Tick-borne diseases, which afflict humans and other animals, are caused by infectious agents transmitted by tick bites. They are caused by infection with a variety of pathogens, including rickettsia and other types of bacteria, viruses, and protozoa. Because individual ticks can harbor more than one disease-causing agent, patients can be infected with more than one pathogen at the same time, compounding the difficulty in diagnosis and treatment. 16 tick-borne diseases of humans are known, of which four have been discovered since 2013.
As the incidence of tick-borne illnesses increases and the geographic areas in which they are found expand, health workers increasingly must be able to distinguish the diverse, and often overlapping, clinical presentations of these diseases. Several high-profile deaths have been caused by the tick–human transmission of disease, including the death of former Senator Kay Hagan in the United States in 2019 at the age of 66Ticks tend to be more active during warmer months, though this varies by geographic region and climate. Areas with woods, bushes, high grass, or leaf litter are likely to have more ticks. Those bitten commonly experience symptoms such as body aches, fever, fatigue, joint pain, or rashes. People can limit their exposure to tick bites by wearing light-colored clothing (including pants and long sleeves), using insect repellent with 20%–30% DEET, tucking their pants legs into their socks, checking for ticks frequently, and washing and drying their clothing (in a hot dryer). Signs and Symptoms: First symptoms appear 5-10 days after tick bite, including fever more than 102°F, headache, and rash. Macular rash, present in 90 percent of patients, begins on the wrists and ankles and spreads inward to trunk, face, palms and soles. Skin lesions often become papular, petechial, or purpuric. Other symptoms that may develop include abdominal pain, diarrhea, conjunctivitis, confusion, meningismus, respiratory failure, renal dysfunction, and myocarditis. Common abnormalities, not specific for RMSF, include depressed leukocyte count, thrombocytopenia, elevated liver enzymes, and hyponatremia. In fulminant cases, widespread vasculitis causes intravascular coagulation and death.
Diagnostic Test: Diagnosis must be made prior to laboratory confirmation, based on clinical presentation and patient history. Serologic tests available to confirm a diagnosis of RMSF include IHA, IFA, and latex agglutination. Antibodies appear within 7-10 days of onset of illness and decline within 2 months. The length of time required and the potential hazard to laboratory personnel make culturing the organism impractical for clinical management.
Treatment: Prompt treatment has reduced mortality from 25 percent to 5 percent. Tetracyclines are recommended in adults with suspected RMSF. Chloramphenicol is the preferred treatment in children under 8 years of age. Intravenous chloramphenicol is recommended when central nervous system symptoms are present. Treatment should continue for 5-7 days or at least 48 hours after resolution of fever. Untreated patients can require weeks to months to recover. Survivors develop permanent immunity against future attacks.
