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A 9-month-old 25-kg (55-lb) female Labrador Retriever was examined in the month of May because of a 2-day history of progressively worsening anorexia and lethargy. The dog and its owner had vacationed at a lake in the North Georgia mountains 2 days earlier. At that time, the owner removed an engorged tick from the dog's ear, and on the day of examination, a male tick was removed.

The dog had a high rectal temperature (40.4 C [104.8 F]), tachypnea (66 breaths/min), and moist respiratory sounds in all lung fields. Popliteal lymph nodes were large. Hematologic abnormalities included a left shift (9,217 WBC/µl, 7,929 neutrophils, 461 band neutrophils), hypoproteinemia (total protein, 5.8 g/dl; albumin, 3.4 g/dl), and hypocalcemia (8.4 mg of Ca++/dl). Thrombocytopenia was detected (119,000 platelets/dl). Evaluation of urine collected by cystocentesis revealed 1.042 sp gr and granular casts (2/hpf [x 40]). Thoracic radiography revealed diffuse pulmonary interstitial density. Bacteria were not isolated from blood.

The dog was given chloramphenicol (250 mg, q 8 h) on day 1 of hospitalization. The rectal temperature decreased to 39.2 C (102.6 F) within 12 hours of antibiotic administration. The dog's mental attitude had improved and it ate well. The exact cause of the dog's illness was not determined, but it had no further signs of clinical illness and was discharged on day 3.

On day 4, the owner was admitted to a hospital for a fever of undetermined origin, anorexia, lethargy, headaches, myalgia, and arthralgia. She became confused and disoriented. Hematologic and biochemical findings were unremarkable. Three days after admission to the hospital, her physicians contacted the veterinarian to determine the cause of the dog's clinical disease. Because of the similarities of the illnesses in the dog and the owner, Rocky Mountain spotted fever (RMSF) titer determinations were performed on serum specimens obtained from the dog, using microimmunofluorescent methods. Antibody titers to Rickettsia rickettsii, R akari, and R typhi were 1:2,048, 1:512, and < 1:8, respectively.

The owner's serum was tested and found to have high immunoglobulin titers to the respective rickettsiae. The owner was given tetracycline (25 mg/kg of body weight/day) for 7 days, and her clinical illness resolved within 3 days.

After recovery, the owner asked her veterinarian the following questions:

Q: Where does RMSF occur and how common is it?

A: Serologically and pathogenically distinct strains of spotted fever-group rickettsiae have been described throughout the world. Rickettsia rickettsii causes tick-borne disease in the western hemisphere, whereas closely related spotted fever-group agents cause similar disease in other parts of the world. Rocky Mountain spotted fever is the most frequently reported rickettsial disease. Nonspotted fever-group zoonotic rickettsial diseases that develop in people in the United States are rickettsial pox, murine (endemic) typhus, louse-borne (epidemic) typhus, and Q fever. Human ehrlichiosis, suspected to be caused by Ehrlichia canis, has been reported recently.¹ In the United States, RMSF distribution centers primarily around the environments of 3 vector ticks, Dermacentor andersoni (American wood tick), D variabilis (American dog tick), and Amblyomma americanum (Lone Star tick). Most of the recent cases have been detected in the southeastern United States.² Cases have been documented in all states except Alaska, Hawaii, Maine, and Vermont. More than two thirds of the human cases have been documented in North and South Carolina, Virginia, Maryland, Georgia, Tennessee, and Oklahoma, whereas only 1% have been reported in the Rocky Mountain region.³ Rocky Mountain spotted fever has been reported in western Canada, Mexico, Panama, Colombia, and Brazil.⁴

Q: What is the rate of infection of RMSF in people?

A: Of the more than 1,000 cases of rickettsial diseases reported each year in the United States, approximately 90% are RMSF.⁵ Since 1980, approximately 50 deaths per year have been attributed to RMSF. Reported cases of RMSF had been increasing since 1960 and peaked in 1981.^3,6 Presumably, this increase was a summation of factors including encroachment of people on undeveloped wooded areas, improved recognition and therefore increased reporting of the disease, and a periodic cyclicity of infection.

Q: How is the disease maintained in nature?

A: Ticks are both the reservoir and vector for R rickettsii. They transmit the organism transovarially, thereby infecting successive generations of ticks without feeding on an infected host. The prevalence of infection in a tick population is increased by simultaneous feeding of infected and uninfected ticks on certain animals, which develop sufficient rickettsemia.⁷ Only certain species of small mammals, which include chipmunks, voles, and ground squirrels, develop sufficient rickettsemia during acute infection to permit infection of naive ticks, thereby maintaining the transmission cycle in nature. Therefore, the primary sylvan cycle exists between small rodents and immature (larval and nymph) tick stages. It is possible that infected medium-sized mammals such as raccoons, opossums, and foxes are additional sources for infecting ticks, although the degree of rickettsemia in these species has not been established. The 2 Dermacentor spp usually only feed on large mammals, such as dogs and people, in their adult and less commonly during their nymphal stages, whereas even larval stages of Amblyomma ticks feed on these larger hosts. Although these larger mammals develop clinical illnesses, their degree of rickettsemia is low, and they do not serve to infect new ticks. Larvae and nymphs usually do not feed more than once before molting. Adult female ticks feed once before laying eggs, after which they die, and only adult males feed repetitively. Although probably not responsible for infecting new ticks, birds may facilitate the mechanical spread of ticks into previously uninfected areas.⁸ Serologic evidence exists for infection in a variety of domestic animal species, however, it is unlikely that they are involved in the maintenance of infection in nature.⁸

Q: What are the factors controlling the prevalence of RMSF in people?

A: According to the Centers for Disease Control,² most of the human cases are reported between mid-April and mid-September, with most of the cases in May through July. The rate of infection of RMSF is highest in children and young adults, compared with other age groups, and is higher in males. Mortality is higher in children and in people over 30 years old. The rate of infection is higher in whites than in blacks.

Patients from rural areas have a greater proportion of confirmed diagnoses (58%), compared with those from suburban (24%) and urban (12%) areas.^3,9 Approximately 60% of infected human beings have reported a tick bite and 30% more said that they were in a wooded area just before clinical illness. The lack of known exposure does not eliminate tick involvement in infection, especially because small larval and nymph stages can feed transiently and undetected. Most exposures occur at the place of residence, but a number have been related to an outdoor recreational activity. Approximately 10% of reported human cases follow only known exposure to dogs or their ticks, but this should not imply an absolute association because common exposure to the same tick population is more likely.

Q: How long must ticks remain attached to cause infection?

A: There is a delay between the time of attachment of infected ticks and actual transmission of infection to its host. Explanations for this delay are controversial. The reactivation theory states that rickettsiae in infected ticks become avirulent during the colder months when ticks have reduced metabolism and that they remain as such in ticks that do not feed. Reactivation of infection within the tick and apparent increased rickettsial virulence take place a period of time after ticks reattach and take their first blood meal of the season.¹⁰ The process of reactivation is poorly understood. A period of feeding may be needed for the production of infective organisms in the salivary glands. It may relate to the need of the tick to produce a cement collar around their mouth parts before their feeding. In any event, ticks usually do not infect a new host until they have been attached for a period of at least 5 to 20 hours. Though infections that people acquire from biting ticks require extended attachment, those acquired from contact with preengorged ticks on animals do not involve extended contact periods, because the organism appears to be more readily able to induce infection.

Q: Does direct transmission from dogs to people occur?

A: No, ticks are essential for the transmission of the disease under natural conditions. The increased prevalence of RMSF in people in recent years may relate to population shifts into rural localities and increased encroachment of people into the habitat of vector ticks. The prevalence of seropositive reactions in dogs within a given geographic region usually parallels the risk of human infection.¹¹ Furthermore, people that develop RMSF often have owned a dog that has had serologic or clinical evidence of the disease, although the role of the dog in human infection is uncertain. lt is most likely related to the fact that these people have common exposure with their dogs to infected ticks in the environment. In addition, feeding on dogs may reactivate the infection in ticks, so that their body fluids can be infectious immediately at the time of contact with people. Infection with rickettsiae is thought to occur in people exposed to dogs by direct contact with rickettsiae from the engorged tick's hemolymph during tick removal or by contact with tick excreta with the person's abraded skin or conjunctivae.

Aerosol exposure from infected dogs or people is unlikely under natural conditions, as the organism does not survive outside host or tick cells. Aerosol exposure has occurred only experimentally.¹² It is not the secretions from infected dogs, but the effluents from infected ticks that are highly infectious, so that handling ticks should be done with caution when they are removed from pets.

Dogs are unlikely reservoir hosts for R rickettsii because they do not develop rickettsemia of sufficient magnitude to simultaneously infect feeding ticks.¹³ Ticks that spontaneously drop off dogs are finished feeding for a while and would only be infectious if they were handled shortly after detachment. Dogs serve as sentinel hosts for human infection, because both are exposed to similar tick populations. Dogs are important as a source for human infections, because they carry infected ticks into closer proximity to people who become exposed by transfer of ticks from dogs to people or by handling ticks during removal procedures. Numerous reports of human infections follow an association with a tick-infested dog or tick removal within 4 weeks of disease onset.

Q: What are the characteristics of dogs affected with RMSF?

A: Seasonal correlation has been found to be similar for diseased dogs and infected people.¹⁴ The presence of ticks has been mentioned in the history or have been found on physical examination in approximately 60% of the dogs.¹⁴ Most infected dogs have been reported to be less than 3 years old.¹⁴ Purebred dogs are more prone to develop illness, compared with mixed-breed dogs, and the German Shepherd Dog has a particularly high prevalence for developing clinical illness. This may parallel that breed's documented reduced cell-mediated immunity to other rickettsiae such as Ehrlichia.¹⁵

Q: What are the clinical signs of disease in people and dogs?

A: The clinical manifestations in affected human beings closely parallel signs seen in dogs (Table 1).

Early signs in people are vague and may mimic an upper respiratory infection. These are followed first by fever with chills, headache, myalgia, and abdominal pain. Only later may a rash appear, first on the soles of the feet and palms. Although the rash is considered typical of RMSF, it never develops in up to 12% of people, and when it does develop, it is seen in less than 50% of the cases within the first 3 days.¹⁶

Not all people develop all of these manifestations, although fever and headache are the most consistent. Neurologic signs usually develop later in the course of illness and consist of nuchal rigidity, stupor, coma, and/or seizures. Death appears to be more of a problem in patients that develop severe hepatomegaly, jaundice, stupor, and a high BUN concentration (> 25 mg/dl). Cardiac arrhythmias from myocarditis, meningoencephalitis, and disseminated intravascular coagulation often are detected in terminal patients.

Although the disease in people and dogs is similar, there are some major differences. Compared with people, dogs have a much lower frequency of developing a petechial rash, as only approximately one fifth of them develop petechiae. When hemorrhages are found in dogs, they usually are confined to the mucous membranes, rather than involving the skin. Neurologic abnormalities in infected dogs include a much higher frequency of vestibular deficits, consisting of abnormal mental status, nystagmus, head tilt, circling, and incoordination. Clinical illness has not been described in cats, although some have been found to be seropositive to R rickettsii.

Q: What factors influence mortality in infected people?

A: The average mortality of 5 to 10% of affected individuals has remained constant despite increased total number of cases and the availability of effective antimicrobial therapy.³ Mortality may be as high as 20% in untreated individuals.^16,17 Rocky Mountain spotted fever often is misdiagnosed. In one study of 262 human cases, only 41% were diagnosed correctly on the initial patient visit.¹⁶ A comparison of fatal and nonfatal cases indicated that diagnosis and proper chemotherapy can have an effect on the reduction of the number of fatal cases.¹⁸ The case fatality also is higher in those patients where a rash is not detected or for those who do not report a tick bite or immediately seek medical care. Similar delays in diagnosis and therapy have increased the mortality and permanent neurologic damage in affected dogs. The burden of reducing this mortality is dependent on the alert and suspicious physician and/or veterinarian to suspect RMSF and then treat accordingly, even before the return of laboratory analyses. Because RMSF can masquerade as many other infectious and immune-mediated disorders, this can delay the diagnosis. The clinician should consider RMSF in any patient with unexplained fever from a RMSF-endemic area that becomes ill in the spring or summer months, regardless of a history of tick exposure. Human ehrlichiosis has a similar clinical picture.^1,19(1,19)

Q: How is a diagnosis confirmed?

A: Serologic testing is the primary means by which RMSF is confirmed in dogs and people. Numerous techniques are available. The complement-fixation and microimmunofluorescent (micro-FA) tests usually are used to precisely determine antibody titers, the latter test being more sensitive. Cross reaction does exist between other spotted fever-group and some typhus-group rickettsiae. Agglutination of sera with Proteus sp antigens (Weil-Felix test) classically has been used to screen for infection; however, high titer (> 1:80) only suggests recent infection because the test lacks sensitivity and specificity. Similarly, high titers have been determined by use of the complement-fixation test (> 1:16) and micro-FA (> 1:128). Using the micro-FA test, infected dogs in the eastern United States generally have higher immunoglobulin (Ig)G titers than those in the West. Absolute serologic confirmation of active RMSF infection with the micro-FA test requires the detection of a fourfold increase in IgG titer with time. Because titers of high magnitude do not persist in dogs for longer than 9 to 12 months, single increased micro-FA IgG titers of > 1:1,024 found in the East and > 1:128 in the West are indicative of recent or active infection.^14,20 A similar disparity in antibody titers from these 2 geographic regions has not been found in human patients. Titers measured by the micro-FA test for IgM or using latex-agglutination methods^a do not remain high for longer than 3 to 4 months.¹⁴ A single high titer would confirm active infection. Unfortunately, they are not consistently high in all infected dogs, so that a low or no titer does not eliminate recent infection.

Antibody titers are not always available at the time the patient is first admitted and, even then, may not be high because it often takes 1 to 3 weeks to develop a maximal rise in IgG titers. For these reasons, response to treatment often is used to increase the index of suspicion because, with the exception of neurologic deficits, dramatic clinical improvement often follows within 24 to 48 hours of initiation of treatment. In human beings, use of tetracycline early in the course of illness is thought to reduce the magnitude of the serologic response that otherwise would be detected and/or abort the development of a rash, which may confuse the diagnosis.¹⁷ Chloramphenicol may thwart the increase in antibody concentration that is detected in infected dogs and interferes with serodiagnosis.^b Tetracycline, on the other hand, has been reported to have less of an effect without interfering with serodiagnosis.^c

Identification of rickettsiae by immunofluorescent methods in the skin of infected people and dogs has been used to establish an earlier diagnosis of RMSF, with a positive correlation of approximately 70% in both species.^14,21 False-positive results are rare; however, negative results do not rule out RMSF. Specimens should be obtained early in the course of infection, because organisms are eliminated from the tissues within a few days, especially after antimicrobial therapy.¹⁸ Biopsy specimens should be obtained from sites of petechial hemorrhage in human patients. Owing to the usual absence of skin petechiae in dogs, biopsy specimens of skin should be obtained from the inguinal region where fine blood vessels are numerous. Specimens can be formalin-fixed and submitted to a diagnostic laboratory, although formalin fixation does cause some decrease in sensitivity of rickettsial detection.²¹

Q: What is the treatment for RMSF?

A: Tetracycline (22 mg/kg, q 8 h, PO) or chloramphenicol (15 to 20 mg/kg, q 8 h, PO) are the drugs of choice for treating infections in people and dogs. Tetracycline is preferred for human beings because of the lesser side effects, compared with chloramphenicol. In addition, it also does not interfere with serodiagnosis in dogs. Chloramphenicol may be preferred for use in young dogs (< 6 months old) and people (< 8 years old) because it does not cause dental staining. Parenteral administration of either drug may be required in patients that are semi-comatose or have nausea or vomiting.

Supportive care must be used in patients with shock or coagulation disorders and clinical or laboratory evidence of organ failure. Intravenous administration of fluids must be done so with caution because of increased vascular permeability, and expanded extracellular fluid volume can give rise to pulmonary and cerebral edema.²²

Mortality in human beings with RMSF often relates to an incorrect or delayed diagnosis, although rapidly progressive and severe cases can result in death despite treatment. To increase the chances for survival, it often is judicious to begin treatment before the return of laboratory test results. Subclinical or mild infections seem to be more common in dogs, which appear to be more frequently exposed and better adapted than people to the organism.^11,20,23,24

Q: Can there be recurrence of infection?

A: Relapses in people are uncommon, but they can occur when antibiotics used early in the course of illness prematurely clear the parasite and reduce the serologic and cell-mediated immune responses against it. Furthermore, relapses can occur when antibiotics are not continued long enough and the organism is not eliminated successfully. Because chloramphenicol and tetracycline are rickettsiostatic, they do not by themselves eliminate the organism, and permanent recovery depends on the host's immune defenses for the final elimination of rickettsiae.

Q: Are there effective vaccines for people and dogs?

A: Spotted fever vaccines developed for use in people have not caused effective immune responses. Although challenge infections after vaccination have been associated with a prolonged incubation period, a shorter and milder course of illness, and a reduced chance of relapse, reinfection is not prevented as it is after recovery from natural infection. Experimental inactivated tissue culture-origin vaccine appears to offer greater protection against infection in animals than the products presently available.²⁵ An inactivated vaccine containing purified surface antigens of R rickettsii, produced by recombinant DNA technology, has been used successfully to protect mice from lethal RMSF.²⁶

Dogs recovering from infection with R rickettsii have been immune to reinfection, with dramatic seroconversion when challenged 6 to 12 months later.²⁷ None of the naturally infected dogs studied by the author has been known to have a second episode. It also appears that dogs in enzootic areas that are infected naturally at an early age become immune, as most infections have been in dogs ≤ 3 years old.¹⁴ Vaccine effectiveness has not been studied in dogs.

Q: What can the veterinarian do to reduce the occurrence of RMSF?

A: Pet owners and veterinary hospital personnel should be educated as to the dangers of contact with infected ticks. The best means of prevention of RMSF are avoidance of tick-infested areas and rapid, safe removal of attached ticks from pets. Ticks should not be squeezed or crushed with bare fingers, as the organism can be transmitted through intact mucosae or abraded skin after contact with tick feces or hemolymph. Ticks should be removed by applying constant traction with forceps, tweezers, or with fingers protected with facial tissue placed as close as possible to the point of insertion.²⁸ Hands should be washed thoroughly with soap and water after removal.

Clients should be encouraged to control tick infestation of their animals. Pets should be dipped in appropriate insecticides repeatedly if they frequent areas inhabited by ticks. Flea and tick collars and topical applications of insecticides may help discourage tick infestations in outdoor pets. Some local reduction of tick numbers has involved application of insecticides in the form of aqueous suspensions or dusts to surrounding vegetation.⁴

Eradication of the reservoir in the environment is impossible because the organism is maintained in nature by ticks that feed on many small feral mammals. Elimination or reduction of ticks and small ground rodents is difficult, if not impossible, to achieve and may not be environmentally correct.

Discussion

Rocky Mountain spotted fever was named during the 1800s by early settlers of the northwestern United States to describe a febrile disease accompanied by a rash that developed in the spring. It was not until 1907 that Howard Taylor Ricketts demonstrated the etiologic agent.²⁹ Rocky Mountain spotted fever was only reported from the western United States until the 1930s, when a typhus survey incidentally revealed serologic evidence of infection in the southeastern states, where most human infections are now known to occur. The overall increase in reports of this human disease since its first recognition relates to improved diagnostic methods and increased recognition by physicians.

In addition to people, evidence of increased antibody titers to spotted fever group-rickettsiae have been detected in a wide variety of mammals and birds. In many instances, seropositivity probably results from infection by antigenically related but avirulent rickettsiae that also are normally harbored by ticks. Serologic information obtained since the 1930s has indicated that dogs were infected with spotted fever-group rickettsiae; however, clinical illness was not appreciated.^{11,20,23-25,30-33} It was not until the late 1970s that experimental studies in dogs confirmed that the organism was capable of producing clinical disease.³⁴ Clinical reports concerning naturally occurring overt RMSF in dogs have been available only since 1980.^9,14,35-40

Rocky Mountain spotted fever infection in dogs seems to parallel most aspects of the human disease. Dogs are not only a good sentinel host for human infection, but important in facilitating exposure of people to infected ticks. On the basis of serologic studies, dogs appear to be better adapted hosts than people. Serosurveys demonstrate a much larger proportion of exposed dogs, compared with the lower reported frequency of clinical illness in a given area.^20,23 In contrast, serologic evidence of subclinical RMSF in people has been recognized only recently.⁴¹

Diagnosis of RMSF in people may be delayed, because some physicians lack a high index of suspicion for the disease and/or because of a late onset or the lack of development of the characteristic rash. Physicians can be alerted to the possibility of infection by veterinarians. Similar to human infections, those in dogs may be missed by veterinarians who were not familiar with the disease and because clinical signs are varied and similar to those of other illnesses. Signs of persistent fever, hyperesthesia, apparent joint pain, vomiting, and diarrhea and the hematologic and biochemical findings may mimic those signs seen in systemic viral infections, septicemia, and immune-mediated disorders. Therespiratory and neurologic signs can be readily confused with canine distemper.

Footnotes

(a) Latex-Rickettsia rickettsii Kit, Integrated Diagnostics Inc, Baltimore, Md.

(b) Greene CE. Update on neurologic and serologic findings on Rocky Mountain spotted fever in dogs (abstr), in Proceedings. 5th Annu Vet Med Forum, Am Coll Vet Intern Med, 1987; 691-692.

(c) Breitschwerdt EB. North Carolina State University, Raleigh, NC: Personal communication, 1987.

Table 1--Frequency of clinical findings in human beings and dogs with Rocky Mountain spotted fever

References

1. Maeda K, Markowitz N, Hawley RC, et al. Human infection with Ehrlichia canis, a leukocyte rickettsia. N Engl J Med 1987; 316:853-856.

2. Bernard KW, Helmick CG, Kaplan JE, et al. Surveillance of Rocky Mountain spotted fever in the United States, 1978-1980. J Infect Dis 1982; 146:297-299.

3. Hattwick MAW, O'Brien RJ, Hanson BF. Rocky Mountain spotted fever: epidemiology of an increasing problem. Arch Intern Med 1976; 84:732-739.

4. Burgdorfer W. Rocky Mountain spotted fever. In: Hubbert WT, McCullough WF, Schneurrenberger PR, eds. Diseases transmitted from animals to man. 6th ed. Springfield, Ill: Charles C Thomas, Publisher 1975; 396-404.

5. Rickettsial surveillance report No. 2 summary: 1979, Atlanta, Centers for Disease Control, 1981.

6. Rocky Mountain spotted fever-United States, 1985. MMWR 1986; 35:247-249.

7. Price WH. The epidemiology of Rocky Mountain spotted fever. II. Studies on the biological survival mechanism of Rickettsia rickettsii. Am J Hyg 1954; 60:292-319.

8. Greene CE, Philip RN. Rocky Mountain spotted fever. In: Greene CE, ed. Clinical microbiology and infectious diseases of the dog and cat. Philadelphia: WB Saunders Co, 1984; 562-575.

9. Smith RC, Gordon JC, Gordon SW, et al. Rocky Mountain spotted fever in an urban canine population. J Am Vet Med Assoc 1983; 183:1451-1453.

10. Spencer RR, Parker RR. Rocky Mountain spotted fever: infectivity of fasting and recently fed ticks. Public Health Rep 1923; 38:333-339.

11. Kelly DJ, Osterman JV, Stephenson EH. Rocky Mountain spotted fever in areas of high and low prevalence: survey for canine antibodies to spotted fever rickettsiae. Am J Vet Res 1982; 43:1429-1431.

12. Fine D, Mosher D, Yamada T, et al. Coagulation and complement studies in Rocky Mountain spotted fever. Arch Intern Med 1978; 138:735-738.

13. Norment BR, Burgdorfer W. Susceptibility and reservoir potential of the dog to spotted fever-group rickettsiae. Am J Vet Res 1984; 45:1706-1710.

14. Greene CE, Burgdorfer W, Cavagnolo R, et al. Rocky Mountain spotted fever in dogs and its differentiation from canine ehrlichiosis. J Am Vet Med Assoc 1985; 186:465-472.

15. Nyindo M, Huxsoll DL, Ristic M, et al. Cell-mediated and humoral immune responses of German Shepherd Dogs and Beagles to experimental infection with Ehrlichia canis. Am J Vet Res 1980; 41:250-254.

16. Helmick CG, Bernard KW, D'Angelo LJ. Rocky Mountain spotted fever: clinical, laboratory, and epidemiological features of 262 cases. J Infect Dis 1984; 150:480-488.

17. Zaki MH. Rocky Mountain spotted fever: epidemiologic and clinical features. NY State J Med 1979; 79:64-65.

18. Woodward TE. Rocky Mountain spotted fever: epidemiological and early clinical signs are keys to treatment and reduced mortality. J Infect Dis 1984; 150:465-468.

19. Fishbein DB, Sawyer LA, Holland CJ, et al. Unexplained febrile illnesses after exposure to ticks. Infection with an Ehrlichia? JAMA 1987; 257:3100-3104.

20. Fiset P, Wisseman CL, Farhand-Azad A. Rocky Mountain spotted fever in Maryland. Serosurvey of dogs, preliminary report. In: Burgdorfer W, Anacker RC, eds. Rickettsiae and rickettsial diseases. New York: Academic Press Inc, 1981; 569-574.

21. Walker DH, Cain BG, Olmstead PM. Laboratory diagnosis of Rocky Mountain spotted fever by immunofluorescent demonstration of Rickettsia rickettsii in cutaneous lesions. Am J Clin Pathol 1978; 69:619-623.

22. Woodward WE, Hornick RB. Rickettsia rickettsii (Rocky Mountain spotted fever). In: Mandell GL, Bennett JE, eds. Principles and practice of infectious diseases. New York: John Wiley & Sons, 1979; 1508-1514.

23. Sexton DJ, Burgdorfer W, Thomas L, et al. Rocky Mountain spotted fever in Mississippi. Survey for spotted fever antibodies in dogs and for spotted fever group rickettsiae in dog ticks. Am J Epidemiol 1976; 103:192-197.

24. Feng WE, Murray ES, Rosenberg GE, et al. Natural infection of dogs on Cape Cod with Rickettsia rickettsii. J Clin Microbiol 1979; 10:322-325.

25. Ascher MS, Oster CN, Harber PI, et al. Initial clinical evaluation of a new Rocky Mountain vaccine of tissue culture origin. J Infect Dis 1978; 138:217-221.

26. McDonald GA, Anacker RL, Garjian K. Cloned gene of Rickettsia rickettsii antigen: candidate vaccine for Rocky Mountain spotted fever. Science 1987; 235:83-85.

27. Keenan KP, Buhles WC, 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 1977; 38:851-856.

28. Needham GR. Evaluation of five popular methods for tick removal. Pediatrics 1985; 75:997-1002.

29. Ricketts HT. A micro-organism which apparently has a specific relationship to Rocky Mountain spotted fever JAMA 1909; 52:379-380.

30. Badger LF. Rocky Mountain spotted fever: susceptibility of the dog and sheep to the virus. Public Health Rep 1933; 48:791-795.

31. Shepard CC, Topping NH. Rocky Mountain spotted fever. A study of the complement fixation in the serum of certain dogs. J Infect Dis 1946; 130:63-68.

32. Amin OM. Expenmental transmission of Rocky Mountain spotted fever rickettsiae. Bull Ga Acad Sci 1973; 31:118-128.

33. Magnarelli LA, Anderson JF, Philip RN, et al. Antibodies to spotted fever group rickettsiae in dogs and prevalence of infected ticks in southern Connecticut. Am J Vet Res 1982; 43:656-659.

34. Keenan KP, Wisseman CL, Farhang-Azad A. Pathogenesis of infection with Rickettsia rickettsii in the dog: a disease model for Rocky Mountain spotted fever. J Infect Dis 1977; 135:911-917.

35. Lissman BA, Benach JL. Rocky Mountain spotted fever in dogs. J Am Vet Med Assoc 1980; 176:994-995.

36. Thornton JT. Rocky Mountain spotted fever in dogs and man. Mod Vet Pract 1981; 62:313-315.

37. Hill GD. Rocky Mountain spotted fever in a dog (letter). J Am Vet Med Assoc 1982; 180:26.

38. Breitschwerdt EB, Meuten DJ, Walker DH, et al. Canine Rocky Mountain spotted fever: a kennel epizootic. Am J Vet Res 1985; 46:2124-2128.

39. Cosenza SF. Rocky Mountain spotted fever in a dog. Mod Vet Pract 1982; 63:567-568.

40. Rutgers C, Kowalski J, Cole CR, et al. Severe Rocky Mountain spotted fever in five dogs. J Am Anim Hosp Assoc 1985; 21:361-369.

41. Taylor JP, Tanner WB, Rawlings JA, et al. Serologic evidence of subclinical Rocky Mountain spotted fever infections in Texas. J Infect Dis 1985; 151:367-369.

Addendum

Since the publication of this report, additional clinical manifestations of infection in dogs have been characterized. Ocular lesions were found to be common in dogs with naturally acquired Rocky Mountain spotted fever (RMSF).¹ Vascular damage included subconjunctival hemorrhage, hyphema, anterior uveitis, retinal petechiae, and focal retinal edema. The ocular lesions were mild and resolved after treatment with antimicrobials. Necrosis of skin of the extremities has been a complication of RMSF in dogs.² This has been reported in a low percentage of cases and may be caused by a delay in recognition and institution of appropriate antimicrobial treatment.

From a diagnostic perspective, direct immunofluorescent staining was performed on biopsy specimens of skin from experimentally infected dogs. Rickettsiae were detected only in biopsy specimens where vesicles (oral mucosal) or macular rash (skin) were detected and not in random biopsy specimens of clinically normal inguinal skin.

Rocky Mountain spotted fever was identified as a cause of human illness in a focal area of urban New York City, an area where the disease has not previously been known to be endemic.⁴ Numerous vacant lots with weeds and tall grass in a densely populated urban environment were characteristic of the area in which the disease was identified. Five percent of Dermacentor variabilis organisms found in local parks were infected with spotted fever-group rickettsiae. The role of pets in the transmission of the disease to people was investigated. Some of the dogs owned by the people were seropositive, indicating exposure to the disease; however, direct tick exposure or contact with dogs could not be found in all of the human cases.

References

1. Davidson MG, Breitschwerdt EB, Nasisse MP, et al. Ocular manifestations of Rocky Mountain spotted fever in dogs. J Am Vet Med Assoc 1989; 194:777-781.

2. Weiser IB, Greene CE. Dermal necrosis associated with Rocky Mountain spotted fever in four dogs. J Am Vet Med Assoc 1989; 195:1756-1758.

3. Davidson MG, Breitschwerdt EB, Walker DH, et al. Identification of rickettsiae in cutaneous biopsy specimens from dogs with experimental Rocky Mountain spotted fever. J Vet Intern Med 1989; 3:8-11.

4. Salgo MP, Telzak EE, Currie B, et al. A focus of Rocky Mountain spotted fever within New York City. N Eng J Med 1988; 318:1345-1348.