Rickettsia (Spotted Fevers)
The "SPOTS" in spotted fevers are often absent.
Do not withold treatment waiting for "SPOTS".
Rule # 1. NEVER DELAY TREATMENT IF SPOTTED FEVER,
EHRLICHIA OR ANAPLASMOSIS IS SUSPECTED.
UPDATE (March 2019)- QUOTE CDC- " During 2010–2015, CDC received 16,807 case reports of SFR meeting the probable or confirmed case definition. The number of cases reported annually increased from 1,617 in 2010 to 2,275 in 2015. As the number of annual cases increased, the percentage of confirmed cases decreased from 1.9% in 2010 to 0.7% in 2015." https://www.cdc.gov/mmwr/volumes/68/wr/mm6810a3.htm?s_cid=mm6810a3_x
UPDATE (March 2019)- Spotted fever group Rickettsia antigens cross-react, and routine serologic assays cannot provide conclusive species-specific diagnoses. https://www.cdc.gov/mmwr/volumes/68/wr/mm6810a3.htm?s_cid=mm6810a3_x
UPDATE (March 2019)- According to the CDC, in 2000, 495 cases of spotted fever rickettsiosis were reported. In 2017, more than 6,248 cases were reported. https://www.cdc.gov/rmsf/stats/index.html
QUOTE (CDC)- "The goal of SFR surveillance is to provide information to health care providers and public health officials about the temporal, geographic, and demographic occurrence of SFR and to facilitate prevention and control (3). During 2010–2015, only 1.0% of SFR cases reported to CDC via case report forms met the criteria for a confirmed SFR case. The majority of probable cases were not confirmed because of incomplete serologic testing." https://www.cdc.gov/mmwr/volumes/68/wr/mm6810a3.htm?s_cid=mm6810a3_e
UPDATE- March 2017- There are a growing number of new Rickettsia strains (spotted fevers) being discovered in the US and foreign countries. Just in the past month (March 2017) seven more were reported from various countries.
UPDATE- May 2017- Five additional strains of spotted fever were documented.
Spotted Fevers (Rickettsia)
QUOTE (CDC)- "People over the age of 40 years account for the highest number of reported cases, however, children under 10 years old represent the highest number of reported deaths." https://www.cdc.gov/rmsf/stats/index.html
"Long-term neurologic sequelae of RMSF include cognitive impairment; paraparesis; hearing loss; blindness; peripheral neuropathy; bowel and bladder incontinence; cerebellar, vestibular, and motor dysfunction; and speech disorders (7,110,121–124).
These complications are observed most frequently in persons recovering from severe, life-threatening disease, often after lengthy hospitalizations, and are most likely the result of R. rickettsii-induced vasculopathy. Cutaneous necrosis and gangrene (Figure 23) might result in amputation of digits or limbs (105)." (CDC- MMWR- May 2016)
QUOTE (CDC)- "The results of these tests (spotted fevers) can take weeks. If your healthcare provider thinks your illness might be RMSF, he or she should recommend antibiotic treatment before test results are available." https://www.cdc.gov/rmsf/diagnosis-testing/index.html
Rocky Mountain spotted fever, Rickettsia rickettsii, (RMSF) is the most common rickettsial disease in the United States. It is potentially fatal with a mortality rate as high as 30%. Early treatment with appropriate antibiotics is required to prevent the disease progression and should be started as soon as the disease is suspected.
The number of reported cases of many strains of spotted fevers are increasing in the United States. Untreated cases may result in death within 20 days after exposure. The hospitalization rate is over 70%, even in treated patients.
Update- September 2014- Study shows a tick attachment time can be as little as 10 minutes before Rocky Mountain Spotted Fever is transmitted.
A second study (2014) indicates various spotted fevers can be missed using tests to detect Rocky Mountain Spotted Fever. (More information on subpages below.)
Update- May 2016- See detailed information and photos below.
Diagnostic tests for rickettsial diseases, particularly for RMSF, are usually not helpful in making a timely diagnosis during the initial stages of illness.
According to the CDC- Treatment decisions for rickettsial pathogens should never be delayed while awaiting laboratory confirmation. Delay in treatment can lead to severe disease and long-term sequelae or death.
Early signs and symptoms of tickborne rickettsial illnesses are nonspecific, and most cases of RMSF are misdiagnosed at the patient’s first visit for medical care, even in areas where awareness of RMSF is high.
Early and empiric treatment with doxycycline
Can prevent severe morbidity or death!
Understand the availability, limitations, and usefulness of confirmatory diagnostic tests.
RMSF is the rickettsiosis in the United States that is associated with the highest rates of severe and fatal outcomes.
The highest incidence occurs in persons aged 60–69 years, and the highest case-fatality rate is among children aged <10 years, although illness occurs in all age groups (4).
Incidence varies considerably by geographic area ( Figure 1). During 2008–2012, 63% of reported SFG rickettsiosis cases originated from five states: Arkansas, Missouri, North Carolina, Oklahoma, and Tennessee (4). However, SFG rickettsiosis cases have been reported from each of the contiguous 48 states and the District of Columbia (4,9,12,14).
A history of a tick bite within 14 days of illness onset is reported in only 55%–60% of RMSF cases and 68% of ehrlichiosis cases. Therefore, absence of a recognized tick bite should never dissuade health care providers from considering tickborne rickettsial disease in the appropriate clinical context.
In fact, the absence of classic features, such as a reported tick bite, has been associated with delays in RMSF diagnosis and increased risk for death.
Temporally and geographically related clusters of illness have occurred among family members (including their pet dogs), coworkers, or persons frequenting a particular common area.
Described clusters include ehrlichiosis among residents of a golfing community, ehrlichiosis and RMSF among soldiers on field maneuvers, and RMSF among family members.
Infections with R. rickettsii and Ehrlichia species have been observed concurrently in humans and their pet dogs. Recognition of a dog’s death from RMSF has even prompted recognition and appropriate treatment of RMSF in the sick owner. Health care providers should ask ill patients about similar illnesses among family members, coworkers, community residents, and pet dogs.
Although the majority of persons have increased IgG titers by the second week of the illness, persons infected with certain Rickettsia species might have delayed development of significant antibody titers or produce none.
PETS- Tickborne rickettsial infection in dogs can range from inapparent to severe. RMSF in dogs manifests with fever, lethargy, decreased appetite, tremors, scleral injection, maculopapular rash on ears and exposed skin, and petechial lesions on mucous membranes.
RMSF- Infection with R. rickettsii leads to systemic vasculitis that manifests externally as characteristic petechial skin lesions.
If disease progresses untreated, it can result in end-organ damage associated with severe morbidity and death. Pathogen-mediated injury to the vascular endothelium results in increased capillary permeability, microhemorrhage, and platelet consumption.
Late-stage manifestations, such as noncardiogenic pulmonary edema (acute respiratory distress syndrome [ARDS]) and cerebral edema, are consequences of microvascular leakage. Hyponatremia occurs as a result of appropriate secretion of antidiuretic hormone in response to hypovolemia.
Spotted Fever symptoms can include:
- Incubation time is often less than 5 days, but could be longer.
- High fever (>102°F), headaches, malaise and myalgias.
- 25% of patients are reported to develop signs of encephalitis.
- Confusion, lethargy, severe vertigo, ataxia, seizures, cranial nerve palsy, photophobia, dysarthria, paralysis and hearing loss may be noted.
- Gastrointestinal symptoms may include abdominal pain, acute pain resembling appendicitis, diarrhea, nausea, cholecystitis or gastroenteritis, anorexia and vomiting. Splenomegaly and hepatomegaly may occur.
- Absence of rash should not preclude consideration of RMSF; less than 50% of patients have a rash in the first 3 days of illness, and a smaller percentage of patients never develop a rash. Some patients develop a maculopapular rash (mild to severe). It often begins later in the illness on the extremities (palms of hands and soles of feet) and spreads toward the trunk.
- Periorbital and peripheral edema, pain in calves, acute transient hearing loss are also symptoms.
- Meningoencephalitis, acute renal failure, ARDS, cutaneous necrosis, shock, arrhythmia and seizures.
- Cutaneous necrosis and gangrene may be present.
- RMSF-associated neurologic manifestations include renal failure, thrombocytopenia, RMSF-associated vasculitis.
- RMSF might also mimic bacterial or viral meningoencephalitis. Focal neurologic deficits, including cranial or peripheral motor nerve paralysis can occur.
- Pulmonary edema, pneumonitis, shortness of breath may be present.
- Petechial conjunctivitis, optic disc edema, anterior uveitis and retinal vascular dysfunction may occur.
- Long-term neurologic sequelae of RMSF include cognitive impairment; paraparesis; hearing loss; blindness; peripheral neuropathy; bowel and bladder incontinence; cerebellar, vestibular, motor dysfunction and speech disorders.
- Amputation of feet/toes, legs, hands/fingers and arms may be necessary due to cutaneous necrosis and gangrene.
Delay in diagnosis and treatment is the most important factor associated with increased likelihood of death.
Early empiric therapy is the best way to prevent RMSF progression.
Without treatment, RMSF progresses rapidly.
Patients treated after the fifth day of illness are more likely to die
Than those treated earlier in the course of illness.
Lab Findings- Total white blood cell count is typically normal or slightly increased in patients with RMSF. Increased numbers of immature neutrophils can be observed. Thrombocytopenia, slight elevations in hepatic transaminases (aspartate transaminase and alanine transaminase), and hyponatremia might be present.
Laboratory values cannot be relied on to guide early treatment decisions because they are often within or slightly deviated from the reference range early in the course of illness.
Indicators of diffuse tissue injury, such as elevated levels of creatine kinase or serum lactate dehydrogenase, might be present later in the course of illness. Disseminated intravascular coagulation (DIC) can occur.
When cerebrospinal fluid (CSF) is evaluated, a lymphocytic (or less commonly, neutrophilic) pleocytosis (usually <100 cells/µL) can be observed.
CSF protein might be moderately elevated (100–200 mg/dL). The glucose level is typically within normal range.
Testing for Spotted Fever
The first manifestation in nearly all patients is an inoculation eschar (a dark, scabbed plaque overlying a shallow ulcer, typically 0.5–2 cm in diameter), which generally is nonpruritic, nontender or mildly tender, and surrounded by an indurated, erythematous halo and occasionally a few petechiae.
The presence of more than one eschar has been described.
Fever typically develops within a few days of the eschar. Shortly after the onset of fever (approximately 0.5–4 days later), a nonpruritic maculopapular or vesiculopapular rash can develop. The rash primarily involves the trunk and extremities and might involve the palms and soles in approximately half of patients and the face in <20% of patients.
Other common symptoms include myalgia (76%) and headache (86%). Regional lymphadenopathy is detected in approximately 25% of patients. Gastrointestinal manifestations, such as nausea or vomiting, can occur.
Mild thrombocytopenia has been observed in 40%, mild leukopenia in 50%, and modest elevation of hepatic transaminase levels in 78% of cases. Because the clinical description of R. parkeri infection is based on observations from a limited number of cases, the full clinical spectrum of illness is likely incomplete.
Rickettsia Species 364D
The first clinical description of a confirmed case of Rickettsia species 364D infection was published in 2010. Although the full spectrum of illness has yet to be described, 364D infection appears to be characterized by an eschar or ulcerative skin lesion with regional lymphadenopathy.
Fever, headache, myalgia, and fatigue have occurred among persons with confirmed infection. Rash has not been a notable feature of this illness. Illnesses among the few described patients can be relatively mild.
Ehrlichia chaffeensis Ehrlichiosis
Last Updated- February 2019
VECTOR-BORNE AND ZOONOTIC DISEASES
Volume 8, Number 1, 2008
Rickettsia amblyommii Infecting Amblyomma americanum Larvae
ELLEN Y. STROMDAHL, 1MARY A. VINCE,1PEGGY M. BILLINGSLEY,2
NICOLE A. DOBBS,3 and PHILLIP C. WILLIAMSON2
Polymerase chain reaction analysis of Amblyomma americanumadults, nymphs, and larvae from Aberdeen Proving Ground, MD (APG), revealed a very high prevalence of a spotted fever group (SFG) rickettsia. Restriction fragment length polymorphism (RFLP) and sequence analysis identified “Rickettsia amblyommii.”
This organism is not yet described or well studied, and its pathogenicity is unknown; however, investigations of the organism are warranted because of its high prevalence in A. americanum. This tick is extremely abundant at military training facilities in the south, central, and Mid-Atlantic United States, and many soldiers experience multiple concurrent tick bites.
Bites by R. amblyommii-infected A. americanummay account for rates of SFG rickettsia seropositivity
that are higher than reported rates of Rocky Mountain spotted fever (RMSF) cases from the same location. Seroconversion to SFG rickettsia following bites of A. americanummay suggest that R. amblyommii is infectious in humans. Subclinical infection in the numerous A. americanumtick bite victims could contaminate donated blood and compromise immunodeficient recipients.
Detection of R. amblyommiiin questing A. americanumlarvae suggests transovarial transmission. The absence of R. rickettsii, the agent of RMSF, in A. americanummay be due to transovarial interference by R. amblyommii. The likelihood of pathogen transmission by larvae is magnified by their habit of mass attack.
The very small size of the larvae is also a risk factor for pathogen transmission. High R. amblyommii prevalence in populations of A. americanumpresage co-infection with other A. americanum-borne pathogens.
A. americanumnymphs and adults from APG were found to be co-infected with R. amblyommii and Borrelia lonestari, Ehrlichia chaffeensisand Ehrlichia ewingii, respectively, and larval pools were infected with both R. amblyommiiand B. lonestari.
Co-infections can compound effects and complicate diagnosis of tick-borne disease.
Key words: Rickettsia amblyommii—Amblyomma americanum—Prevalence—Pathogenicity—Co-infection.
Address reprint requests to:
Entomological Science Program
U.S. Army Center for Health Promotion &
5158 Blackhawk Rd.
Aberdeen Proving Ground, MD 21010-5403
RMSF vs. Lyme
Rocky Mountain Spotted Fever & Lyme
According to the CDC
Two potentially fatal infections treated differently?
According to CDC, Rocky Mountain Spotted Fever (RMSF) was responsible for 19 deaths between 2004 and 2007. In contrast, CDC reported Lyme disease was responsible for 26 deaths during the same time period.
The national incidence rate for RMSF (1997-2002) was 2.2 cases per million persons; incidence rates for Lyme disease (2009) was reported as 12.71. There were 38,468 cases of Lyme disease reported by the CDC in 2009 and 1,815 cases of Rocky Mountain Spotted Fever during that same year.
In spite of the higher number of deaths from Lyme disease, a six times higher incident rate over the tick borne RMSF, and an additional 37,000 plus more reported cases of Lyme over RMSF, only RMSF is said by the CDC to be “life-threatening”, and a “cause [of] severe illness and death”.
This same warning is not offered to those seeking information on Lyme disease. Neither is the RMSF related statement, “early empiric antibiotic therapy can prevent severe morbidity and death”, shared with the public on the CDC website in regards to Lyme disease.
In fact, the CDC casually states Lyme disease “is diagnosed based on symptoms, physical findings (e.g., rash), and the possibility of exposure to infected ticks; laboratory testing is helpful if used correctly and performed with validated methods. Typical symptoms include fever, headache, fatigue, and a characteristic skin rash called erythema migrans.”
CDC warns readers about specific difficulties regarding RMSF - “Early signs and symptoms of these illnesses are notoriously nonspecific or mimic benign viral illnesses, making diagnosis difficult.” In contrast, although Lyme disease has been referred to across the globe as “a multisystem disease” and is known as the '”great imitator” due to diversity of its clinical manifestations, the CDC has no similar warning of the difficulty with diagnosing Lyme disease on its website.
The CDC website gives the impression diagnosing Lyme early is not a priority, discourages the use of testing until weeks after possible exposure and indicates testing is not even necessary in the event a person exhibits “typical” symptoms -“Laboratory blood tests are helpful if used correctly and performed with validated methods. Laboratory tests are not recommended for patients who do not have symptoms typical of Lyme disease.” Describing Lyme disease symptoms as “typical” is a misnomer, as presentations can be varied, certain stages and symptoms may never appear, and one or more symptoms can wax and wane throughout the course of the illness, including after what is reported to be adequate treatment.
CDC states- “For example, even in areas where awareness of RMSF is high, approximately 60%--75% of patients with this TBRD receive an alternate diagnosis on their first visit for medical care (8,9).” This may be accurate, however, it is important to note that Lyme disease patients often receive multiple incorrect diagnoses, even after visiting several physicians, and the correct diagnosis is often not discovered until years after the original exposure to infected ticks, if at all.
The results of a 2009 CALDA survey, which included 2,424 Lyme patients whose clinical diagnosis was supported by positive test results, was reported at the IOM Workshop. The study determined- “More than half of patients saw 7 or more physicians to obtain a diagnosis; over a third saw 10 or more physicians. Nearly half of these Lyme patients had traveled over 50 miles to receive healthcare; 30% had traveled more than 100 miles; and 9% had traveled over 500 miles. (Travel distances of 30 miles or more are considered to impose a high healthcare access burden on a patient.) Roughly 40% had sought services at their local hospital, and approximately 82% of these Lyme patients had difficulty obtaining care.”
Additionally, the CALDA study revealed 95% of respondents had suffered with Lyme disease for more than 2 years.
The CDC warns, regarding RMSF- “The lack of a specific initial syndrome, however, does not imply that the course of these diseases will be benign.” It does not alert the public to the fact that people exposed to Lyme disease may experience the same situation.
The negative, chronic health effects from RMSF are also mentioned in detail- “Long-term health effects persisting for >1 year after acute RMSF infection include partial paralysis of the lower extremities; gangrene requiring amputation of fingers, toes, arms, or legs; hearing loss; blindness; loss of bowel or bladder control; movement disorders; and speech disorders (79).”
The literature concerning Lyme disease does not include the fact it can also cause blindness; partial paralysis of the lower extremities; hearing loss; loss of bowel or bladder control; movement disorders; or speech disorders. It also additional fails to mention many mild to severe symptoms documented in the scientific literature, such as:
Facial and dental pain- “clinical manifestations may include facial and dental pain, facial nerve palsy, headache, temporomandibular joint pain, and masticpain.” (1) Laryngoscope, 101(6 Pt 1):592-5. 1991.
Headaches- “Our patients show that headache can be the first, and for a long time the only, prominent sign of Lyme
neuroborreliosis” Headache resembling tension-type headache as the single manifestation of Lyme
neuroborreliosis. Brinck T; Hansen K; Olesen J. Cephalalgia, 13(3):207-9. 1993
...“headaches resembling migraine... tension-type headache” (3) Headache characteristics in hospitalized patients with Lyme disease. Scelsa SN; Lipton RB; Sander H; Herskovitz S. Headache, 35(3):125-30. 1995.
TMJ Pain- “Fourteen patients demonstrated temporomandibular joint pain. temporomandibular joint
disorder (TMJ) Otolaryngologic aspects of Lyme disease. Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F. Laryngoscope, 101(6 Pt 1):592-5. 1991.
Tongue Paresthesia- “he developed paresthesia in his tongue” [A patient with neuroborreliosis presenting gadolinium-enhanced MRI lesions in bilateral facial nerves.] Tokunaga H; Ohyagi Y; Furuya H; Araki T; Yamada T; Isogai E; Kira J. Rinsho Shinkeigaku, 41(9):632-4. 2001.
Facial Swelling- Otolaryngologic aspects of Lyme disease. Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F. Laryngoscope, 101(6 Pt 1):592-5. 1991.
Difficulty Swallowing- “Dysphagia” (1) Otolaryngologic aspects of Lyme disease. Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F. Laryngoscope, 101(6 Pt 1):592-5. 1991.
Twitching of facial or other muscles - “the other [patient] has had intermittent facial twitches for eight
months. [post treatment]” Isolation of Borrelia burgdorferi from the blood of seven patients with Lyme disease.
Nadelman RB; Pavia CS; Magnarelle LA; Wormser GP. American Journal of Medicine, 88:21-6. 1990.
Vocal Paralysis- Paralysis of recurrent laryngeal nerve in Lyme disease. Schroeter V; Belz GG; Blenk H.
Lancet, 2(8622):1245. 1988.
Hypersensitivity to noise- “Lyme disease-induced hyperacusis can be an intensely disabling, chronic condition that is accompanied by posttraumatic stress disorder-like psychobehavioral sequelae. Carbamazepine in the treatment of Lyme disease-induced hyperacusis." Nields JA; Fallon BA; Jastreboff PJ. J Neuropsychiatry Clin Neurosci, 11(1):97-9. 1999.
Pain in Ears- Otolaryngologic aspects of Lyme disease. Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F. Laryngoscope, 101(6 Pt 1):592-5. 1991.
“...it should be emphasized that marked variation is possible in the clinical expression of the disease. Even without treatment, some patients have very mild disease... At the opposite end of the spectrum, an occasional patient will have severe involvement of the skin, nerves, heart, and joints at the same time.” Steere AC; Malawista SE; et al. The clinical spectrum and treatment of Lyme disease. Yale Journal of Biology and Medicine 1984;57(4):453-64.
“Clinically, this borrelial infection is most like syphilis in its multisystem involvement, occurrence in stages, and mimicry of other diseases. ...Lyme disease’s great range of presentations can make recognition difficult.” Steere AC. Lyme disease. New England Journal of Medicine 1989;321:586-596.
“Symptoms can be surprisingly variable, so that days of near normality can alternate with days of profound debility.”
Pachner AR. Early disseminated Lyme disease. American Journal of Medicine 1995;98 (suppl):4A-30S-43S.
“As in other spirochetoses, such as syphilis, the symptoms may be fulminant, with a sudden onset, or may develop insidiously over many years. The variable clinical manifestations have led to an awareness of this disorder as a “great imitator” that must be considered in the differential diagnosis of numerous complaints, especially in those geographic areas where the spirochete is endemic.” Cooke WD; Dattwyler RJ. Complications of Lyme borreliosis. Annual Review of Medicine 1992;43:93-103.
“Lyme disease has now been shown to involve nearly every organ and organ system in both sexes.”
Duray PH. Clinical pathologic correlations of Lyme disease. Rev Infect Dis 1989;Vol 11(Suppl. 6):S1487-S1493.
“In syphilis, ...staging is particularly useful because it is likely that the pathophysiology of stage 2 and stage 3 disease differs; this is far less clear with neuroborreliosis. Considerable data suggest that the differences between early and late neuroborreliosis are more quantitative than qualitative, with the different syndromes representing different points on a continuum, all with the same pathophysiologic mechanism. Moreover, the clinical phenomena in neuroborreliosis often do not follow an obligatory temporal sequence; any symptoms may develop without an antecedent stage 1 illness. For example, arthritis (generally considered stage 3 disease) may occur
early, on occasion even preceding EM; meningitis (nominally stage 2) may develop after arthritis, and so on. All this suggests that dividing neuroborreliosis into early versus late phenomena, while occasionally reassuring to the physician and patient, may lack pathophysiologic validity.” Halperin JJ. Neuroborreliosis. Am J Med 1995;Vol 98(4A):52S-56S.
“This pattern of persistent infection, acute disease, disease remission, and intermittent bouts of exacerbation is typical of untreated human Lyme disease.” Barthold SW; de Souza MS; Janotka JL; Smith AL; Persing DH. Chronic Lyme borreliosis in the laboratory mouse. Am J Path 1993;143(3):959-71.
“The syphilis spirochete can live in the CNS for long periods, as evidenced by the fact that patients with general paresis usually do not manifest neurologic symptoms until 15 years after infection. A lengthy latency within the CNS also appears to exist in Lyme disease, with neurologic symptoms not becoming manifest for months or even years.” Pachner AR. Neurologic manifestations of Lyme disease, the new “Great Imitator.” Rev Inf Dis 1989;Vol. 11(Suppl 6):S1482-6.
Fatigue- “often constant and may be incapacitating”. The clinical spectrum and treatment of Lyme disease.
Steere AC; Malawista SE; Bartenhagen NH; Spieler PN; Newman JH; Rahn DW; et al. Yale Journal of Biology and Medicine, 57(4):453-64. 1984.
Lyme from CDC site- “There is some evidence that PTLDS is caused by an autoimmune response, in which a person's immune system continues to respond, doing damage to the body’s tissues, even after the infection has been cleared.”
Also on CDC site- “As with many infectious diseases, there is no test that can "prove" cure.”
In comparison, the CDC website reports:
“Tickborne rickettsial diseases (TBRD) continue to cause severe illness and death in otherwise healthy adults and children, despite the availability of low cost, effective antimicrobial therapy.”
RMSF- “…greatest challenge to clinicians is diagnosing these infections early in their clinical course, when antibiotic therapy is most effective.”
“…understand that early empiric antibiotic therapy can prevent severe morbidity and death.”
“Early signs and symptoms of these illnesses are notoriously nonspecific or mimic benign viral illnesses, making diagnosis difficult.”
“Early signs and symptoms of these illnesses are notoriously nonspecific, or they might mimic benign viral illnesses, making diagnosis difficult. For example, even in areas where awareness of RMSF is high, approximately 60%--75% of patients with this TBRD receive an alternate diagnosis on their first visit for medical care (8,9).”
“The lack of a specific initial syndrome, however, does not imply that the course of these diseases will be benign.”
“Two recent cross-sectional studies in the southeastern and south central United States* have indicated that up to 22% of children have serologic evidence of previous exposure to antigens of both E. chaffeensis (15) and R. rickettsii (16), suggesting that rickettsial and ehrlichial infection might be more common than previously recognized.”
“Long-term health effects persisting for >1 year after acute RMSF infection include partial paralysis of the lower extremities; gangrene requiring amputation of fingers, toes, arms, or legs; hearing loss; blindness; loss of bowel or bladder control; movement disorders; and speech disorders (79).”
“Similarly, HME and HGA can cause serious or fatal disease as well, although at lower rates than are observed for RMSF.”
“Approximately 3% of HME patients and less than 1% of HGA patients with symptoms severe enough to seek medical attention will die from the infection (25,34,47).”
“In addition, advanced patient age and delay in diagnosis and the onset of specific antibiotic therapy are predictors of a more severe course of HGA (53).”
“TBRD can be life-threatening.”
“TBRD can be life-threatening. Severe manifestations of TBRD include prolonged fever, renal failure, myocarditis, meningoencephalitis, hypotension, acute respiratory distress syndrome, and multiple organ failure. Patients usually do not have diagnostic serum antibody levels during the first week of illness; therefore, an inability to detect antibodies (IgG or IgM) in acute-phase serum does not exclude TBRD.
RMSF- “Health-care providers should not delay treatment while waiting for a diagnosis; rather, they should empirically provide treatment if they suspect TBRD. Doxycycline is the drug of choice for the treatment of presumptive or confirmed TBRD in both adults and children.” … “Several laboratory methods are available to diagnose TBRD. However, they vary in the time required to obtain results and in the type of information they provide the clinician. Therefore, treatment decisions should be based on epidemiologic and clinical clues and should never be delayed while waiting for laboratory confirmation of a diagnosis. “
Lyme- “Several weeks after infection, currently available ELISA, EIA and IFA tests and two-tier testing have very good sensitivity.” “Just as it is important to correctly diagnose Lyme disease when a patient has it, it is important to avoid misdiagnosis and treatment of Lyme disease when the true cause of the illness is something else.”
Lyme- “Lyme disease is diagnosed based on symptoms, physical findings (e.g., rash), and the possibility of exposure to infected ticks; laboratory testing is helpful if used correctly and performed with validated methods.”
Lyme- “You may have heard that the blood test for Lyme disease is correctly positive only 65% of the time or less. This is misleading information. As with serologic tests for other infectious diseases, the accuracy of the test depends upon the stage of disease. During the first few weeks of infection, such as when a patient has an erythema migrans rash, the test is expected to be negative.
“Long-term health effects persisting for >1 year after acute RMSF infection include partial paralysis of the lower extremities; gangrene requiring amputation of fingers, toes, arms, or legs; hearing loss; blindness; loss of bowel or bladder control; movement disorders; and speech disorders (79).”
Lyme- Lingering symptoms after treatment (post-treatment Lyme disease syndrome)
Approximately 10-20% of patients with Lyme disease have symptoms that last months to years after treatment with antibiotics5. These symptoms can include muscle and joint pains, cognitive defects, sleep disturbance, or fatigue. The cause of these symptoms is not known, but there is no evidence that these symptoms are due to ongoing infection with B. burgdorferi. This condition is referred to as Post-treatment Lyme disease syndrome (PTLDS).