Mouse Mycoplasma pulmonis EcoELISA Kit (DEIA2115)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Species Reactivity
Intended Use
This kit is to be used for the Detection of Viral/Mycosomal Infections in Laboratory Animals.
Contents of Kit
1. Microtiter Strips
2. Dilution Buffer
3. HRP Conjugate
4. Positive Control Conjugate
5. Substrate Solution
6. Stop Solution
7. Wash Solution 40X
8. Positve Control Serum
9. Negative Control Serum
Upon receipt store entire microwell plate and remnant removawell-strips at -20°C or below.


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Contagious Bovine and Caprine Pleuropneumonia: a research community's recommendations for the development of better vaccines


Authors: Jores, Joerg; Baldwin, Cynthia; Blanchard, Alain; Browning, Glenn F.; Colston, Angie; Gerdts, Volker; Goovaerts, Danny; Heller, Martin; Juleff, Nick; Labroussaa, Fabien; Liljander, Anne; Muuka, Geoffrey; Nene, Vish; Nir-Paz, Ran; Sacchini, Flavio; Summerfield, Artur; Thiaucourt, Francois; Unger, Hermann; Vashee, Sanjay; Wang, Xiumei; Salt, Jeremy

Contagious bovine pleuropneumonia (CBPP) and contagious caprine pleuropneumonia (CCPP) are major infectious diseases of ruminants caused by mycoplasmas in Africa and Asia. In contrast with the limited pathology in the respiratory tract of humans infected with mycoplasmas, CBPP and CCPP are devastating diseases associated with high morbidity and mortality. Beyond their obvious impact on animal health, CBPP and CCPP negatively impact the livelihood and wellbeing of a substantial proportion of livestock-dependent people affecting their culture, economy, trade and nutrition. The causative agents of CBPP and CCPP are Mycoplasma mycoides subspecies mycoides and Mycoplasma capricolum subspecies capripneumoniae, respectively, which have been eradicated in most of the developed world. The current vaccines used for disease control consist of a live attenuated CBPP vaccine and a bacterin vaccine for CCPP, which were developed in the 1960s and 1980s, respectively. Both of these vaccines have many limitations, so better vaccines are urgently needed to improve disease control. In this article the research community prioritized biomedical research needs related to challenge models, rational vaccine design and protective immune responses. Therefore, we scrutinized the current vaccines as well as the challenge-, pathogenicity- and immunity models. We highlight research gaps and provide recommendations towards developing safer and more efficacious vaccines against CBPP and CCPP.

Causes and Clinical Features of Childhood Encephalitis: A Multicenter, Prospective Cohort Study


Authors: Britton, Philip N.; Dale, Russell C.; Blyth, Christopher C.; Clark, Julia E.; Crawford, Nigel; Marshall, Helen; Elliott, Elizabeth J.; Macartney, Kristine; Booy, Robert; Jones, Cheryl A.

Background. We aimed to determine the contemporary causes, clinical features, and short-term outcome of encephalitis in Australian children. Methods. We prospectively identified children (<= 14 years of age) admitted with suspected encephalitis at 5 major pediatric hospitals nationally between May 2013 and December 2016 using the Paediatric Active Enhanced Disease Surveillance (PAEDS) Network. A multidisciplinary expert panel reviewed cases and categorized them using published definitions. Confirmed encephalitis cases were categorized into etiologic subgroups. Results. From 526 cases of suspected encephalitis, 287 children met criteria for confirmed encephalitis: 57% (95% confidence interval [CI], 52%-63%) had infectious causes, 10% enterovirus, 10% parechovirus, 8% bacterial meningoencephalitis, 6% influenza, 6% herpes simplex virus (HSV), and 6% Mycoplasma pneumoniae; 25% (95% CI, 20%-30%) had immune-mediated encephalitis, 18% acute disseminated encephalomyelitis, and 6% anti-N-methyl-d-aspartate receptor encephalitis; and 17% (95% CI, 13%-21%) had an unknown cause. Infectious encephalitis occurred in younger children (median age, 1.7 years [interquartile range {IQR}, 0.1-6.9]) compared with immune-mediated encephalitis (median age, 7.6 years [IQR, 4.6-12.4]). Varicella zoster virus encephalitis was infrequent following high vaccination coverage since 2007. Thirteen children (5%) died: 11 with infectious causes (2 influenza; 2 human herpesvirus 6; 2 group B Streptococcus; 2 Streptococcus pneumoniae; 1 HSV; 1 parechovirus; 1 enterovirus) and 2 with no cause identified. Twenty-seven percent (95% CI, 21%-31%) of children showed moderate to severe neurological sequelae at discharge. Conclusions. Epidemic viral infections predominated as causes of childhood encephalitis in Australia. The leading causes include vaccine-preventable diseases. There were significant differences in age, clinical features, and outcome among leading causes. Mortality or short-term neurological morbidity occurred in one-third of cases.

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