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Query: UMLS:C0026936 (Mycoplasma)
 14,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The excretion of cellular per litre of urine amounted in healthy persons to, in round figures, one million epithelial cells (2.5 cells per visual field) in both sexes, one million leukocytes in males, one million erythrocytes in females and 0.5 million in males. The maximal excretion was calculated to be 5-6 million per litre. In acute infections the number of epithelial cells and leukocytes in the urine rose to more than the double. Pathological microscopic haematuria, judged by exceeding of the maximal value for normal excretion during the acute phase (24 or more erythrocytes per visual field), occurred in no case of mycoplasma infection, in about 4% of measles, mononucleosis, serous meningitis and hepatitis cases, in about 8% of mumps and streptococcal infections, and in more than 20% of influenza A2 cases. Statistical significance or probable significant existed between influenza and other diseases. The haematuria was unrelated either to the general degenerative or to the specific inclusion-provocative reaction within the renal and urinary tract epithelium. The cause is sought in an involvement of glomeruli with increased diapedesis. The special position of influenza may be explained by the marked haemorrhagic reactions produced by this infection. In one case persistent haematuria combined with increased content of inclusion-bearing cells occurred after influenza. Immunoglobulin deposition in glomerular mesangium may perhaps be one explanation of this haematuria.
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PMID:Cellular elements in the urine in health and in acute infectious diseases, especially with respect to the presence of haematuria. A study with application of millipore procedure and Papanicolaou staining. 5 90

Two cases of Mycoplasma hominis meningitis in the newborn are described. These infants demonstrate the need to consider M. hominis as a cause of neonatal meningitis, especially if the Gram stain is negative, conventional cultures yield no growth, and there is a history of maternal infection. CSF cultures on appropriate medium can quickly confirm the diagnosis.
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PMID:Mycoplasma hominis. A cause of neonatal meningitis. 43 11

Details are given of all serologically confirmed Mycoplasma pneumoniae infections in children referred to Bristol hospitals during an epidemic lasting 18 months. 44 children, many below school age, had lower respiratory infections. The majority had cough and malaise which had failed to respond to antibiotics given before referral. Chest x-rays showed no pathognomonic features: segmental or patchy consolidation was common; 3 cases of lobar consolidation. Cold agglutinins were raised in 9 out of 12 cases. In the majority of cases the total leucocyte count was normal and the absolute neutrophil count raised. Mean duration of symptoms was 4.2 weeks (range 1-16). Treatment with erythromycin or tetracycline appeared to have little effect in most cases. Seven nonrespiratory manifestations were seen in 6 children. These were meningitis (2 cases), Stevens-Johnson syndrome (4 cases, 1 case complicated by toxic epidermal necrolysis), and acute haemolytic anaemia (1 case).
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PMID:Mycoplasma pneumoniae infections in children. 62 17

Twenty goats and four sheep were experimentally infected with Mycoplasma mycoides var. capri and examined histopathologically. Death occurred or a moribund state developed in most of them within a week after parenteral inoculation with mycoplasmas. Histopathological examination revealed severe serofibrinous inflammation on the serosa and interstitial connective tissue at the site of inoculation. Marked inflammatory edema with infiltrating polymorphs was found in the early stage of infection. As the infection progressed, the lesion became a cellulitis; necrosis, sometimes with focal liquefaction, was a constant feature. Organization with infiltration by lymphocytes and histiocytes had begun in some tissues. Acutely infected organs had evidence of systemic involvement. Lesions included splenitis, lymphadenitis, meningitis, metastatic foci in the intestine and urinary bladder, and parenchymatous degeneration in the liver, heart, and kidneys. Mycoplasmas were isolated from many tissues of critically ill animals. Other goats which had received mycoplasmas by instillation escaped severe illness. Even so, mycoplasmas were isolated from one or two of their tissues at necropsy. The great variation in clinical and pathological response was apparently dependent upon the route of inoculation. Recovery of mycoplasmas from two contact control goats which remained healthy is suggestive of the clinically undectable carrier state. As other workers have reported, the clinical and pathological changes in sheep were similar to those in parenterally inoculated goats.
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PMID:Pathology of goats and sheep experimentally infected with Mycoplasma mycoides var. capri. 78 42

Pocket mice are facultative homoiotherms with the ability to drop their metabolic rate dramatically while at rest or in response to environmental stresses. Under these conditions, they characteristically enter a state of prolonged torpor. These animals require no drinking water and they can live in darkness for many months without apparent ill effect. They tolerate a wide range of ambient temperature, ralative humidity, and oxygen pressure and have survied without food for a mean of 14 d at an ambient temperature of 20 degrees C (68 degrees F). Studies carried out on the pocket mouse colony used for the Apollo XVII flight revealed, in the animals tested, no serological evidence of viral disease, no pathogenic enterobacteria or respiratory Mycoplasma on culture, a 25% incidence of sarcosporidiosis, and a 2% incidence of chronic meningitis or meningoencephalitis. The conclusion reached is that the pocket mouse is a highly adaptive animal and very well suited for space flight.
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PMID:The effects of cosmic particle radiation on pocket mice aboard Apollo XVII: II. Characteristics and tolerances of the pocket mouse and incidence of disease. 80 8

Measurement of cerebrospinal fluid lactic acid by gas liquid chromatography and by an enzymatic Monotest lactate test was evaluated for the early detection of bacterial meningitis in 396 patients. Spinal fluid specimens from 62/62 patients with a bacterial or mycoplasma etiology yielded lactate levels greater than the upper limits of normal, whereas specimens from 334 patients with no bacterial involvement gave values within the normal range. The duration of elevated CSF lactate values coincided with the clinical response to therapy. When considered along with the history and physical examination of the patient, determination of lactic acid proved to be a rapid and reliable diagnostic test for the early detection of untreated as well as partially treated pyogenic meningitis.
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PMID:Cerebrospinal fluid lactic acid levels in meningitis. 89 5

This is a case-report about a 4 year old boy with "cherry red" epiglottis, purulent meningitis and pleuropneumonia. Purulent meningitis and pleuropneumonia are not complications of treatment of "cherry red" epiglottis but an entity caused by Hemophilus influenzae-infection and is called Kleinschmidt's syndrome (Hemophilus influenzae type B-infection-syndrome). This severe illness is successfully treated if recognized early enough. At present, chloramphenicol is the therapy of choice. Intubation or tracheotomy are important but supportive measures.
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PMID:[Kleinschmidt's syndrome (author's transl)]. 98 30

Infants with myelomeningocele are liable to develop bacterial colonisation of the lesion which, in the case of Gram-negative bacteria, often progresses to meningitis because of the infants' immature immune status. The time and origin of the bacterial colonisation usually are uncertain. This study reports seven cases of meningitis caused by Mycoplasma hominis, an organism not previously reported to cause meningitis. The commensal status of Mycoplasma hominis in the vagina of many women, and its isolation from the mother of one patient in this group, suggests that the infant acquired the organism in the birth canal and that infection developed over a period of days. Routine cultures from the sac or wound did not show the presence of organisms until after the child had developed signs and symptoms of meningitis. Commensal organisms from the vagina may lie dormant for several days within the closed myelomeningocele and their more virulent strains may then produce meningitis. It is suggested that neonatal meningitis may be caused by organisms acquired during birth, as well as by those to which the infant is exposed later.
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PMID:Mycoplasma meningitis in infants with spina bifida. 110 9

Polymerase chain reaction (PCR) was prospectively performed with cerebrospinal fluid (CSF) from 51 patients whose CSF was available for analysis and was submitted for viral culture and/or herpes simplex virus (HSV) serology and 20 patients whose CSF was submitted exclusively to the Clinical Biochemistry Laboratory. Primers were used that flanked a 92 bp segment of the HSV DNA polymerase gene (35 cycles). Amplified products were electrophoresed on agarose gel, blotted onto nylon membrane, and probed with a 32P-labelled sequence internal to the primers. For nested PCR, 1 microliter of PCR product was amplified for an additional 35 cycles before electrophoresis and Southern blot analysis. Review of the clinical records revealed that 15 patients had central nervous system (CNS) infections. Specific HSV DNA sequences were detected in CSF specimens of three of the individuals [PCR(2), nested PCR(1)]. Two of these patients had disseminated HSV infection including encephalitis and one patient had aseptic meningitis. The diagnoses of the 12 patients with CNS infection who did not have HSV DNA detected in CSF included encephalitis [varicella-zoster virus (1), cytomegalovirus (1), Mycoplasma pneumoniae (1)], meningitis [Neisseria meningitidis (1), Coccidioides immitis (1), Enterovirus (1), aseptic meningitis (1)], varicella-zoster radiculitis (2), human immunodeficiency virus dementia (2), and transverse myelitis due to Epstein-Barr virus (1). Importantly, HSV DNA was also not detected in the CSF of the 36 patients who did not have CNS infection and 20 samples submitted exclusively to the Clinical Biochemistry Laboratory. Our findings demonstrate the utility of PCR as a rapid, non-invasive method for the routine laboratory diagnosis of CNS infection due to HSV.
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PMID:A prospective study of the polymerase chain reaction for detection of herpes simplex virus in cerebrospinal fluid submitted to the clinical virology laboratory. 133 47

Group G streptococci which have been isolated from the oral flora of rats are also normal inhabitants of the human skin, oropharynx, gastrointestinal tract, and female genital tract. This group of streptococci can cause a wide variety of clinical diseases in humans, including septicemia, pharyngitis, endocarditis, pneumonia, and meningitis. Ten days after oral gavage with 7,12-dimethylbenz[a]anthracene, 12 of 22 two-month-old, female, outbred, viral-antibody-free rats presented with red ocular and nasal discharges and marked swelling of the cervical region. Various degrees of firm, nonpitting edema in the region of the cervical lymph nodes and salivary glands as well as pale mucous membranes and dehydration were observed. Pure cultures of beta-hemolytic streptococci were obtained from the cervical lymph nodes of three rats that were necropsied. A rapid latex test system identified the isolates to have group G-specific antigen. These streptococcal isolates fermented trehalose and lactose but not sorbitol and inulin and did not hydrolize sodium hippurate or bile esculin. A Voges-Proskauer test was negative for all six isolates. Serologic tests to detect the presence of immunoglobulin G antibody to rat viral pathogens and Mycoplasma pulmonis were negative. Histopathologic changes included acute necrotizing inflammation of the cervical lymph nodes with multiple large colonies of coccoid bacteria at the perimeter of the necrotiz zone. To our knowledge, this is the first report of naturally occurring disease attributed to group G streptococci in rats.
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PMID:Group G streptococcal lymphadenitis in rats. 175 39


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