Rocky Mountain spotted fever

Rickettsiae are strict intracellular bacteria requiring a host cell to replicate. Within the genus Rickettsia three groups are differentiated, one of which is the spotted fever group (SFG), whose members are associated mainly with ticks, but also with fleas and mites (Raoult and Roux, 1997). Within the SFG Rickettsia rickettsii is the pathogenic agent of Rocky Mountain spotted fever (RMSF), a potentially fatal rickettsial disease of dogs and humans. The pathogen has been reported throughout the USA, Central and South America, and is transmitted by ticks of the Dermacentor, Rhipicephalus and Amblyomma genera, respectively.

Pathogens

The genus Rickettsia is included in the bacterial tribe Rickettsiae, order Rickettsiales, family Rickettsiaceae. It comprises many species of bacteria associated with important and severe human or animal disease, including those in the spotted fever group (SFG), which currently recognises more than 20 valid species.

Rickettsia rickettsii is a very small, gram-negative, rod-shaped bacterium that obligatory lives inside the cells of its hosts, ranging in size from 0.2 x 0.5 µm to 0.3 x 2.0 µm. The pathogen disseminates to infect the endothelium of the microcirculation and is difficult to detect in tissues by using routine histologic staining, generally requiring the use of special staining methods (i.e., Giemsa, Gimenez, or immunohistochemical) (Greene and Breitschwerdt, 1998; Paddock et al., 1999).

The clinical illness of what is called now Rocky Mountain spotted fever (RMSF) was first described in Montana and Idaho during the late 1890s (Maxey, 1899; Wood, 1896). The causative organism, R. rickettsii, was isolated and characterized between 1906 and 1910 by Howard T. Ricketts, also demonstrating that it circulated among ticks and mammals in the wild and that it could be transmitted transovarially by ticks to their offspring (Ricketts, 1906, 1908, 1909; Ricketts and Gomez, 1908). 

Transmission electron microscopic image of Rickettsia ricketsii, showing rod-like appearance and a trilaminar wall, with a measurement bar of 0.16 µm length.
Transmission electron microscopic image of Rickettsia ricketsii, showing rod-like appearance and a trilaminar wall, with a measurement bar of 0.16 µm length.

In respect to dogs, early reports indicated that dogs are susceptible to RMSF and could be infected and become rickettsaemic (Badger, 1933; Shepard and Topping, 1946), but more detailed work on dogs only started in the late 1970s (e.g., Kennan et al., 1977a, 1977b; Lissman and Benach, 1980).

Other SFG rickettsiae are also known for causing diseases of animals and humans around the world. Belonging into the same group of rickettsiae, Rickettsia conorii, the agent of Boutonneuse or Mediterranean spotted fever (MSF) in humans is occurring in Southern Europe, the Middle East and Southern Africa. This pathogen is rarely detected in dogs and has not been reported with clinical signs in dogs so far.

Light microscopic image of a Gimenez stain of tick haemolymph cells infected with Rickettsia rickettsii.
Light microscopic image of a Gimenez stain of tick haemolymph cells infected with Rickettsia rickettsii.

Epidemiology

Geographical and seasonal distribution

The distribution of Rocky Mountain spotted fever (RMSF) as the most severe and most frequently reported human rickettsial illness in the United States has been monitored extensively. Generally, dogs may be effective sentinels for the prevalence of human disease.

Over half of the human RMSF infections are reported from the South-Atlantic region of the United States (Delaware, Maryland, Washington D.C., Virginia, West Virginia, North Carolina, South Carolina, Georgia, and Florida). Infection also occurs in other parts of the United States, namely the Pacific region (Washington, Oregon, and California) and the west South-central region (Arkansas, Louisiana, Oklahoma, and Texas).

Human infections with Rickettsia rickettsii have also been documented in Argentina, Brazil, Colombia, Costa Rica, Mexico, and Panama.

R. rickettsii is not naturally transmitted dog-to-dog, dog-to-human, or human-to-human, but is vectored by ixodid ticks to larger mammals.

In southeastern and mid-Atlantic regions of the United States, the most common vector of R. rickettsii is Dermacentor variabilis (American dog tick); in the northwestern United States and southwestern Canada, the common vector is Dermacentor andersoni (Rocky Mountain wood tick). In Latin America, Amblyomma cajennense (Cayenne tick) is reported to be the primary vector of R. rickettsii (Greene and Breitschwerdt, 1998; Goddard, 1989; Thorner et al., 1998).

In the United States, two further tick species have been suggested to vector R. rickettsii: Amblyomma americanum (Lone Star tick), which is found from central Texas to the Gulf of Mexico and Atlantic coasts, as far north as Iowa and New Jersey and Rhipicephalus sanguineus (Brown dog tick), which is found from southern Canada into tropical South America.

In general, the risk of exposure to a tick carrying R. rickettsii in the USA is low. Only about 1-3% of the tick population carries R. rickettsii, even in endemic areas. There may be significant variation in prevalence of R. rickettsii and RMSF within geographic areas. Since canine infection is supposed to mirror human infection, geographic and seasonal distribution can be considered identical for humans and dogs.

Over 90% of human RMSF infections occur between April and September. This period is the season for increased activity of adult and nymphal Dermacentor ticks.

Host spectrum

Studies suggest that sporting and working breeds and young dogs (< 2 years) are over-represented for RMSF in dogs. 5 to 15% of dogs in endemic areas may have positive serology for R. rickettsii.

Certain small mammal hosts (chipmunks, squirrels) become infected, but clinical signs of RMSF are transient. Despite the short infection, these small mammals serve as amplifiers of the infection in the tick population, allowing the spread of the organisms from infected to uninfected individuals, like e.g. dogs.

In cats, seropositivity has been reported, but a clinical disease has not been described so far.

Transmission

Ticks are the natural hosts of Rickettsia rickettsii, serving both as reservoirs and as vectors. The two major vectors of R. rickettsii in the United States are the American dog tick (Dermacentor variabilis) and the Rocky Mountain wood tick (Dermacentor andersoni).

Ticks may obtain the pathogen by feeding on small mammals such as chipmunks and squirrels functioning as reservoirs for R. rickettsii. During feeding on small rodents with acute rickettsaemia, naïve larval and nymphal tick stages become infected (Greene and Breitschwerdt, 1998; Goddard, 1989). Once infected, ticks may spread the infectious agent transstadially within their own population, or transovarially (horizontal) from the female tick to its offspring. The latter seems to be the primary way by which R. rickettsii propagates in nature. Male ticks can transfer R. rickettsii to females during the mating process via spermatozoa or other body fluids, thus contributing to the maintenance of the organism from one generation to another. Ticks can remain infective for life (possibly 2 to 5 years), especially if there are long periods between blood meals (Greene and Breitschwerdt, 1998; Thorner et al., 1998).

It usually requires several (6 to 20) hours of tick attachment and feeding before the rickettsiae are transferred to a vertebrate, depending on the developmental stage and species of tick (Greene and Breitschwerdt, 1998; Goddard, 1989; Walker, 1995). Consequently, the risk of exposure to R. rickettsii following an individual tick bite is considered to be low. Less commonly, infections may occur following exposure to crushed tick tissues, fluids (haemolymph), or tick faeces. Manual removal of engorged ticks from dogs has been identified as a potential risk factor for human infection (Goddard, 1997), and can occur by inoculation of the pathogen onto mucous membranes by contaminated fingers as has been shown with Rickettsia conorii.

Dogs and humans may function also as reservoirs, but in the natural history of R. rickettsii transmission, human and domestic dog infections are considered incidental events. Even in areas where RMSF is most endemic, only 1 to 5% of ticks (in a particular econiche) harbour R. rickettsii (Burgdorfer, 1975; Greene and Breitschwerdt, 1998; Walker, 1995). In contrast to Rickettsia conorii, the agent of Boutonneuse or Mediterranean spotted fever (MSF) in humans, for which dogs have been shown to be competent reservoirs (Levin et al., 2012 12), R. rickettsii infected dogs have proven relatively inefficient at transmitting rickettsiae to naïve ticks and therefore may not play a large role in maintenance or amplification of the R. rickettsii transmission cycle (Norment and Burgdorfer, 1984).

Pathogenesis

Rickettsia rickettsii enters the circulation system after being inoculated into the host body during the tick bite and subsequently disseminates throughout the body. The pathogens are obligate intracellular bacteria that grow and multiply primarily within the cytoplasm and, occasionally, in the nuclei of endothelial cells lining arterioles and venules resulting in vasculitis, increased vascular permeability and thrombosis in many organs, notably those with an abundant endarterial circulation (e.g., brain, dermis, gastrointestinal organs, heart, lungs, kidneys, and skeletal muscles) (Greene and Breitschwerdt, 1998; Paddock et al., 1999; Thorner et al., 1998). This vasculitis and increased vascular permeability causes blood leakage into adjacent tissues leading to a rash that is traditionally associated with Rocky Mountain spotted fever (RMSF) (only typical in humans) and causing damage to organs and tissues, eventually with interstitial pneumonia, meningoencephalitis, acute kidney injury, multiorgan failure, and death. Activation of the coagulation cascade leads to thrombosis and thrombocytopenia. Plasma loss leads to increased interstitial fluid volume and oedema. For more details on the immunopathology of RMSF see Mansueto et al. (2012).

Although platelet consumption is considered as the primary cause of thrombocytopenia in clinical cases, anti-platelet antibodies have also been identified in infected dogs. A tendency towards a more fulminant disease has been reported in Springer spaniels with phosphofructokinase deficiency and in German shepherd dogs.

Transmission electron microscopic image showing in vitro infection of chick embryo fibroblasts with Rickettsia rickettsii (R).   Infected cells grown for 92 hours. Some bacteria appear to be enclosed within host cell membranes. View the greatly swollen cisterna of the rough endoplasmatic reticulum (RER).
Transmission electron microscopic image showing chick embryo fibroblasts infected with Rickettsia rickettsii (R). Infected cells grown for 92 hours. View the greatly swollen cisterna of the rough endoplasmatic reticulum (RER) (measurement bar 3 µm).

Infected cell grown in culture for 117 hours. Measurement bar with a length of 3 µm.
Transmission electron microscopic image showing in vitro infection of chick embryo fibroblasts with Rickettsia rickettsii (R). Infected cells grown for 117 hours (measurement bar 3 µm).

Diagnosis

A diagnosis of Rocky Mountain spotted fever (RMSF) is based on a combination of clinical signs, epidemiological data and specialised confirmatory laboratory tests. Because of the rapidly progressive nature of certain rickettsial diseases, antibacterial treatment should never be delayed while awaiting laboratory confirmation of a rickettsial illness (Walker and Dumler, 1995), nor should treatment be discontinued solely on the basis of a negative test result with an acute phase specimen (Biggs et al., 2016).

Laboratory tests

There is no widely available laboratory assay that provides rapid confirmation of early RMSF. Routine clinical laboratory findings suggestive of RMSF may include normal white blood cell count, thrombocytopenia, hyponatraemia, or elevated liver enzyme levels.
Serological assays are the most widely available and frequently used methods for confirming cases of RMSF. Indirect immunofluorescence assays (IFA) using paired acute and convalescent sera are the reference standard for serologic confirmation of rickettsial infection in humans (Reller and Dumler, 2015; Walker and Bouyer, 2015).

IFA reaction of a positive human serum on Rickettsia rickettsii, grown in chicken yolk sacs, 400x enlargement.
IFA reaction of a positive human serum on Rickettsia rickettsii, grown in chicken yolk sacs, 400x enlargement.

IFA can be used to detect either IgG or IgM antibodies. Blood samples taken early (acute) and late (convalescent) in the disease are the preferred specimens for evaluation. Most human patients demonstrate increased IgM titres by the end of the first week of illness. Diagnostic levels of IgG antibody generally do not appear until 7-10 days after the onset of illness. However, IgM antibodies reactive with Rickettsia rickettsii are frequently detected in patients for whom no other supportive evidence of a recent rickettsiosis exists (McQuiston et al., 2014). So that the majority of commercial reference laboratories that conduct testing for rickettsial pathogens test for IgG antibodies. It is important to consider the time it takes for antibodies to appear. The value of testing two 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 titres may persist in some patients for years after the original exposure.

These factors also have to be considered for diagnosis of RMSF in dogs. Infected dogs may not have increased titres, so a convalescent sample should be obtained. Furthermore, 5% to 15% of dogs in endemic areas may have positive serology, so a positive diagnosis should never be based upon a single sample unless it is a quite high titre.

PCR detection of R. rickettsii in whole blood is possible but less sensitive because low numbers of rickettsiae typically circulate in the blood in the absence of advanced disease (Demma et al., 2005; Kaplowitz et al., 1983; Walker and Bouyer, 2015). Tissue specimens are a more useful source of SFG rickettsial DNA than acute blood samples (Chapman et al., 2006). Doxycycline treatment decreases the sensitivity of PCR (Bakken and Dumler, 2004; Olano et al., 2003); therefore, obtaining blood for molecular testing before antibacterial agents are administered is recommended to minimize the likelihood of a false-negative result.

Another approach to RMSF diagnostics mainly for human patients is immunostaining by taking a skin biopsy of the rash or the eschar prior to therapy or within the first 48 hours after antibiotic therapy has been started. Immunostaining of skin biopsy specimens is 100% specific and 70% sensitive in diagnosing RMSF (Kaplowitz et al., 1983; Walker et al., 1980). Sensitivities might be higher for tests using eschars than for those using rash lesions (Walker and Bouyer, 2015). This assay may also be used to test tissues obtained at autopsy and has been used to confirm RMSF in otherwise unexplained deaths. 
For more detailed considerations on RMSF diagnosis (especially in humans) see Biggs et al. (2016).

Immunohistological staining of a blood vessel from a human patient with fatal Rocky Mountain spotted fever (RMSF). Red structures indicate Rickettsia rickettsii in endothelial cells.
Immunohistological staining of a blood vessel from a human patient with fatal Rocky Mountain spotted fever (RMSF). Red structures indicate Rickettsia rickettsii in endothelial cells.

Clinical Signs

Rocky Mountain spotted fever (RMSF) in humans initially presents as sudden onset of fever, severe headache and generalized malaise, although patients often also develop myalgia, nausea, vomiting and photophobia. Within two weeks of infection the classic triad of fever, headache and generalized maculopapular rash is present in the majority of patients. The appearance of skin rash is more prevalent as the disease progresses, although some individuals never develop the typical rash (Chapman et al., 2006; Dantas-Torres, 2007).

Mortality rates of RMSF have been estimated at 20% in people in the absence of appropriate antibiotic treatment and 5% in patients who receive antibiotics (Chapman et al., 2006).

In dogs, RMSF can be very difficult to diagnose in its early stages, even among experienced veterinarians who are familiar with the disease. A rash occurs in only 1 out of 5 cases, or even less. But the clinical signs together with the serology, the geographic location and the time of the year will assist in diagnosis. Co-infection with other tick-transmitted pathogens may occur.

Most infected dogs are less than 3 years old and have a recent history of exposure to a tick habitat. First clinical signs may occur about one week after tick attachment and include fever (>39°C), anorexia, depression, lethargy, reluctance to move and stiffness, oedema, lymphadenopathy and neurological signs.

Petechiae and ecchymotic haemorrhages associated with destruction of platelets in response to vasculitis are often seen on exposed mucosal surfaces in the dog. Due to the vasculitis, oedema in the body appendages may also occur. These are including the scrotum, prepuce, and ears of affected dogs. While the disease is generally thought to be self-limiting with duration of approximately 2 weeks in dogs, it may also be fatal.

As primary reservoir hosts, the ticks vector Rickettsia rickettsii to larger mammals; however, dogs and humans are the only ones that display clinically recognizable illnesses (Warner and Marsh, 2002).

Treatment & Prevention

Appropriate antibiotic treatment should be initiated immediately after suspicion of fever and observation of Rickettsia infection on the basis of clinical and epidemiological findings. Treatment should not be delayed until laboratory confirmation is obtained.

Infected dogs (as well as humans) may rapidly and completely recover if the infection is mild or appropriate antimicrobial therapy is initiated promptly. However, thrombosis may lead to organ dysfunction in severe cases. Death occurs in less than 5% of human and canine patients. Dogs that recover from the clinical disease have not shown to become re-infected.

As with other rickettsial infections, the treatment of choice for RMSF is doxycycline or tetracycline. Chloramphenicol may also be used.

Supportive therapy should be initiated concomitantly with antibiotic administration; however, fluid therapy should be administered conservatively due to the vasculitis and subsequent risk of pulmonary and cerebral oedema.

For more detailed considerations on human treatment, please see Biggs et al. (2016). For detailed information on canine treatment see also Warner and Marsh (2002).

Finally, as with other vector-transmitted infections, ectoparasite control is the basis of prevention

References

Introduction

Raoult D, Roux V: Rickettsioses as paradigms of new or emerging infectious diseases. Clin Microbiol Rev. 1997, 10, 694-719

Pathogens

Badger LF: Rocky Mountain spotted fever: susceptibility of the dog and sheep to the virus. U.S. Public Health Service, Public Health Reports. 1933, 48, 791-5

Greene CE, Breitschwerdt EB: Rocky Mountain spotted fever, Q Fever, and typhus. In: Greene CE (ed.): Infectious Diseases of the Dog and Cat. 2nd edn., 1998, WB Saunder Co., Philadelphia, pp 155-62

Keenan KP, Buhles WC Jr., Huxsoll DL, et al.: Pathogenesis of infection with Rickettsia rickettsii in the dog: a disease model for Rocky Mountain spotted fever. J Infect Dis. 1977a, 135, 911-7

Keenan KP, Buhles WC Jr., Huxsoll DL, et al.: Studies on the pathogenesis of Rickettsia rickettsii in the dog: clinical and clinicopathologic changes of experimental infection. Am J Vet Res. 1977b, 38, 851-6

Lissman BA, Benach JL: Rocky Mountain spotted fever in dogs. J Am Vet Med Assoc. 1980, 176, 994-5

Maxey E: Some observations on the so-called spotted fever of Idaho. Medical Sentinel. 1899, 7, 433-8

Paddock CD, Greer PW, Ferebee TL, et al.: Hidden mortality attributable to Rocky Mountain spotted fever: immunohistochemical detection of fatal, serologically unconfirmed disease. J Infect Dis. 1999, 179, 1469-76

Ricketts HT: The study of “Rocky Mountain spotted fever” (tick fever?) by means of animal inoculations. A preliminary communication. J Am Med Assoc. 1906, 47, 33-6

Ricketts H: Recent studies on Rocky Mountain spotted fever in Montana and Idaho. Medical Sentinel. 1908, 16, 688-97

Ricketts HT: Some aspects of Rocky Mountain spotted fever as shown by recent investigations. Med Rec. 1909, 76, 843–55

Ricketts HT, Gomez L: Studies on immunity in Rocky Mountain spotted fever: first communication. J Infect Dis. 1908, 5, 221–44

Shepard CC, Topping NH: Rocky Mountain spotted fever – A study of complement fixation in the serum of certain dogs. J Infect Dis. 1946, 78, 63-8

Wood MW: Spotted fever as reported from Idaho. Report Surgeon General, U.S. Army, Washington, Govt. Print. Office, 1896, 60-5

Epidemiology

Greene CE, Breitschwerdt EB: Rocky Mountain spotted fever, Q Fever, and typhus. In: Greene CE (ed.): Infectious Diseases of the Dog and Cat. 2nd edn., 1998, WB Saunder Co., Philadelphia, pp 155-62

Goddard J: Ixodidae (hard ticks). In: Ticks and tickborne diseases affecting military personnel. San Antonio, Tex: USAF School of Aerospace Medicine, 1989, 70-125

Thorner AR, Walker DH, Petri WA Jr.: Rocky Mountain spotted fever. Clin Infect Dis. 1998, 27, 1353-9

Transmission

Burgdorfer W: A review of Rocky Mountain spotted fever, its agent, and its tick vectors in the United States. J Med Entomol. 1975, 12, 269-78

Greene CE, Breitschwerdt EB: Rocky Mountain spotted fever, Q Fever, and typhus. In: Greene CE (ed.): Infectious Diseases of the Dog and Cat. 2nd edn., 1998, WB Saunder Co., Philadelphia, pp 155-62

Goddard J: Basic tick biology and ecology. In: Ticks and tickborne diseases affecting military personnel. San Antonio, Tex: USAF School of Aerospace Medicine, 1989, 13–19

Goddard J: Rickettsial organisms in ticks: Rocky Mountain spotted fever. Infect Med. 1997, 14, 18-20

Levin ML, Killmaster LF, Zemtsova GE: Domestic dogs (Canis familiaris) as reservoir for Rickettsia conorii. Vector Borne Zoonotic Dis. 2012, 12, 28–33

Norment BR, Burgdorfer W: Susceptibility and reservoir potential of the dog to spotted fever-group rickettsiae. Am J Vet Res. 1984, 45, 1706–10

Thorner AR, Walker DH, Petri WA Jr.: Rocky Mountain spotted fever. Clin Infect Dis. 1998, 27, 1353-9

Walker DH: Rocky Mountain spotted fever: a seasonal alert. Clin Infect Dis 1995, 20, 1111-7

Pathogenesis

Greene CE, Breitschwerdt EB: Rocky Mountain spotted fever, Q Fever, and typhus. In: Greene CE (ed.): Infectious Diseases of the Dog and Cat. 2nd edn., 1998, WB Saunder Co., Philadelphia, pp 155-62

Mansueto P, Vitale G, Cascio A, et al.: New insight into immunity and immunopathology of rickettsial diseases. Clin Dev Immunol. 2012, 967852

Paddock CD, Greer PW, Ferebee TL, et al.: Hidden mortality attributable to Rocky Mountain spotted fever: immunohistochemical detection of fatal, serologically unconfirmed disease. J Infect Dis. 1999, 179, 1469-76

Thorner AR, Walker DH, Petri WA Jr.: Rocky Mountain spotted fever. Clin Infect Dis. 1998, 27, 1353-9

Diagnosis

Bakken JS, Dumler JS: Ehrlichiosis and anaplasmosis. Infect Med. 2004, 21, 433-51

Biggs HM, Barton Behravesh C, Bradley KK: Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever and other spotted fever group rickettsioses, ehrlichioses, and anaplasmosis – United States: A practical guide for health care and public health professionals. MMWR Recomm Rep. 2016, 65 (No. RR-2)

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, 55 (No. RR-4)

Demma LJ, Traeger MS, Nicholson WL, et al.: Rocky Mountain spotted fever from an unexpected tick vector in Arizona. N Engl J Med. 2005, 353, 587-94

Kaplowitz LG, Lange JV, Fischer JJ, et al.: Correlation of rickettsial titers, circulating endotoxin, and clinical features in Rocky Mountain spotted fever. Arch Intern Med. 1983, 143, 1149-51

McQuiston JH, Wiedeman C, Singleton J, et al.: Inadequacy of IgM antibody tests for diagnosis of Rocky Mountain spotted fever. Am J Trop Med Hyg. 2014, 91, 767-70

Olano JP, Masters E, Hogrefe W, et al.: Human monocytotropic ehrlichiosis, Missouri. Emerg Infect Dis. 2003, 9, 1579-86

Reller ME, Dumler JS: Ehrlichia, Anaplasma, and related intracellular bacteria. In: Jorgensen JH, Pfaller MA, Carroll KC, et al. (eds.): Manual of Clinical Microbiology. 11th edn., 2015, American Society of Microbiology Press, Washington, DC, pp 1135-49 

Walker DH, Bouyer DH: Rickettsia and Orientia. In: Jorgensen JH, Pfaller MA, Carroll KC, et al. (eds.): Manual of Clinical Microbiology. 11th edn., 2015, American Society of Microbiology Press, Washington, DC, pp 1122-34

Walker DH, Dumler JS: Rickettsiae: spotted fever and typhus group. In: Lennette EH, Lennette DA, Lennette ET, (eds.): Diagnostic procedures for viral, rickettsial, and chlamydial infections. 7th edn., 1995, American Public Health Association, Washington, DC, pp 575-81 

Walker DH, Burday MS, Folds JD: Laboratory diagnosis of Rocky Mountain spotted fever. South Med J. 1980, 73, 1443-6, 1449

Clinical Signs

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, 55 (No. RR-4), 1-27

Dantas-Torres F. Rocky Mountain spotted fever. Lancet Infect Dis. 2007, 7, 724-32

Warner RD, Marsh WW: Rocky Mountain spotted fever. J Am Vet Med Assoc. 2002, 221, 1413-7

Treatment

Biggs HM, Barton Behravesh C, Bradley KK: Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever and other spotted fever group rickettsioses, ehrlichioses, and anaplasmosis – United States: A practical guide for health care and public health professionals. MMWR Recomm Rep. 2016, 65 (No. RR-2)

Warner RD, Marsh WW: Rocky Mountain spotted fever. J Am Vet Med Assoc. 2002, 221, 1413-7

Further Reading

Dantas-Torres F. Rocky Mountain spotted fever. Lancet Infect Dis. 2007, 7, 724-32

https://www.cdc.gov/rmsf/index.html

EXPLORE OUR CONTENT

CVBD Maps

The CVBD Occurence World Map presents country-specific situations based on current scientific knowledge and feed-back from experts around the world in an easy-to-grasped way.

Resources

Bayer Animal Health supports education in parasitology and especially in the field of Vector-Borne Disease.  Access picture and video collections, discover the World Forum calendar, interesting links and our glossary.

CVBD World Forum

The CVBD World Forum is a working group of leading international experts with the mission to enhance knowledge and communication on companion animal vector-borne diseases for the improvement of animal, human, and environmental health.