses through a sequence of stages and distribution that are never pathognomonic. The effects of disseminated Rickettsia rickettsii infection of endothelial cells include increased vascular permeability, edema, hypovolemia, hypotension, prerenal azotemia, and, in life-threatening cases, pulmonary edema, shock, acute tubular necrosis, and meningoencephalitis. In severe cases, fluid management is a challenge. The clinical diagnosis, which is difficult, is rarely assisted by laboratory findings because antibodies are usually detected only in convalescence, and immunohistologic methods for detection of rickettsiae are unavailable in most clinics. Doxycycline is the treatment of choice except for pregnant or allergic patients, who are treated with chloramphenicol.
 ...
PMID:Rocky Mountain spotted fever: a seasonal alert. 761 84

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
 ...
PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

Fifty 3-4-mo-old piglets died of accumulative sodium poisoning, but none of the 60 adult pigs with the same feeding and management did. The average ambient temperature throughout the period was 32 C. The herd had been regulary fed whey, ground corn and vegetables, but for at least 2 d the pigs were deprived of water and then water was offered ad libitum. Twenty hours later 20 piglets had died and the remaining exhibited classical nervous signs and died within 14 h. Only the piglets had a high degree of dehydration caused by water deprivation and exacerbated by the high average ambient temperature. Pulmonary edema was evident in most piglets. Acute cerebral edema and meningoencephalitis were present in all animals, but there was no polioencephalomalacia. The sodium accumulation was caused by the continuing intake of whey which contained 10,810 mg sodium/L. To produce the whey, 2 kg of sodium chloride had been added to every 100 kg of milk.
 ...
PMID:Accumulative sodium poisoning in Brazilian swine fed whey. 1130 26

Pleuropulmonary amebiasis is the common and pericardial amebiasis the rare form of thoracic amebiasis. Low socioeconomic conditions, malnutrition, chronic alcoholism, and ASD with left to right shunt are contributing factors to the development of pulmonary amebiasis. Although no age is exempt, it commonly occurs in patients aged 20 to 40 years, with an adult male to female ratio of 10:1. Children rarely develop thoracic amebiasis: when it does occur there is an equal sex distribution. The infection usually spreads to the lungs by extension of an amebic liver abscess. Infection may pass to the thorax directly from the primary intestinal lesion through hematogenous spread, however. Lymphatic spread is one possible route. Inhalation of dust containing cysts and aspiration of cysts or trophozoites of E histolytica in the lungs are some other hypothetical routes. The lung is the second most common extraintestinal site of amebic involvement after the liver. Usually the lower lobe, and sometimes the middle lobe of the right lung, are affected, but it may affect any lobe of the lungs. The patient develops fever and right upper quadrant pain that is referred to the tip of the right shoulder or in between the scapula. Hemophtysis is common. The diagnosis of thoracic amebiasis is suggested by the combination of an elevated hemidiaphragm (usually right), hepatomegaly, pleural effusion, and involvement of the right lung base in the form of haziness and obliteration of costophrenic and costodiaphragmatic angles. Infection is usually extended to the thorax by perforation of a hepatic abscess through the diaphragm and across an obliterated pleural space, producing pulmonary consolidation, abscesses, or broncho-hepatic fistula. Empyema develops when a liver abscess ruptures into the pleural space. Rarely, a posterior amebic liver abscess can burst into the inferior vena cava and develop an embolism of the inferior vena cava and thromboembolic disease of the lungs with congestive cardiac failure or corpulmonale. Diagnosis by finding E histolytica in stool specimens is of limited value. In a limited number of cases amebae might be found in aspirated pus or expectorated sputum. "Anchovy sauce-like" pus or sputum may be found. Presence of bile in sputum indicates that the pus is of liver origin. Serological tests are of immense value in diagnosis. Liver enzymes are usually normal and neutrophilic leucocytosis may or may not be found. ESR is invariably elevated. Anti-amebic antibodies can be detected by ELISA, IFAT, and IHA. Amebic antigen can be detected from serum and pus by ELISA. Detection of Entamoeba DNA in pus or sputum may be a sensitive and specific method. Pleuropulmonary amebiasis is easily confused with other illnesses and is treated as pulmonary TB, bacterial lung abscesses, and carcinoma of the lung. A single drug regimen with metronidazole with supportive therapy usually cures patients without residual anomalies. Aspiration of pus from empyema thoracis may be needed for confirmation and therapeutic purposes. The pericardium is usually involved by direct extension from the amebic abscess of the left lobe of the liver, sometimes from the right lobe of the liver, and rarely from the lungs or pleura. An initial accumulation of serous fluid due to reactive pericarditis followed by intrapericardial rupture may develop either (1) acute onset of severe symptoms with chest pain, dyspnea, and cardiac tamponade, shock, and death, or (2) progressive effusion with thoracic cage pain, progressive dyspnea, and fever. Chest radiograph, ultrasound examination, and CT scan usually confirm the presence of a liver abscess in continuity with the pericardium and fluid within the pericardial sac with or without the fistulous tract. Echocardiography may demonstrate fluid in the pericardial cavity. Patients should be cared for in the ICU and ambecides should be started without delay. Pericardiocentesis usually confirms the diagnosis and improves the general condition of the patient. Aspiration of the accumulated fluid should be performed urgently in cardiac tamponade; repeated aspiration may be needed. Surgical drainage should be done if needed. Acanthamoeba, a free-living ameba, may also infect the lungs in the form of pulmonary nodular infiltration and pulmonary edema in association with amebic meningoencephalitis in immunocompromised patients. It usually spreads to the meninges of the brain by way of the blood from its primary lesion in the lung or skin. Early diagnosis and institution of treatment may be life saving for these patients. A literature review shows that HIV/AIDS patients are not prone to infection with E histolytica. It is now clear that there are an increasing number of HIV-seropositive patients among amebic liver abscess patients, however, which suggests that although the incidence of intestinal infection is not high among HIV-seropositive or AIDS patients they are more susceptible to an invasive form of the disease.
 ...
PMID:Thoracic amebiasis. 1209 41

Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal meningoencephalitis complicated with neurogenic pulmonary oedema. Its pathogenesis, especially the CNS involvement, is not clearly understood. The aim of this study was to set up a mouse EV71 infection model with CNS involvement. EV71 virus was administrated orally to neonatal mice. The EV71-infected mice manifested a skin rash at an early stage and hind limb paralysis or death at a later stage. Immunohistochemical staining and virus isolation demonstrated that EV71 replicated in the small intestine, induced viraemia and spread to various organs. Kinetic studies showed that EV71 antigen was first detected in the intestine at 6 h, in the thoracic spinal cord at 24 h, in the cervical spinal cord at 50 h and in the brain stem at 78 h post-infection. Leukocyte infiltration was evident in the spinal cord and brain stem. Furthermore, EV71 virus could be transmitted to littermates within the same cage.
 ...
PMID:A murine oral enterovirus 71 infection model with central nervous system involvement. 1471 21

A 29-year-old woman was admitted to our hospital with a 7-day history of elevated temperature to 39.5 degrees C associated with headache and nausea. She had been diagnosed with tuberous sclerosis complex 10 years earlier. Her unconsciousness progressed, and she was diagnosed as having aseptic meningoencephalitis. The next day, she had a generalized seizure with severe hemoptysis, and she suddenly fell into severe respiratory failure (PaO2/FiO2 = 76.9). Transbronchial lung biopsy revealed the findings of lymphangioleiomyomatosis. It was suggested that neurogenic pulmonary edema accompanied with venous flow obstruction by lymphangioleiomyomatosis lesions resulted in diffuse pulmonary hemorrhage with resultant gross hemoptysis accelerating to severe hypoxemia.
 ...
PMID:Acute respiratory failure with gross hemoptysis in a patient with lymphangioleiomyomatosis as part of tuberous sclerosis complex. 1546 81

Highly pathogenic avian influenza (HPAI) was diagnosed in broiler breeders, submitted to the National Veterinary Research and Quarantine Service in South Korea. Grossly, the dead breeders had lesions consistent with HPAI, including pancreatic mottling, splenomegaly, pulmonary edema and congestion, and hemorrhages in the mucosa of the proventriculus, gizzard and small intestine, and on the serosal surface. Microscopically, there were necrotized hepatitis and pancreatitis, lymphocytic meningoencephalitis, myocarditis, and interstitial pneumonia. Influenza viral antigen was demonstrated in areas closely associated with histopathologic lesions. The AI virus was isolated from cecal tonsils, feces, trachea, and kidney of the chickens. The isolated virus was identified as the highly pathogenic H5N1, with a hemagglutinin proteolytic cleavage site deduced amino acid sequences of QREKRKKR/GLFGAGLFGAIAG. In order to determine the pathogenicity of the isolate, eight 6-week-old specific pathogen free chickens were inoculated intravenously with the virus, and all the birds died within 24 hr after inoculation. This is the first report of an outbreak of HPAI in the chickens in South Korea.
 ...
PMID:An outbreak of highly pathogenic avian influenza subtype H5N1 in broiler breeders, Korea. 1632 36

We report the echocardiographic findings in a 27-year-old woman with viral meningoencephalitis and a positive test for cardiac troponin. Initially, the basal parts of the left ventricle were severely hypokinetic, whereas contraction in the mid-ventricle and apex was normal. A second echocardiogram obtained 19 days after the development of pulmonary edema showed a generalized, severe myocardial thickening, the left ventricular ejection fraction being normal. Three months after the initial examination the "hypertrophy" had disappeared. The serial echocardiograms along with a positive cardiac troponin led to the diagnosis of myocarditis, which can very rarely present with the echocardiographic picture of severe left ventricular thickening.
 ...
PMID:Transient left ventricular "hypertrophy" in a woman with meningoencephalitis. 1691 32


1 2 Next >>