Zoonoses - Science topic
A zoonosis or zoonose is any infectious disease that can be transmitted between species (in some instances, by a vector) from animals to humans or from humans to animals (the latter is sometimes called reverse zoonosis or anthroponosis). In a study of 1415 pathogens known to affect humans, 61% were zoonotic.
Questions related to Zoonoses
Does anyone have experience with CAEV in immortalized cell lines? Some publications show use of goat synovial membrane cells or goat milk epithelial cells, but these cell lines are not available through commercial companies.
We have been pursuing the possibility that a cluster of unusual chronic illnesses among a group of veterinarian colleagues and some of their extended family, might be caused by infection/colonization with a novel type of organism.
Thorough standard medical work-up has not determined the underlying cause of this “syndrome”, involving chronic hematuria, calcium/phosphate metabolism dysregulation, and development of pain and small nodules especially in areas of fascia or loose connective tissue.
However, simple wet-mounts of what Should be sterile tissues from several of those affected showed objects not normal for those areas, including objects staining positive for cellulose or chitin, and small, motile objects moving with a eukaryotic flagellar swimming pattern.
We attempted to culture these tissues and found that surface colonies only rarely developed, and even then, not usually till 6+ weeks after the culture was started. Oddly, contaminant colonies almost never developed on the test-subject agar plates, and, if continued to incubate, they began developing small spheres within the matrix of the agar, followed by visible fern-like ridges, all developing within the deeper layers of the agar. This did not occur in the control plates.
We initially suspected some type of inorganic crystal formation, but still checked for evidence of an organic process by using sterile technique to cut pieces of the agar, which we rehydrated in sterile water and stained with sterile cotton blue.
To our amazement, the piece of agar stained in a pattern of millions of very small blue dots embedded within the matrix of the agar, and within 45 minutes, there was obvious motility and free-swimming of huge numbers of these blue dots. They resemble motile zoospores of some type of spore-producing organism. When that same slide was allowed to dry, the “dots” produced germ-tube like extensions and formed a network of what appeared to be thin hyphae or pseudohyphae.
This finding was repeatable in cultures from several of the affected patients and absent in controls from healthy donors. We hypothesize that this may be some form of oomycete, or other stramnopile relative, and are hoping to find experts in these types of organism/infection who might be able to comment on if they have seen similar patterns in cultured stramnopiles, (or something else) and/or help us connect with anyone else pursuing this type of research.
Hello and regards, our study investigates the relationship between latent toxoplasmosis and psychiatric and psychological mental disorders. It is part of my research (Ashkan Latifi, postgraduate student of psychology at University of Tehran- Iran) in partial fulfilment of the requirements of my master’s degree. By filling in this questionnaire, you have been of great help to me and to those with toxoplasmosis. In addition, by optionally sharing your email with me, you allow me to inform you of any possible toxoplasmosis-associated psychological/psychiatric problems in you under the supervision of two professors of University of Tehran (Dr. Abbas Rahiminezhad, psychologist and Dr. Reza Rostami, psychiatrist) for free. You can participate in this study if you have latent toxoplasmosis (other than congenital toxoplasmosis) and are at least 18 years old. The approximate response time to the questionnaire is ten to fifteen minutes. Thank you in advance for your participation in this research.
Link to the questionnaire: https://docs.google.com/forms/d/1Qvu3J0MuXz56r1d1dZtpWBYHKUmXDByx_3eQ37LRsg0/viewform?edit_requested=true
Do we need to understand zoonotic diseases better to avoid more pandemics in future? Should we all turn vegetarians? Is eating animals the only issue or there are some other human-animal interactions which need to be understood? Will vising the zoos be safe? Or even keeping pet animals?
Please have a logical discussion around these and ask related questions.
I broadly understand the scale at which Zoonoses develop, but would be deeply curious to understand if there is a similar risk of entomopathogenic diseases jumping the biological border to vertebrates (more specifically humans).
Our project description page details the unusual origins of our research project/group- looking for the identity of a (likely novel) organism that may be causing a form of chronic illness.
We have successfully cultured an organism from blood donated by affected individuals, and failed to culture it from healthy control blood samples. The organism appears to grow preferentially in the deep matrix of the agar, and only the sporulation stage is visible as surface colonies.
Microscopically, the organism forms structures resembling pseudohyphae, fruiting bodies, and birefringent walled cysts. We hypothesize that it may be related to myxomycetes, oomycetes, apicomplexia and/or other Stramenopile organisms. This is based on morphology and also early metagenomics studies (done on tissue samples rather than the cultured colonies). We are pursuing additional sequencing studies as well asTEM, but have run into complications with DNA extraction (low yields) presumably due to the tendency for the spore nuclei to be encasked in a crystal-like capsule within the agar matrix, as well as the tiny size of the spores/zoospores (1-3 microns)
A recurring finding is that once the organism has infiltrated the agar matrix in the Petri dish, it begins to form spheres and pseudohyphae-like structures WITHIN the deep layers of the agar matrix. Grossly, the agar plate will look like there is no growth for three to six weeks (though samples of agar removed by sterile loop show infiltration of thousands of nuclei-which can be induced to form motile zoospores within 20 min of re-hydration) during this time. Contaminant growth is very rare during this time window. Then, as moisture is removed from the agar, sphere-like objects with a fibrous outer ring, and then fern-like patterns begin to become visible in the dessicated agar. This happens only in the samples cultured from affected individuals, and not in the sham or negative control samples.
I am wondering if anyone else has seen these patterns before in the deep layers of agar (and ideally confirmed presence of an organism by removing/staining blocks of the affected agar). If so, what organism was growing in the agar and, did you find any way of extracting good yields of DNA from the dried/crystallized agar?
PS- photos below are of surface of agar plate/Petri dish as viewed 100x-250x through dissecting microscope. Cultured tissues represented include blood, subcutaneous adipose collected by needle biopsy, and water from a hot tub that might have been a source of infection.
It is excellent news about the COVID-19 vaccination programme and the vaccination trials where both humoral and cellular immune responses to challenge, after vaccination are observed. These positive responses will be required to neutralise the virus before immune escape mechanisms can be triggered from viral mutation and evolution.
Another similar single stranded positive (+ve SS) virus (HCV) has a continuous emergence of resistant strains of virus in HCV, resulting from the quasispecies that evolve, resulting in escape mutations, due to a rapid change in viral proteins. In the case of HCV, the high level of genetic diversity of the virus hampers the vaccination progress, whereas in the case of SARSCoV-2, genetic variation has also been reported where the coronavirus accumulates about two changes per month but most do not affect the behaviour of the virus, however, one SNP causes a change on the spike from aspartic acid to glycine at position 641 of the coronavirus spike and this is thought to make the virus more transmittable or more severe. G641 variant is now more prevalent than the aspartic acid version, globally. This is a genetically distinct variant but closely related to other variants within the same genotype-designated quasi species. These successful members of the quasispecies arise as a result of weak conservation of sequence and high evolutionary selection. Highly changeable quasispecies, generated as a consequence of evolutionary pressure from human immune responses, such as from antibodies, should be taken into consideration when considering candidates for the vaccine trials.
Although we do not have any evidence that immune pressure causes RNA rearrangement or mutation of the COVID-19 genome, as often occurs in other virus species or between other species, however, it is clear that these events did take place zoonotically, resulting in the SARSCoV-2 emergence after jumping between different animal species. The existence of COVID-19 and ability to infect humans is evidence of this rearrangement through the process of zoonosis with bats, pangolin and civet cats. Frequent and rapid rearrangements in other chronic viral infections, such as, HCV often render therapeutics ineffective.
I am concerned that there may be selection pressure on the virus during the vaccination process resulting in escape variants that are even more resilient and transmittable than the current SARSCoV-2. Administering the vaccine to many immunologically naïve individuals could drive many more escape variants, forced to evolve due to immune pressure but I presume that virus genetic mutation will be monitored throughout the trials. (This process slightly reminds me of the RAG gene recombinant rearrangement activation of genes in antibody and T ell receptor differentiation but an unregulated mirror image of the process in the case of the virus, both achieving a ‘’best fit’ of the antigen). Thus, the immune response of entirely healthy individuals, that receives the vaccine, could drive viral mutation inducing unknown viral escape mechanisms that may impair recognition by human immune systems. The similar SS +ve RNA virus of HCV has rapid and frequent viral mutations.
Should scientists also be cautious about viral RNA rearrangement between different viruses and tread carefully as to which individuals are vaccinated, in case they have a chronic RNA virus that could rearrange with COVID-19? We do know that +ve SS RNA viruses mutate, like HIV and HCV and some of these viruses evolve through rearrangement of the RNA.
Could it be possible that the presence of HIV or HCV virus, as indeed many other virus strains, may enable a more dangerous evolution of escape quasi-species to arise? It was reported that the exclusion of HIV patients as vaccine recipients for COVID-19 has been described as discriminatory but perhaps it should be considered as cautionary, based on basic knowledge and understanding about the behaviour of viruses and its engagement with human immune systems. Anything that may possibly influence a high mutation rate, further enabling viral persistence by evading the innate, humoral and cellular immune responses, should be avoided. Scientists have already witnessed lymphopenia in severely affected patients due to the virus attaching to ACE2 on Th1 cytotoxic cells thus affecting the cellular response in severely affected patients. HIV attaches to CD4+ T cells via the CCR5 receptor also causing lymphopenia.
Should these factors be considered or endorsed in the selection of vaccine recipient candidates in this highly uncertain phase of experimentation, with the above considerations included in the exclusion criteria for the participants?
Do any others have any of these concerns, please discuss.
Highly Pathogenic Avian Influenza (HPAI) commonly known as Bird Flu is a viral infection caused by strains of influenza that occur among birds. Veterinary extension and community interventions have a great effect in changing knowledge and practice toward avian influenza.
A 1969 paper reports prevalence of Zika virus in Malaysia (Marchette NJ, Garcia R, Rudnick A (1969) Isolation of Zika virus from Aedes aegypti mosquitoes in Malaysia. Am J Trop Med Hyg 18: 411–415).
About the bacteria causing rat bite fever, Str. moniliformis, I have read it was renamed as Actinobacillus muris, which also was renamed later as Muribacter muris, is this information right?, or there are different agents causing this zoonose?
Thanks a lot,
I need the Literature related to Studies on Environmental Drivers of Zoonoses. It is actually survey study, so need methodologies to adopted to achieve below goals;
The objectives of the study are
. To identify and evaluate pathogenic and zoonotic diseases
. To establish the prevalence of diseases in wild, live stock and domestic animals
. To access the gravity of animal-human diseases transmission.
So anyone having papers related to the study could please send the same.
I want any suggestions for online websites which contain updated information concerning emerging infectious diseases.
Thanks in advance
Newcastle disease virus is one of the important viruses in poultry it causes outbreaks with high mortality and morbidity moreover,it has zoonotic importance it can affect human result in conjunctivitis with flu-like signs my question is how does it affect human cell ? .Is there are specific receptors for which ? and if so how does it replicate inside human cells .
I know that regarding the concentration of primers I've have to used 4 to 5x more and I've done that. However only one species amplifies. Any suggestions? Thanks in advance! :)
I am looking for a hyper-variable region/suitable gene good enough to conduct phylogenetics for canine babesiosis. Any one with and idea whether ITS-2 can serve that purpose pls!
All researchers are welcome to send camel sera from suspected areas together with retropharngeal and/ or supramammary lymph nodes. Sera will be screened with the buffered acidified plate antigen test and confirmed with the complement fixation test. Lymph nodes will be bacteriological examined for Brucella and isolates identified to the biovar level. The sender will be responsible for sending the samples by a suitable means according to the international regulations. Lab testing will be performed at no charge to the sender. Any additional lab work can be arranged for by the cooperating parties. Results will be included in a collaborative publication. I’m looking forward to hearing from you soon.
Non-host mechanical vectors are frequently overlooked as transmitters and/or disseminators of pathogens in agricultural, sylvatic, and urban systems. This may be particularly important for zoonotic pathogens in agricultural ecosystems, but depending on the geographical location and the particular pathogens involved, there may be a range of possibilities. For example, trachoma is transmitted among humans by synanthropic flies even in some urban settings. We have been studying this at various locations, focusing on zoonotic enteric protists such as Cryptosporidium and Giardia, as well as microsporidia. To gain a more comprehensive understanding of non-host vectors of pathogens around the world, I seek input on diverse specific experiences.
I am looking for experimental evidence (or convincing non-experimental evidence) that the number of fleas or ticks an individual animal harbors is related to that individual's risk of infection by a vector-borne pathogen. Can anyone point me to some compelling literature?
According to Wikipedia, eating feces occurs in a wide range of circumstances: in invertebrates; in vertebrates including great apes; as ancient and modern medical treatments; as sexual fetish: in some mental illness; in pica; in developmentally abnormal children, or normal babies; in trapped miners. While some parasites can be spread this way, I can find no evidence that bacterial infections are. It seems unlikely that indirect ingestion of fecal matter can cause gastrointestinal infections when direct fecal ingestion seem not to. Is there really no evidence base for the public sanitation interventions against diarrheal diseases?
See also my RG question on Ingestion of Feces or Urine.
the wolf scats (from isle royale) were collected since 2000, and frozen but have been thawed by other students in the previous years and stored in fridge 4-5 celsius.My project aims to identify helminth eggs.
i performed volumetric dilution using distilled water, analysed 1ml under compound microscope and found no eggs, so i stored the faecal mixture under fridge conditions for a week. i returned to the mixture, took 1ml out and performed microscopy: found alot of the live organisms under x400 magnification. There were about 10 organisms per ml. is it possible that tiny cysts of ..some protozoan flagellate laid dormant for YEARS and only hatched when i applied distilled water? if so, what parasite could this be? or is this just contamination from other students?
Giardia intestinalis is divided into different groups based on rRNA sequences, although grouping and taxonomy is changing rapidly from year to year.
Rodents are reservoirs of many zoonotic diseases to human and their infested fleas,mites,ticks and lice act as vehicles transmitters of infections to man.What is best apply ant-ratting or insecticide first?
Two patients infected with Ebola virus have now entered the U.S. for treatment, but they are in a highly controlled environment. However, while the press and the public have been very aware of this, we still have black market transfer of "bush meat", fresh animal flesh from Africa to other parts of the world, outside any regulation for potential disease transmission. Could it be that while the media and public focus on a contained and controlled situation that is unlikely to result in an Ebola outbreak outside Africa, we are largely ignoring a more significant Ebola threat via other means of introduction?
In regard to vector borne diseases and their transmission cycle, from your previous experience in general where is the weakest point in this cycle? Is it the vector or the pathogens or maybe the presence of the host?
Thousands of tourists go to protected areas. Many of them move from one area to another and use the same backpacks, raincoats, boots, pants. .. even without cleaning them enough. What mechanism or substance can be used to clean the visitors without damaging the elements that they carry... but reducing human-mediated risk dispersal?
The study of health sciences is often compartmentalized: human diseases, live-stock diseases, wild animal diseases. Some of us grew up thinking that doctors were responsible for human health, and vets for animal health.
But for the past decade, we have had severe diseases that involve both human and animal hosts. In Malaysia, we had the fear of H1N1 or swine flu.
What is being done in your country or institution concerning this compartmentalization of health science studies? What innovative collaborations are being put in place to control diseases that involve human and animal hosts?
I am planning to use a BALB/C mice for inducing humoral or immunogenic responses. In literature it is reported that the authors used female mice for this kind of experiments, and this same procedure is reported in all articles that I read. What is the scientific reason for this? The ethical committee need this justification before they approve my proposal.
Please help identify the egg species from this image .
1 and 2 (not the capillaria egg) look like same species. (2 is next to capillaria egg)
3 and 6 look like same species
sizes- 1 is 90um length by 60um width
-2 is 99um
-3 is 51um
-4 is 87um by 42um
-5 is 81um by 20um
-6 is 54um
These eggs are taken from ethiopian wolf (canis simensis) faeces
1 looks more like hymenolepsis diminuta ( it has hooks)- AND RODENTS are main host + ethiopian wolves are known to eat alot of rodents
2 is very confusing, maybe toxocara
4 is acanthocephala
3, 5, 6 TOXOCARA
The scats were from bale mountains, known for high populations of human, their livestock and dogs living close to the wolf's environment. I am looking for possible routes of transmissions of Ascaris onto the wolves. These eggs are NOT toxocaris, they look exactly like ascaris eggs (A. lumbricoides or suum ) HOWever, i also found toxocaris eggs but i know the route of transmission, i just dont know how ascaris lumbricoides can now be found in canid faeces.
Could be due to wolves ingesting infective larval stage from rodents (Jebessa, 2009)
Could also be due to eating human faeces.
But I am not certain. Is there any source that could back up one of these suggestions?
Legionella occurs in many environments, but the potential to infect humans is variable and complex.