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Host-Parasite Relationships
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
One of the more unique mechanisms for spread of a parasite, and one which is damaging to the host, was developed by the neurotrophic rabies virus. The virus, which grows in the host′s brain and its salivary glands, causes changes in the host′s behavior so that it attacks other potential hosts, inoculating infected saliva during the attack. In most of the host species of the rabies virus, the damage to the nervous system that causes these changes is finally fatal to the host. However, in bats and skunks, which are probably the hosts in which the rabies virus maintains itself between epidemics, damage is limited and spread is not dependent on changes in the host′s behavior. The occurrence of some damage as a result of parasitization does not change the fact that it is usually not in the interest of a parasite to severely damage its host.
Bacteria are harmless
Published in Dinesh Kumar Jain, Homeopathy, 2022
In example one, Hahnemann observed that after a dog bite, part was cleaned and removed from the body still the patient suffered from hydrophobia and died. That's why he concluded that external microorganisms were not responsible for hydrophobia and death. Then he presumed that the cause of hydrophobia was within the person and not related to dog bite. Truth was missed by Hahnemann. But it was the reality. Rabies, also known as hydrophobia, is an acute highly fatal viral disease of the central nervous system. It is transmitted to man by bites or licks of rabid animals. Rabies virus spreads from the site of infection via the peripheral nerves toward the central nervous system. Bite wounds should not be immediately sutured to prevent extra trauma, which may help spread the virus into the deeper tissues (Park, 1997, pp. 207–210). In this example, dissection at the site of dog bite exposed nerve endings that facilitated virus transmission to the central nervous system. “Once the virus reaches the central nervous system, it replicates almost exclusively within the gray matter and then passes centrifugally along autonomic nerves to reach other tissue” (Corey, 1983, p. 1136), causing death.
Neuroinfectious Diseases
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Jeremy D. Young, Jesica A. Herrick, Scott Borgetti
Rabies virus is present in high concentrations in the saliva of clinically ill mammals due to viral shedding from nerve endings in the oral mucosa and local replication in the salivary glands.2 Rabies is typically acquired from an animal bite, but it can rarely be transmitted via large mucous membrane exposures or aerosolized virus.
Child survivor of rabies in India: a case report
Published in Paediatrics and International Child Health, 2020
Biju John, Shyam Kumar, Sudeep Kumar, S. S. Dalal, Aneesh Mohimen
In the last few decades, reports of cases of rabies who survived beyond 6 months have been increasing. A review of the world literature estimates that there were 27 rabies survivors beyond 6 months, most of whom have significant neurological sequelae [5]. Many of these cases were related to dog bites and patients had not received the complete WHO-recommended post-exposure prophylaxis [6–11]. A lack of adherence to WHO guidelines and improving supportive care has probably contributed to this group of rabies survivors. According to WHO, a diagnosis of rabies should be: (i) suspected if it is compatible with the clinical case definition; (ii) probable if the clinical suspicion is accompanied by contact with a rabid animal; and (iii) confirmed if a suspected or probable case is confirmed in a laboratory [1]. Although ante-mortem laboratory diagnosis of rabies can be difficult, it can be made by one of the following: demonstration of (i) rabies virus or antigen or RNA in CSF, saliva, nuchal skin or a tissue specimen; (ii) rabies antibody in serum or CSF in unvaccinated individuals; or (iii) rabies antibody in the CSF or a four-fold rise (7–10 days apart) in the serum antibody titre in those who have been vaccinated [1,6].
Current status of human rabies prevention: remaining barriers to global biologics accessibility and disease elimination
Published in Expert Review of Vaccines, 2019
Charles E. Rupprecht, Naseem Salahuddin
While not ignoring the limitations of overall supply availability in LDCs, the basic quality of current biologics, as evident in Table 1, is more than adequate to meet the basic goals of the GEHRD program [17,79,80]. Future products would obviously benefit the global initiative, if able to meet the cost and schedule recommendations needed for LDCs, using a variety of realistic approaches [92]. Today, highly purified, serum-free, thermo-stable Vero cell-based vaccines are poised to become the next major human rabies product to be licensed in over 40 years [93]. Other approaches will take longer. For example, simian-based recombinant adenovirus vaccines, expressing the rabies virus glycoprotein, have demonstrated pre-clinical safety and efficacy after a single administration, in comparison to conventional-licensed biologics [94]. Additionally, phase one human clinical trials have begun with rabies virus RNA as an immunogen [95]. An imaginative tactic of using flaviviruses as a platform to express rabies virus glycoprotein could fill some major NTD needs, for both the New and Old World Tropics alike [96,97]. Recombinant rabies virus vectors also offer opportunities for human and veterinary interventions, such as combined vaccines against rabies and hemorrhagic fever viruses, as well as options for oral immunization of both wildlife and dogs [98,99].
Multi-Patient Rabies Exposure on a Colorado River Rafting Expedition: Urgent vs. Emergent Transport Decision Making in an Austere Setting
Published in Prehospital Emergency Care, 2018
Emily A. Pearce, Aaron N. Farney, Laura Banks, Andrew J. Harrell
Once introduced to a human or animal via a bite or other exposure, the rabies virus travels proximally along the neurons of the peripheral nervous system until it reaches the CNS.20 The time during which the virus travels along the peripheral nervous system is called the incubation period. The incubation period is highly variable, ranging from 1 week to 3 months and as long as 1 year.4,20 The duration of the incubation period is directly affected by the bite location; the farther the bite is located from the CNS, the longer the incubation period.20 Hence, a patient who sustained a bite in the foot will have a longer window before becoming symptomatic than a victim who was bitten in the face. During the incubation period, the infected person or animal is neither symptomatic nor capable of transmitting the disease.20 It is during this time that rabies can be treated and halted from progressing.