Rocky Mountain spotted fever (RMSF) is a zoonosis which means it can be spread between animals and humans. Many such zoonotic diseases are transmitted through insects like mosquitoes and ticks. RMSF is caused by a very small type of bacteria called Rickettsia rickettsii which is injected into people and dogs by feeding ticks. However, direct transmission of organisms from dogs to people is not known to occur.
Once established inside the animal, the rickettsial organisms cause damage and inflammation in tiny blood vessels resulting in the ‘spots’ referred to in the common name for the disease. These little areas of hemorrhage are often visible on the skin but they also occur in other internal organs like the heart, brain and kidney and can result in serious, potentially life-threatening/fatal illness.
The incubation period from infection to onset of clinical signs can vary from just a few days to two weeks; often times the connection may not be made between the presence of a tick and the later development of illness.
Symptoms of Rocky Mountain spotted fever
Symptoms can be very non-specific in dogs and in people:
Diagnosing Rocky Mountain spotted fever
True diagnostic testing is based on demonstrating RMSF DNA in the patient’s blood by polymerase chain reaction (PCR) testing. Serology, which tests for a rising immune response over time, can also be performed. That means the results are not available until well into the illness. Unfortunately, Not every patient develops a rash, and when they do it is often a few days after they become clinically ill.
Treatment of Rocky Mountain spotted fever
Since treatment with the antibiotic doxycycline is most effective when started before the fifth day of symptoms, any delay in diagnosis and treatment can be profoundly significant in terms of outcome and prognosis. As a result, treatment is typically instituted based on clinical symptoms, location, and risk of exposure alone (with or without known tick bites).
What regions are at risk for Rocky Mountain spotted fever?
First and foremost, do not let the name of the disease fool you into a false sense of security based on where you live. Even though the disease was first recognized in the Rocky Mountains, only a small percentage of all cases are now found there. The CDC says, “RMSF cases have been reported throughout most of the contiguous United States, with five states (North Carolina, Oklahoma, Arkansas, Tennessee, and Missouri) accounting for over 60% of RMSF cases.” Also, while according to the CDC “the proportion of RMSF cases resulting in death has declined to a low of less than 0.5, the incidence of the disease itself has increased during the last decade.”
Prevention of Rocky Mountain spotted fever
Tick control and prevention of transmission are your best defense for both you and your pet. The Companion Animal Parasite Council recommends that, "all dogs be maintained year round on tick control products.” (See your veterinarian about what to use for your particular pet.) In addition tick control efforts can be aided by removing tick habitats around the home:
Of course, you should always carefully check your pets, yourselves, your clothing, and your belongings for ticks.
The timely removal of ticks is absolutely essential in preventing RMSF because, unlike other tick borne illness, e.g., Lyme or ehrlichia where the ticks need to be feeding for approximately 24-48 hours before transmitting infectious organisms, with RMSF “transmission generally occurs 5 to 20 hours after tick attachment,” says capcvet.com. Tick removal and handling must be done very carefully because the rickettsial bacteria can also be transmitted through fluids, tissues, blood, or feces through cuts or sores on your skin.
In conclusion, RMSF is a serious, sometimes fatal illness for both dogs and people that occurs to some degree in most areas of the United States. Because it can be difficult to diagnose early enough for effective treatment, the best defense is to guard against exposure in the first place.
[Editor's Note: Annual testing is important to protect your dog from ticks. Learn more here.]
If you have any questions or concerns, you should always visit or call your veterinarian – they are your best resource to ensure the health and well-being of your pets.
Beware the Bug
By Dr. Ruth MacPete
Anaplasma is spread by ticks. As the weather gets warmer and dogs spend more time outside, they’re more likely to be exposed to these creepy parasites and all of the diseases they carry. Read more> Or learn more about dogs and parasites >
Tuesday, September 22, 2015
Infected ticks placed on dogs engorged normally and dropped off within time limits expected for D. variabilis – 4 days for larvae, 5–6 days for nymphs, and 7–10 days for adult females . Overall, 76 (22.4% of the placed) larvae and 56 (74.7%) nymphs successfully fed to repletion on dogs 181 and 424 respectively. Out the total of 34 adult D. variabilis placed on dogs 362 and 664, 33 (97%) ticks were collected after feeding. All 20 female ticks (10 per dog) completed their engorgement plus 6 and 7 male ticks were collected from dogs 362 and 664 respectively at the end of the infestation (one dead male tick was removed on day 7).
Body temperature charts and a summary of clinical signs observed in dogs following exposure to R. rickettsii-infected ticks are presented in Fig. 1 and Table 1 . An increase of body temperature above 39.5°C was the earliest sign of infection in all dogs. It was recorded on the 3rd day post-infestation (DPI) in one dog, 5 DPI – in two, and 7 DPI – in one, and lasted continuously for three to nine days ( Fig.1 ). Regardless of the time of fever onset in individual dogs, the highest temperatures (40.1 to 41.3°C) were observed at 7–8 DPI. In the two younger dogs (4 months old), febrile response to infection appeared earlier and lasted longer than in the older ones (9 months old). Following the peak of fever, the body temperature in each dog gradually declined, and by 10–12 DPI dropped to or below the pre-exposure levels. After the subsidence of fever, body temperatures continued to fluctuate (±1.5°C) throughout the period of treatment and recovery in both the antibiotic-treated (424 and 664) and the untreated (181) dogs before permanently returning to the normal – pre-exposure levels. The fall of body temperature, however, did not indicate recovery or alleviation of other clinical signs.
(Shaded area marks the period of antibiotic treatment in dogs 424 and 664).
|Dog (age)||Tick life stage||Fever above 39.5°C||Depression||Lethargy||Decreased appetite||Tremors||Petechiae on ocular mucosa||Petechiae on oral mucosa||Skin rash||PCR +|
|181 (4 mo.)||Larvae||5–11||5–17||9–11||6–11||8–11||8–17||7–11||7–13||5–13|
|424 b (4 mo.)||Nymphs||3–11||5–17||none||6–17||6–15||6–17||11–13||6–15||7–13|
|362 a (9 mo.)||Adults||5–8||7–14 a||8–14 a||8–14 a||7–8, 13–14 a||11–14 a||11–14 a||8–11||6–8|
|664 b (9 mo.)||Adults||7–9||7–14||8–13||8–11, 14–15||7–14||8–18||8–17||8–17||8|
Within one or two days after the appearance of fever, dogs became depressed, showing less interest in interaction or play and spending most of their time resting. This depressed state lasted for approximately a week – beyond the subsidence of fever – and in three dogs progressed into either continuous or intermittent lethargic states ( Table 1 ). Beginning 6–8 DPI, all dogs exhibited a decrease in appetite that lasted from 6–7 to 12 days with a total refusal of food for one or two days coinciding with the peak of lethargy. Tremors of the head, limbs, and body also appeared within 6–8 DPI. Appetite returned to normal and tremors subsided either on their own in the untreated dog (11 DPI), or within 24–72 hours after initiation of the antibiotic regimen ( Table 1 ).
Widespread abundant petechiae on gums and buccal mucosa, as well as macular skin rash, became noticeable 6–11 DPI and lasted well into the period of recovery or treatment ( Table 1 ). Vascular injection of the sclera with petechiae in the conjunctiva appeared in both eyes. Extensive maculopapular rash was observed in exposed areas of the skin starting with ears and spreading to the trunk and limbs ( Fig. 2 ).
A– maculopapular rash on the ear of dog 181 at 11 days postinfection (DPI), B – petechiae on oral mucosa of dog 362 at 12 DPI.
In addition to the above signs of infection, dog 181 exhibited slightly swollen testes on 6 DPI and crusty eyes on 14 DPI. Dog 424 had clear nasal discharge on 8–13 DPI and crusty eyes on 11–13 DPI. Only one of the four dogs – 362 - appeared dehydrated on 7–12 DPI, even though it retained its body weight it also displayed excessive salivation and scrotal edema on 7 and 12 DPI respectively. Dog 664 had excessive salivation (7 DPI), slight scrotal edema (12 DPI), and hematochezia (13–14 DPI).
Although fever in dogs 181 and 424 was higher and longer than in 362 and 664, they developed a less severe illness overall. Dogs 362 and 664 had more pronounced, acute, and longer lasting clinical signs, according to the daily overall health assessments. It is noteworthy that the less severely ill dogs were approximately five months younger. Differences in disease severity also corresponded with the fact that dogs 362 and 664 were infested with adult ticks and potentially received higher infectious doses than those infested with either infected larvae or nymphs.
Significant changes in differential blood counts were observed in all experimental animals with the most prominent findings being normocytic, normochromic anemia and severe thrombocytopenia. Thrombocytopenia lasted for approximately 10 days and was followed by secondary thrombocytosis during the third and fourth weeks postinfection ( Fig. 3 A–D ). Platelet counts gradually returned to the pre-infection levels by 28–30 DPI in one antibiotic-treated dog (424, Fig. 3 B ) as well as in the untreated dog (181, Fig. 3 A ). Conversely, in the second dog treated with doxycycline, platelet numbers began decreasing within a week after the initiation of treatment, but remained higher than the pre-infection level for extended period of time (664, Fig. 3 D ). Lymphocytopenia also developed in all dogs within 5 days after placement of infected ticks and was followed by lymphocytosis. Lymphocyte counts returned to normal levels by 30–35 DPI in one antibiotic-treated dog (424) and the untreated dog (181), but remained significantly elevated in the other antibiotic-treated dog (664).
A– dog 181, B – dog 424, C – dog 362 (euthanized for pathological evaluation at 14 DPI), D – dog 664: •••••••••• Hematocrit value (%) ——— White blood cells (x10 3 /µl) - - - - - Granulocytes (x10 3 /µl) – – – – Lymphocytes (x10 3 /µl) – • – • – • Monocytes (x10 3 /µl) – •• – •• – •• Platelets (x10 3 /µl). Shaded areas mark periods of antibiotic treatment in dogs 424 and 664.
All four dogs developed marked monocytosis from 4–7 DPI. Monocyte counts remained above normal for at least 2 weeks regardless of the treatment history ( Fig. 3 A–D ). Again, one of the two antibiotic-treated dogs (664) retained high monocyte levels well beyond the 2-wk treatment period. Three dogs - 424, 362, and 664 – also developed significant granulocytosis, which dissipated in the antibiotic-treated dogs within the first week of treatment. Eosinophil and basophil counts remained within normal limits for all dogs throughout the study. The overall changes in white blood cell counts resulted in leukocytosis in three dogs ( Fig. 3 A–D ).
Rickettsial DNA was detected in the peripheral blood of the dogs on one to four occasions between 5 and 13 DPI ( Fig. 1 ). PCR-positive blood samples generally coincided with the period of fever, with the exception of samples collected from dogs 181 and 424 at 13 DPI, after the sharp decline of body temperature. As with the febrile reaction, the duration of detectable rickettsemia in 4 month old dogs (181 and 424) was somewhat longer than in the 9 month old (362 and 664), but was inconsistent with the severity of clinical symptoms ( Fig. 1 , Table 1 ). In the older dogs, the last appearance of rickettsial DNA in peripheral blood was recorded at 8 DPI, prior to exacerbation of clinical symptoms and approximately a week before administration of doxycycline. Conversely, in the younger dogs – 181 (untreated) and 424 (treated), rickettsial DNA was detectable not only throughout the clinical illness, but after the most severe manifestation of infection had subsided. Therefore, the apparent ending of detectable rickettsemia could not be explained by either initiation of antibiotic treatment or spontaneous recovery from infection.
All dogs seroconverted within 10–13 DPI. In the three dogs whose immune responses were monitored throughout treatment and recovery, reciprocal titers of IgG antibodies peaked at 2048 by 17–28 DPI ( Fig. 4 ). In a dog with a more severe illness (664), the peak titers were recorded earlier than in the one with the least severe clinical signs (181). Noteworthy, antibody titers continued to rise after the subsidence of clinical signs in both treated and untreated dogs.
Shaded area marks the period of antibiotic treatment in dogs 424 and 664.
At 14 DPI, dog 362 exhibited convulsions and was euthanized. Pathologic evaluation revealed multisystem involvement typical of acute rickettsial infection. Pertinent gross findings included pulmonary, gastrointestinal, and urinary bladder hemorrhage, and diffuse lymphadenopathy. Histopathological findings included widespread lymphohistiocytic and, to a lesser extent, neutrophilic vasculitis in multiple tissues, including: heart, lung, urinary bladder, testicle, and all examined segments of the gastrointestinal tract ( Fig. 5A and B ). Fibrin thrombi were seen in urinary bladder and gastrointestinal tissues ( Fig. 5B ). Hepatic sinusoids and pulmonary alveolar walls contained increased leukocytes throughout. Examination of brain revealed meningoencephalitis with nonsuppurative perivascular infiltrates and scattered glial nodules involving cerebrum, cerebellum, and brainstem ( Fig. 5C ). Mild extramedullary hematopoiesis was present in the spleen, and kidney showed minimal lymphoplasmacytic interstitial inflammatory infiltrates.
A - Canine lung with lymphohistiocytic and neutrophilic vasculitis and interstitial leukocytosis (hematoxylin and eosin staining original magnification ×400). B - Canine colon, submucosa with vasculitis with thrombosis (hematoxylin and eosin staining original magnification ×400). C - Canine brainstem with nonsuppurative perivascular infiltrate and glial nodule (hematoxylin and eosin staining original magnification ×400). D - Canine brainstem Immunostaining of spotted fever group rickettsial antigens in multiple vessels, immunoalkaline phosphatase staining, naphthol fast red substrate with hematoxylin counterstain (original magnification ×400).
Immunohistochemical (IHC) testing for spotted fever group rickettsiae was performed on tissue specimens from brain, heart, lung, spleen, small intestine, and colon. An immunoalkaline phosphatase technique with a polyclonal anti-R. rickettsii antiserum was used, with appropriate positive and negative controls. Spotted fever group rickettsiae were detected by IHC in all evaluated tissues ( Fig. 5D ).
At 14 DPI, dogs 424 and 664 were placed on pharmaceutical treatment, which included doxycycline (Vibramycin calcium, oral syrup Pfizer Labs, Inc. New York, NY) at 5 mg/kg orally twice a day for 14 days meloxicam (Metacam oral suspension Boehringer Ingelheim Vetmedica, Inc St. Joseph, MO) at 0.2 mg/kg orally once a day then 0.1 mg/kg for the next two days and Vitamin K-1 injectable (K-Ject Butler Schein Animal Health Dublin, OH) at 2 mg/kg subcutaneous injection once a day then 0.25 mg/kg subcutaneous injections for the next two days. Due to miscommunication during a weekend, the treatment with doxycycline was maintained for a total of 16 days – two days longer than originally prescribed.
At the start of antibiotic treatment, both dogs were lethargic, anorexic, and had petechiae on the gums extensive maculopapular rash was observed in exposed areas of the skin on the trunk and limbs, but neither dog had a fever by this time point ( Table 1 Fig. 1 ). In addition, dog 664 appeared lethargic, reluctant to stand, and had a mild ambulatory ataxia. A complete blood count (CBC) cell differential showed an acute thrombocytopenia, leukocytosis, neutrophilia, monocytosis, and low hematocrit values in both dogs ( Fig. 2 ).
Within 24–48 hours after the start of the treatment regimen, the tremors and anorexia resolved the dogs became more active and began eating normal food. Scleral blood vessel injection, as well as petechiae of the oral mucosa and the rash on the skin, gradually faded away by 11–18 DPI with no apparent correlation to either antibiotic treatment or the severity of other signs ( Table 1 ).
Platelet counts not only returned to normal, but surpassed the upper limit of the pre-infection range ( Fig. 2 ). Total white blood cell counts as well as differential counts of granulocytes and monocytes began declining immediately after initiation of treatment. However, the reversal of neither the thrombocytopenia, granulocytosis nor monocytosis at the start of treatment could not be attributed solely to the effects of the antibiotic as exactly the same dynamics were observed in the untreated dog 181 ( Fig. 2 ). By the end of the 16-day course of treatment, all clinical signs of infection completely resolved in both treated dogs. The dogs' body temperature, appetite, demeanor, defecation and urination remained normal. Blood-PCR remained negative throughout the treatment. Both the total and differential white blood cell counts levelled off after approximately 5–7 days after initiation of treatment and remained virtually unchanged from then on ( Fig. 2 ).
It was noted that in one of the dogs (664) lymphocytes, monocytes, and especially granulocytes remained elevated above the canine reference levels as well as above the pre-infection values. In view of the completely resolved clinical signs, these abnormal differential counts were not considered attributable to the pathogen persistence. However, at 44 DPI - two weeks after the completion of doxycycline treatment, this dog (664) suddenly developed severe scrotal inflammation and the core body temperature increased to 39.5°C ( Fig. 6A ). The dog presented as anorexic and restless. Reappearance of sparse petechiae on the gums and macular rash on exposed skin of the trunk was noted, but there was no scleral injection or conjunctivitis. Bilateral testicular edema was accompanied by acute moist dermatitis of the scrotal skin ( Fig. 7 ). Upon palpation, testes appeared swollen and tender suggestive of underlying orchitis. The blood-PCR at this time was negative, but IgG titers against R. rickettsii antigen abruptly increased to 8,192 ( Fig. 6C ).
Shaded area marks the period of antibiotic re-treatment.
The dog was immediately prescribed doxycycline syrup at 5 mg/kg twice a day for a total of 27 days enrofloxacin injectable (Baytril 2.27% solution Bayer HealthCare, Animal Health Division, Monheim, Germany) at 3 mg/kg intramuscularly twice a day for 7 days meloxicam oral suspension at 0.2 mg/kg once a day then 0.1 mg/kg for the next two days and a topical triple antibiotic ointment twice a day on the affected scrotal area until resolution of the dermatitis.
Enrofloxacin (Baytril) can potentially cause damage to joint cartilage in dogs less than 8 months of age. Considering the age of dog 664 (10 months) at the time of the episode and the severity of clinical presentation, bactericidal qualities of enrofloxacin were judged to outweigh potential side effects. Meloxicam was considered the best choice among non-steroidal anti-inflammatory analgesics as it has lower potential for gastrointestinal side effects and does not impair the platelet function. Vitamin K was administered to assist in blood coagulation.
As in the previous round of antibiotic treatment, the body temperature returned to the normal range within 24 hours after the first dose of doxycycline ( Fig. 6A ) petechiae on oral mucosa decreased and faded within 72 hours. Conversely, the testicular inflammation persisted for over 2 weeks it completely resolved only by 59 DPI – after 25 days of the antibiotic. Moreover, a blood sample collected at 60 DPI (16 days after initiation of treatment) was PCR-positive for rickettsial DNA. CBC differential analysis showed a gradual rise in hematocrit values and a decline in white blood cell counts to within the reference ranges. Serum IgG titers reached 32,768 by 50 DPI and then gradually declined throughout the treatment period and the following two months of observation ( Fig. 6C ). Together, the recurrence of rash on the oral mucosa and skin, a significant boost in anti-rickettsial antibody titers, and the reappearance of rickettsial DNA in the dog's blood strongly suggested that the testicular edema and erythema were due to a relapse of rickettsial infection.
However, because the scrotal edema and dermatitis persisted for 15 days despite intensive antibiotic treatment, the possibility of alternate causality was considered and samples of serum and urine were submitted for additional analyses. Serological testing ruled out infections with Anaplasma phagocytophilum, Borrelia burgdorferi, Babesia microti, Bartonella henselae, B. vinsonii, Ehrlichia canis, E. ewingii, E. chaffeensis, and canine distemper virus as a cause of testicular edema in this dog. Urine culture did not recover either aerobic or anaerobic bacteria after 96 hours of observation, and results of urinalysis were unremarkable. The negative results generated in all additional testing supported a conclusion that the orchitis, as well as the accompanying fever, were caused by a relapse of R. rickettsii infection and not by an alternative pathogen.
The second round of antibiotic treatment in dog 664 was concluded at 71 DPI. By that time, all clinical and hematological abnormalities had completely resolved and dog remained healthy during the additional 8.5 weeks of observation. The acute moist dermatitis resolved in parallel with the scrotal edema. Serum IgG titers gradually decreased to 512 by 130 DPI and all hematological values have remained within the normal limits ( Fig. 6 ). No complications or sequelae were noted in dogs 181 and 424 after their recovery from the original illness up to 130 DPI (data not shown).
Rocky Mountain Spotted Fever (RMSF) is a tick borne illness found in dogs in many US states, that causes a host of symptoms ranging from mild to potentially life-threatening. Today our Charlotte vets explain what causes Rocky Mountain Spotted Fever in dogs, as well as the most common symptoms and treatments.
Rocky Mountain spotted fever (RMSF) is an acute, tick-borne disease seen in dogs throughout the USA, with higher numbers of reported cases in southern Atlantic states, western central states, and areas of the mid-Atlantic and southern New England coastal states.
Caused by an intracellular parasite called rickettsia rickettsii, this disease is transmitted to dogs through the bite of an infected Rocky Mountain wood tick, American dog tick, or brown dog tick.
For transmission to occur an unfed tick needs to be attached to your dog for more than 10 hours, however if a tick has already fed it is capable of transmitting the disease to your dog in as little as 10 minutes after attachment.
Signs and symptoms of Rocky Mountain Spotted Fever begin to appear between 2 - 14 days after the bite occurred and can be extremely varied. Since many of the symptoms of this disease are common to other conditions also, knowing if and when your dog may have been exposed to ticks can help your vet diagnose your dog's condition.
Common signs and symptoms of Rocky Mountain Spotted Fever include:
About 20% of dogs may also experience tiny hemorrhages in the skin, and up to 1/3 of dogs infected dogs will experience symptoms related to the central nervous system such as lack of voluntary coordination of muscle movements, weakness, balance problems, seizures, or spinal pain. Any organ in the dog's body could be affected by Rocky Mountain spotted fever and the symptoms can range from mild to severe or even life-threatening.
When diagnosing Rocky Mountain Spotted Fever in dogs, your vet will look for any of the signs of the symptoms listed above, and possibly perform a series of diagnostic tests including: basic blood tests, urinalysis and x-rays.
Test results that point to Rocky Mountain Spotted Fever include low numbers of platelets, red blood cells (anemia), and abnormal white blood cell counts on complete blood count (CBC) results. Other diagnostic tests could detect low protein levels, abnormal calcium levels, electrolyte abnormalities, and abnormal liver or kidney values which point towards a diagnosis of this condition.
Antibiotics are the main form of treatment for dogs diagnosed with Rocky Mountain Spotted Fever. Most dogs respond to the antibiotic treatment within 24 to 48 hours, although dogs with severe cases of the disease may not respond at all to treatment. The most common antibiotics used are tetracycline, doxycycline, and minocycline. In some cases, your vet may also recommend a blood transfusion to treat anemia or other supportive therapies.
In dogs that are diagnosed and treated for Rocky Mountain Spotted Fever early, the prognosis is good and there tends to be few complications associated with the condition. In many cases lifelong immunity will occur after the infection has been cleared.
Dogs with more advanced cases of Rocky Mountain Spotted Fever, which are treated later are at higher risk for complications of the disease such as kidney disease, neurological disease, vasculitis, and coagulopathies. In these cases the prognosis is guarded since complications can be severe.
To help prevent your dog from Rocky Mountain Spotted Fever, limit your dog's exposure to ticks and tick-infested areas, particularly during peak tick months from March through October.
Whenever your dog has been out in areas known to have ticks, inspect your dog closely. The sooner you can remove a tick after it attaches to your dog, the better your chance that the organism will not have had time to infect your pet. Always wear gloves when removing ticks from your dog to avoid being infected through cuts and scratches on your hand. Tick remover tools are inexpensive and readily available at pet stores and vet's offices. These small tools can make removing ticks faster and safer for you and your dog.
Use of year round tick prevention medications is also recommended to help protect your dog against a host of tick borne diseases including Rocky Mountain Spotted Fever, Canine Ehrlichiosis, Lyme disease, tularemia, and Canine Babesiosis. Contact your vet to learn more about parasite prevention.
Tick populations are on the rise across the United States, and our beautiful state is no exception. Of the 30 plus species of ticks that make their home in Colorado, there are several that have the potential to make your pet, and you, very sick. Rocky Mountain Spotted Fever is one of many diseases that can be transmitted to both people and pets via the bite of an infected tick, and is of particular concern in our region.
Despite its name, Rocky Mountain spotted fever is found in several other parts of the United States. The disease is caused by the bacterium Rickettsia rickettsii, and is spread primarily through the bite of an infected tick. The ticks usually responsible for the transmission of Rocky Mountain Spotted Fever are the American Dog Tick and the Rocky Mountain Wood Tick.
The symptoms of Rocky Mountain Spotted Fever in dogs tend to be vague and may mimic the symptoms of other illnesses. An infected dog may experience fever, muscle or joint pain, vomiting, swollen lymph nodes, or depression. Other signs include abnormal bruising, especially of the gums, but may also be noted on the skin.
If you are concerned about your dog or think it may have been bitten by a tick, bring him or her in to see us right away. With early diagnosis and treatment, most pets make a full recovery.
Rocky Mountain Spotted Fever isn’t the only tick-related disease putting our pets at risk. Tularemia, also known as Rabbit Fever, is prevalent in our area and can be spread via tick to both people and pets. Ehrlichiosis is another dangerous tick-borne disease that is present throughout the United States. While Lyme disease has become more prevalent in eastern, southern, and coastal areas of the country, it still is not as common in Colorado.
It is not uncommon for a pet to be infected with more than one tick-borne illness when bitten by a tick. These are called “co-infections” and are particularly common with Ehrlichiosis.
As with most health issues, including Rocky Mountain Spotted Fever, preventing your pet from being exposed to a tick-borne illness in the first place is far better than trying to treat your pet once infected. Besides keeping your pet on a Spring through Fall flea and tick preventive medication (which we recommend), you can reduce your pet’s chances of coming into contact with ticks in the following ways:
If you haven’t started your pet on a seasonal parasite prevention protocol, or need a refill, please contact us at Lone Tree Veterinary Medical Center, and we’ll be happy to help you.
Rocky Mountain Spotted Fever is carried by a tick and passed onto people as well as dogs when they are bitten. When a tick feeds, the bacteria in their saliva travels to the bloodstream and reproduces in the cells of the blood vessels. This causes problems with blood flow because the blood vessels become inflamed and constricted. In humans, this infection may also be referred to as Spotted Fever Rickettsiosis but this name also includes infections of Rickettsia parkeri, Pacific Coast tick fever, and rickettsialpox.