Rickettsial Infection Workup: Laboratory Studies, Imaging Studies, Procedures
Rickettsial Infection Workup: Laboratory Studies, Imaging Studies, Procedures
Rickettsiae are not evident on blood smear findings and do not stain with most conventional stains.
No rapid laboratory tests are available to diagnose rickettsial diseases early in the course of illness.
Serologic assays that demonstrate antibodies to rickettsial antigens (eg, indirect immunofluorescence, complement fixation, indirect hemagglutination, latex fixation, enzyme immunoassay, microagglutination) are preferable to the nonspecific and insensitive Weil-Felix test based on the cross-reactive antigens of Proteus vulgaris strains. Serologic findings usually take 10-12 days to become positive. The value of testing 2 sequential serum or plasma samples together to show a rising antibody level is considerably more important in confirming acute infection with rickettsial agents because antibody titers may persist in some patients for years after the original exposure.
Immunofluorescence assay (IFA) is currently considered to be the reference serological method. However, it cannot determine the causative agent to the species level.
Polymerase chain reaction (PCR) to detect rickettsiae in blood or tissue provides promise for early diagnosis. PCR testing and immunohistochemical staining of skin specimen obtained by performing a biopsy may help confirm the clinical diagnosis in patients with rash (high expertise is usually needed to interpret the biopsy result).
Preliminary findings of new research is indicating that swabs of eschars may be used for molecular detection of rickettsial infections when biopsies are difficult to perform.However, serology remains the mainstay of diagnosis because these other tests are expensive and less available to clinicians.
Rickettsial isolation in culture is unnecessary, laborious, and hazardous to laboratory personnel.
Serology is the mainstay to confirm diagnosis.
Another approach to RMSF diagnostics is immunostaining whereby a skin biopsy of the rash from an infected patient is tested prior to therapy or within the first 48 hours after antibiotic therapy has been started. This test's use remains highly operator-dependent.
Other tests, such as PCR, are rather expensive and not readily available.
Nonspecific laboratory findings, such as thrombocytopenia, leukopenia, and mild hyponatremia, may give helpful clues to the treating physician.
If cerebrospinal fluid is examined, pleocytosis (generally < 100 cells/μ L) is typically observed with polymorphonuclear or lymphocyte predominance, moderately elevated protein levels (100-200 mg/dL), and normal glucose levels.
As with other rickettsial infections, diagnosis is clinical and may be confirmed by serology.
The Weil-Felix test is not useful because R akari does not produce Weil-Felix agglutinins.
R akari has a soluble antigen that cross-reacts with R rickettsii (the cause of RMSF) and other spotted fever groups of rickettsiae.
Serologic laboratory confirmation (complement fixation, microagglutination, western blot, indirect immunofluorescent tests) usually provides support for the diagnosis made on clinical and epidemiologic grounds. Additionally, a latex agglutination test for detection of antibodies to R conorii that is both specific and sensitive now can be performed in specialized laboratories.
R conorii has been detected from the tache noire by restriction fragment length polymorphism (RFLP) and by PCR.
Serologic laboratory confirmatory tests are available as in RMSF. Patients initially have an IgM response followed by production of immunoglobulin G (IgG) antibodies.
However, a significant antigenic crossing is noted between this rickettsial organism and those of the spotted fever group.
PCR promises to be a rapid diagnostic test but is expensive and not yet widely available.
Laboratory studies are similar to those for primary louse-borne epidemic typhus. However, patients develop an anamnestic immune response whereby only IgG is produced.
Laboratory studies are analogous to those mentioned for epidemic louse-borne typhus.
Additionally, a mild-to-moderate elevation of serum aspartate aminotransferase (AST) level is present in approximately 90% of patients. Other indices of hepatocellular injury (alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase) are often also elevated.
Serologic testing using specific methods (eg, immunofluorescence antibody test, indirect immunoperoxidase test, enzyme immunoassay) is superior to the Weil-Felix reaction.
However, these tests are cumbersome and only available in a few special laboratories.
Laboratory findings in acute Q fever infection may include thrombocytopenia in approximately 25% of cases and elevated hepatic transaminases. In prolonged infections, autoantibodies (eg, anti-smooth muscle antibodies) may be found.
In addition to clinical and epidemiologic features, serology (eg, microimmunofluorescence, complement fixation, enzyme immunoassay) remains the mainstay of diagnosis in acute and chronic illnesses.
As with other rickettsiae, attempts to isolate the organism are biohazardous and unnecessary.
PCR may be used; however, it remains less available and more expensive than serology.
Chronic Q fever endocarditis is diagnosed by demonstration of high antibody (IgG and IgA) titers against C burnetii in patients with signs of endocarditis whose blood cultures contain no organisms (ie, culture-negative endocarditis). These patients may have elevated erythrocyte sedimentation rate, anemia, thrombocytopenia, and hematuria.
See the list below:
See the list below:
See the list below:
Treatment & Management
Mobeen H Rathore, MD, CPE, FAAP, FIDSA Chief of Division of Pediatric Infectious Diseases/Immunology, Associate Chairman of Department of Pediatrics, University of Florida College of Medicine at Jacksonville; Hospital Epidemiologist and Section Chief of Infectious Disease and Immunology, Wolfson Children's Hospital; Director of University of Florida Center for HIV/AIDS Research, Education and Service (UF CARES)
Mobeen H Rathore, MD, CPE, FAAP, FIDSA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Florida Medical Association, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Healthcare Epidemiology of America, Society for Pediatric Research, Southern Medical Association, Southern Society for Pediatric Research, Florida Chapter of The American Academy of Pediatrics, Florida Pediatric Society, European Society for Paediatric Infectious Diseases
Coauthor(s)
Nizar F Maraqa, MD, FAAP Associate Professor of Pediatrics, Fellowship Program Director, Pediatric Infectious Diseases, University of Florida College of Medicine at Jacksonville
Nizar F Maraqa, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society
Saran A Wells, MD Fellow in Pediatric Infectious Disease, University of Florida College of Medicine at Jacksonville
Saran A Wells, MD is a member of the following medical societies: American Academy of Pediatrics, Pediatric Infectious Diseases Society
Specialty Editor Board
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America
Chief Editor
Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association
José Rafael Romero, MD Director of Pediatric Infectious Diseases Fellowship Program, Associate Professor, Department of Pediatrics, Combined Division of Pediatric Infectious Diseases, Creighton University/University of Nebraska Medical Center
José Rafael Romero, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, New York Academy of Sciences, Pediatric Infectious Diseases Society
References
This photo shows the relative sizes of the adult forms of Ixodes scapularis (right) and Dermacentor variabilis (left). These ticks are shown next to a common match for scale. I scapularis is also referred to as Ixodes dammini. Photo by Darlyne Murawski; reproduced with permission.
This photo is of an adult female, Amblyomma americanum, and a nymphal form of the same species (shown next to a common match for scale). Photo by Darlyne Murawski; reproduced with permission.
Laboratory Studies
Rickettsiae are not evident on blood smear findings and do not stain with most conventional stains.
No rapid laboratory tests are available to diagnose rickettsial diseases early in the course of illness.
Serologic assays that demonstrate antibodies to rickettsial antigens (eg, indirect immunofluorescence, complement fixation, indirect hemagglutination, latex fixation, enzyme immunoassay, microagglutination) are preferable to the nonspecific and insensitive Weil-Felix test based on the cross-reactive antigens of Proteus vulgaris strains. Serologic findings usually take 10-12 days to become positive. The value of testing 2 sequential serum or plasma samples together to show a rising antibody level is considerably more important in confirming acute infection with rickettsial agents because antibody titers may persist in some patients for years after the original exposure.
Immunofluorescence assay (IFA) is currently considered to be the reference serological method. However, it cannot determine the causative agent to the species level.
Polymerase chain reaction (PCR) to detect rickettsiae in blood or tissue provides promise for early diagnosis. PCR testing and immunohistochemical staining of skin specimen obtained by performing a biopsy may help confirm the clinical diagnosis in patients with rash (high expertise is usually needed to interpret the biopsy result).
Preliminary findings of new research is indicating that swabs of eschars may be used for molecular detection of rickettsial infections when biopsies are difficult to perform.However, serology remains the mainstay of diagnosis because these other tests are expensive and less available to clinicians.
Rickettsial isolation in culture is unnecessary, laborious, and hazardous to laboratory personnel.
Rocky Mountain spotted fever (RMSF)
Serology is the mainstay to confirm diagnosis.
Another approach to RMSF diagnostics is immunostaining whereby a skin biopsy of the rash from an infected patient is tested prior to therapy or within the first 48 hours after antibiotic therapy has been started. This test's use remains highly operator-dependent.
Other tests, such as PCR, are rather expensive and not readily available.
Nonspecific laboratory findings, such as thrombocytopenia, leukopenia, and mild hyponatremia, may give helpful clues to the treating physician.
If cerebrospinal fluid is examined, pleocytosis (generally < 100 cells/μ L) is typically observed with polymorphonuclear or lymphocyte predominance, moderately elevated protein levels (100-200 mg/dL), and normal glucose levels.
Rickettsialpox
As with other rickettsial infections, diagnosis is clinical and may be confirmed by serology.
The Weil-Felix test is not useful because R akari does not produce Weil-Felix agglutinins.
R akari has a soluble antigen that cross-reacts with R rickettsii (the cause of RMSF) and other spotted fever groups of rickettsiae.
Boutonneuse fever
Serologic laboratory confirmation (complement fixation, microagglutination, western blot, indirect immunofluorescent tests) usually provides support for the diagnosis made on clinical and epidemiologic grounds. Additionally, a latex agglutination test for detection of antibodies to R conorii that is both specific and sensitive now can be performed in specialized laboratories.
R conorii has been detected from the tache noire by restriction fragment length polymorphism (RFLP) and by PCR.
Louse-borne (epidemic) typhus
Serologic laboratory confirmatory tests are available as in RMSF. Patients initially have an IgM response followed by production of immunoglobulin G (IgG) antibodies.
However, a significant antigenic crossing is noted between this rickettsial organism and those of the spotted fever group.
PCR promises to be a rapid diagnostic test but is expensive and not yet widely available.
Brill-Zinsser disease (ie, relapsing louse-borne typhus)
Laboratory studies are similar to those for primary louse-borne epidemic typhus. However, patients develop an anamnestic immune response whereby only IgG is produced.
Murine (endemic or flea-borne) typhus
Laboratory studies are analogous to those mentioned for epidemic louse-borne typhus.
Additionally, a mild-to-moderate elevation of serum aspartate aminotransferase (AST) level is present in approximately 90% of patients. Other indices of hepatocellular injury (alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase) are often also elevated.
Tsutsugamushi disease (ie, scrub typhus)
Serologic testing using specific methods (eg, immunofluorescence antibody test, indirect immunoperoxidase test, enzyme immunoassay) is superior to the Weil-Felix reaction.
However, these tests are cumbersome and only available in a few special laboratories.
Q fever
Laboratory findings in acute Q fever infection may include thrombocytopenia in approximately 25% of cases and elevated hepatic transaminases. In prolonged infections, autoantibodies (eg, anti-smooth muscle antibodies) may be found.
In addition to clinical and epidemiologic features, serology (eg, microimmunofluorescence, complement fixation, enzyme immunoassay) remains the mainstay of diagnosis in acute and chronic illnesses.
As with other rickettsiae, attempts to isolate the organism are biohazardous and unnecessary.
PCR may be used; however, it remains less available and more expensive than serology.
Chronic Q fever endocarditis is diagnosed by demonstration of high antibody (IgG and IgA) titers against C burnetii in patients with signs of endocarditis whose blood cultures contain no organisms (ie, culture-negative endocarditis). These patients may have elevated erythrocyte sedimentation rate, anemia, thrombocytopenia, and hematuria.
Imaging Studies
See the list below:
- Chest radiography may be required in patients with severe illness or pulmonary manifestations, especially in patients with RMSF and Q fever.
- Other imaging studies may be necessary, depending on the severity of organ involvement and development of complications.
Procedures
See the list below:
- A Lumbar Puncture and other procedures may be needed to exclude other possible etiologies.
Histologic Findings
See the list below:
- Evidence of vasculitis, angiitis, and perivascular mononuclear cell infiltration may be evident in involved organs.
- Chronic Q fever infection of the skeletal system causes the formation of granulomatous lesions.
Treatment & Management
Mobeen H Rathore, MD, CPE, FAAP, FIDSA Chief of Division of Pediatric Infectious Diseases/Immunology, Associate Chairman of Department of Pediatrics, University of Florida College of Medicine at Jacksonville; Hospital Epidemiologist and Section Chief of Infectious Disease and Immunology, Wolfson Children's Hospital; Director of University of Florida Center for HIV/AIDS Research, Education and Service (UF CARES)
Mobeen H Rathore, MD, CPE, FAAP, FIDSA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Florida Medical Association, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Healthcare Epidemiology of America, Society for Pediatric Research, Southern Medical Association, Southern Society for Pediatric Research, Florida Chapter of The American Academy of Pediatrics, Florida Pediatric Society, European Society for Paediatric Infectious Diseases
Coauthor(s)
Nizar F Maraqa, MD, FAAP Associate Professor of Pediatrics, Fellowship Program Director, Pediatric Infectious Diseases, University of Florida College of Medicine at Jacksonville
Nizar F Maraqa, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society
Saran A Wells, MD Fellow in Pediatric Infectious Disease, University of Florida College of Medicine at Jacksonville
Saran A Wells, MD is a member of the following medical societies: American Academy of Pediatrics, Pediatric Infectious Diseases Society
Specialty Editor Board
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America
Chief Editor
Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association
José Rafael Romero, MD Director of Pediatric Infectious Diseases Fellowship Program, Associate Professor, Department of Pediatrics, Combined Division of Pediatric Infectious Diseases, Creighton University/University of Nebraska Medical Center
José Rafael Romero, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, New York Academy of Sciences, Pediatric Infectious Diseases Society
References
- Walker DH. Rickettsiae and rickettsial infections: the current state of knowledge. Clin Infect Dis. 2007 Jul 15. 45 Suppl 1:S39-44. [Medline].
- Jensenius M, Fournier P, Raoult D. Rickettsioses and the international traveler. Clin Infect Dis. 2004. 34(10):1493-9. [Medline].
- Center of Disease Control and Prevention (CDC). Rickettsial Diseases. Infectious Disease Information. Available at http://www.cdc.gov/ncidod/dvrd/branch/vrzb.htm.
- Edwards MS, Feigin RD. Rickettsial diseases. Feigin RD, Cherry JD, Demmler GJ, Kaplan SL, eds. Textbook of Pediatric Infectious Diseases. 5th ed. WB Saunders Co; 2004. 2497-2515/Chapter 195.
- Tissot-Dupont H, Raoult D. Q Fever. Infect Dis Clin N Am. Sept 2008. 22:505-514. [Medline].
- Walker DH. Rickettsiae. Baron S, ed. Medical Microbiology. 4th ed. University of Texas Medical Branch; 1996. [Full Text].
- Shapiro MR, Fritz CL, Tait K, Paddock CD, Nicholson WL, Abramowicz KF, et al. Rickettsia 364D: a newly recognized cause of eschar-associated illness in California. Clin Infect Dis. 2010 Feb 15. 50(4):541-8. [Medline].
- Johnston SH, Glaser CA, Padgett K, Wadford DA, Espinosa A, Espinosa N, et al. Rickettsia spp. 364D causing a cluster of eschar-associated illness, California. Pediatr Infect Dis J. 2013 Sep. 32 (9):1036-9. [Medline].
- Azad AF. Pathogenic Rickettsiae as Bioterrorism Agents. Clin Infect Dis. 2007 Jul 15. 45 Suppl 1:S52-55. [Medline].
- Rovery C, Raoult D. Meditteranean Spotted Fever. Infect Dis Clin N Am. Sept 2008. 22:515-530. [Medline].
- Drexler NA, Dahlgren FS, Heitman KN, Massung RF, Paddock CD, Behravesh CB. National Surveillance of Spotted Fever Group Rickettsioses in the United States, 2008-2012. Am J Trop Med Hyg. 2015 Aug 31. [Medline].
- Dumler JS, Walker DH. Rocky Mountain spotted fever--changing ecology and persisting virulence. N Engl J Med. 2005 Aug 11. 353(6):551-3. [Medline].
- Graf PC, Chertien JP, Ung L, et al. Prevalence of serpositivity to spotted fever group rickettsiae and Anaplasma phagocytophilum in a large, dempgraphically diverse US sample. Clin Infect Dis. Jan 2008. 46 (1):70-77. [Medline].
- Cowan G. Rickettsial diseases: the typhus group of fevers--a review. Postgrad Med J. 2000 May. 76(895):269-72. [Medline].
- Marshall GS. Rickettsia typhi seroprevalence among children in the Southeast United States. Tick-Borne Infections in Children Study (TICKS) Group. Pediatr Infect Dis J. 2000 Nov. 19(11):1103-4. [Medline].
- Fergie JE, Purcell K, Wanat D. Murine Typhus in South Texas children. Pediatr Infect Dis J. 2000. 19(6):535-38. [Medline].
- Aung AK, Spelman DW, Murray RJ, Graves S. Rickettsial infections in Southeast Asia: implications for local populace and febrile returned travelers. Am J Trop Med Hyg. 2014 Sep. 91 (3):451-60. [Medline]. [Full Text].
- Centers for Disease Control and Prevention. Q Fever- Statistics and Epidemiology. Centers for Disease Control and Prevention. Available at http://www.cdc.gov/qfever/stats/index.html. Accessed: 02/23/2013.
- Williams M, Izzard L, Graves SR, et al. First probable Australian cases of human infection with Rickettsia felis (cat-flea typhus). Med J Aust. Jan 2011. 194(1):41-43. [Medline].
- Walker DH, Dumler JS. Emerging and reemerging rickettsial diseases. N Engl J Med. 1994 Dec 15. 331(24):1651-2. [Medline].
- Rombola F. Mediterranean spotted fever presenting as an acute pancreatitis. Acta Gastroenterol Belg. Mar 2011. 74(1):91-92. [Medline].
- Cascio A, Giordano S, Dones P, et al. Haemophagocytic syndrome and rickettsial diseases. J Med Microbiol. Apr 2011. 60(4):537-542. [Medline].
- Abramson JS, Givner LB. Rocky Mountain spotted fever. Pediatr Infect Dis J. 1999 Jun. 18(6):539-40. [Medline].
- Parola P, Davoust B, Raoult D. Tick- and flea-borne rickettsial emerging zoonoses. Vet Res. May-Jun 2005. 36:469-492. [Medline].
- Ruiz-Contreras J, Gonzalez Montero R, Ramos Amador JT, et al. Q fever in children. Am J Dis Child. 1993 Mar. 147(3):300-2. [Medline].
- Nourse C, Allworth A, Jones A, et al. Three cases of Q fever osteomyelitis in children and a review of the literature. Clin Infect Dis. 2004 Oct 1. 39(7):e61-6. [Medline].
- Sexton DJ, Corey GR. Rocky Mountain "spotless" and "almost spotless" fever: a wolf in sheep's clothing. Clin Infect Dis. 1992 Sep. 15(3):439-48. [Medline].
- Demma LJ, Traeger MS, Nicholson et al. Rocky Mountain spotted fever from an unexpected tick vector in Arizona. N Engl J Med. 2005 Aug 11. 353(6):587-94. [Medline].
- Nicholson WL, Allen KE, McQuiston JH, et al. The increasing recognition of rickettsial pathogens in dogs and people. Trends Parasitol. Apr 2010. 26(4):205-212. [Medline].
- Hildebrandt A, Franke J, Meier F, et al. The potential role of migratory birds in transmission cycles of Babesia spp., Anaplasma phagocytophilum, and Rickettsia spp. Ticks Tick Borne Dis. Jun 2010. 1(2):105-107. [Medline].
- Raoult D, Paddock CD. Rickettsia parkeri infection and other spotted fevers in the United States. N Eng J Med. 2005. 353:626-7. [Medline].
- Bechah Y, Socolovschi C, Raoult D. Identification of Rickettsial Infections by Using Cutaneous Swab Specimens and PCR. Emerg Infect Dis. Jan 2011. 17(1):83-86.
- Angelakis E, Richet H, Rolain JM, La Scola B, Raoult D. Comparison of real-time quantitative PCR and culture for the diagnosis of emerging Rickettsioses. PLoS Negl Trop Dis. 2012. 6(3):e1540. [Medline].
- Giulieri S, Jaton K, Cometta A, Trellu LT, Greub G. Development of a duplex real-time PCR for the detection of Rickettsia spp. and typhus group rickettsia in clinical samples. FEMS Immunol Med Microbiol. 2012 Feb. 64(1):92-7. [Medline].
- Raoult D, Drancourt M. Antimicrobial therapy of rickettsial diseases. Antimicrob Agents Chemother. 1991 Dec. 35(12):2457-62. [Medline].
- Purvis JJ, Edwards MS. Doxycycline use for rickettsial disease in pediatric patients. Pediatr Infect Dis J. 2000 Sep. 19(9):871-4. [Medline].
- Kim CO, Huh AJ, Yeom JS, Lee KS, Chin BS, Han SH. Lack of effect of dexamethasone on growth of Orientia tsutsugamushi Gilliam in mouse L929 cells. Yonsei Med J. 2011 Jul. 52(4):624-9. [Medline].
- Richards AL. Rickettsial Vaccines: the old and the new. Expert Rev Vaccines. October 2004. 3:541-555. [Medline].
- Chapman AS, Bakken JS, Folk SM, et al. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrlichioses, and anaplasmosis--United States: a practical guide for physicians and other health-care and public health professionals. MMWR Recomm Rep. 2006 Mar 31. 55(RR-4):1-27. [Medline].
- Fournier PE, Gouriet F, Brouqui P. Lymphangitis-associated rickettsiosis, a new rickettsiosis caused by Rickettsia sibirica mongolotimonae: seven new cases and review of the literature. Clin Infect Dis. 2005 May 15. 40(10):1435-44. [Medline].
- Jensenius M, Fournier P, Kelly P. African tick bite fever. Lancet Infect Dis. 2003. 3(9):557-64. [Medline].
- Spach DH, Liles WC, Campbell GL, et al. Tick-borne diseases in the United States. N Engl J Med. 1993 Sep 23. 329(13):936-47. [Medline].
This photo shows the relative sizes of the adult forms of Ixodes scapularis (right) and Dermacentor variabilis (left). These ticks are shown next to a common match for scale. I scapularis is also referred to as Ixodes dammini. Photo by Darlyne Murawski; reproduced with permission.
This photo is of an adult female, Amblyomma americanum, and a nymphal form of the same species (shown next to a common match for scale). Photo by Darlyne Murawski; reproduced with permission.
