China
Africa
Explore chapters and articles related to this topic
Diagnostic Approach to Rash and Fever in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Lee S. Engel, Charles V. Sanders, Fred A. Lopez
Rocky Mountain spotted fever, the most lethal rickettsial disease in the United States, is caused by Rickettsia rickettsii [31–36]. Infection occurs approximately 7 days after a bite by a tick vector (Dermacentor or Rhipicephalus). As of 2010, cases of RMSF are reported as spotted fever rickettsiosis (SFR) to capture cases of RMSF, R. parkeri rickettsiosis, Pacific Coast tick fever, and rickettsialpox [37]. The incidence of SFR has increased since 2000 from 495 reported cases to 4269 reported cases in 2016 [38]. Patients who have frequent exposure to dogs and live near wooded areas or areas with high grass may be at an increased risk of infection. The RMSF is more common in men and is most prevalent in the southern Atlantic and southern central states. North Carolina and Oklahoma are the states with the highest incidence, accounting for over 35% of the cases. Greater than 90% of patients are infected between April and September. During this season, there are increased numbers of ticks. Furthermore, research has demonstrated a link between warmer temperatures and increased tick aggressiveness [39].
Pneumonitis In Rickettsial Infections
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
The causative agent Rickettsia rickettsii is transmitted to man via the bite of a tick. Dermacentor variabilis (dog tick) in the East, D. andersoni (wood tick) in the West, and Amblyomma americanum (Lone Star tick) in the Southwest are vectors and reservoirs of RMSF. The spring-summer (April to September) prevalence reflects the peak period of tick activity.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Borrelia burgorferi is spread by ticks and is caused by Lyme disease. Rickettsia rickettsii is also usually spread by ticks. Clostridium tetani enters the body through wounds. Neisseria meningitidis and Corynebacterium diphtheriae both enter via the respiratory tract.
Tick transmission of toxoplasmosis
Published in Expert Review of Anti-infective Therapy, 2019
Studies on the possible transmission of T. gondii from infected ticks to mammalian hosts are limited. Given the incidence of this parasite in the human population and the neurologic consequences of latent infection [68,69], it is important to identify if ticks play a role in the distribution of T. gondii. Among the questions to be answered by future research are which species of ticks are most likely to be viable transmitters, including the study of Ixodes scapularis (Blacklegged or Deer tick) – another tick with a rapidly expanding habitat within the US [70]. Early studies indicate a short lifespan of T. gondii within the tick. Newer studies to determine if the parasite has developed mechanisms to survive long-term inside these vectors are needed. Also, if ticks are firmly established as vectors of T. gondii, determining if the parasite can be transmitted to offspring transovarially will provide a better understanding of which life stage ticks are able to transmit the disease. Transmission time for ticks to convey the parasite to a host after attachment will also need to be established. Recent studies have found rapid transmission time after tick attachment for some tick-borne pathogens, such as Rickettsia rickettsii (Rocky Mountain Spotted Fever) in just 10 min of attachment if the tick has been feeding on prior hosts [71] and Powhassan virus in just 15 min of tick attachment [72].
More than just Borrelia? A study of co-infection and etiology in erythema migrans patients from southernmost Sweden
Published in Infectious Diseases, 2019
Lukas Frans Ocias, Ram Benny Dessau, Charlotte Sværke Jørgensen, Karen Angeliki Krogfelt, Katharina Ornstein
The study patients were clinically diagnosed with EM by experienced physicians, thus reflecting the day-to-day practice at Swedish clinics. Further, as 43% of the cultured biopsies were verified by PCR, we can be sure that ticks were attached to these patients for a time of sufficient duration to transmit Bbsl. However, the samples tested were obtained in the years 1994–1997 and it is possible that the presence and distribution of tick-borne organisms in southernmost Sweden has changed over the years. This has to be kept in mind when extrapolating the results to a more contemporary setting. Moreover, long-term storage of the samples could have reduced the sensitivity of the molecular analysis. However, as all samples were stored in −80 °C, we do not expect this to have been a major problem. It is also important to keep in mind that some patients exposed to SFG rickettsiae or A. phagocytophilum could have seroconverted or displayed an increase in IgG titer prior to the initial visit thus eluding detection in our study. Finally, Rickettsia rickettsii was used as antigen which could have reduced the sensitivity of our serological assay to other species of SFG rickettsiae. Nevertheless, due to the general homology among the SFG rickettsiae we expect our assay to be capable of detecting most SFG rickettsiae, including Rickettsia helvetica, the most common SFG rickettsiae in field-collected ticks from Sweden.
DRESS syndrome associated with influenza virus
Published in Baylor University Medical Center Proceedings, 2019
Raghavendra L. Girijala, Aishwarya Ramamurthi, David Wright, Young Kwak, Leonard H. Goldberg
Laboratory testing demonstrated positive influenza A and B antigens, transaminitis, and eosinophilia (1.26 × 109/L); blood cultures and serological testing for Rickettsia rickettsii, human immunodeficiency virus, and hepatitis A, B, and C were negative. Epstein-Barr virus (EBV) serology was consistent with past infection. A punch biopsy revealed a lymphocytic perivascular infiltrate in the dermis, with prominent extravasation of red blood cells; fibrinoid necrosis was not appreciated. Given the clinical constellation (with a RegiSCAR score of 4), treatment was started with 60 mg methylprednisolone intravenously twice a day, resulting in improvement over the course of a week. She was subsequently switched to oral prednisone (to be tapered over 6 weeks) and discharged for outpatient management.