Rocky Mountain Spotted Fever

Is your pet suddenly lame when you have seen no indication of trauma?  Have you recently removed ticks from your pet or are you late on your tick treatment this month?  Has your dog had any abnormal bleeding or are his joints swollen or painful?  Then you may want to consider the possibility that your dog could be suffering from Rocky Mountain Spotted Fever (RMSF).

Rocky Mountain Spotted Fever is one of the most prevalent tick-transmitted diseases in the United States.  Contrary to what the name implies, RMSF is not just confined to the Rocky Mountains of the United States, but is endemic in most of North and South America.  The name comes from a syndrome first described by settlers in the late 1800’s moving west in the United States.  These settlers reported outbreaks of a distinct skin rash, fever, and general malaise (feeling poorly) with lymphadenopathy (enlarged lymph nodes), which came to be known as Rocky Mountain Spotted Fever.    

The parasitic agent responsible for RMSF is Rickettsia rickettsii.  Rickettsia are a group of obligatory intracellular parasites (can only exist within the cells of a host animal) of the family Rickettsiaceae.  A similar organism by the name of Rickettsia conorii, is the causative agent of Mediterranean Spotted Fever.  Both syndromes and organisms are similar and may affect both dogs and people.  Even in the Americas infection can occur due to either rickettsia species because of the world-wide transport of animals.  

The natural host, reservoir, and vectors (agents responsible for disease transmission) for Rocky Mountain Spotted Fever are ticks.  Two ticks, Dermacentor variabilis, also known as the Rocky Mountain wood tick, and Dermacentor variabilis, the “American dog tick,” are the primary vectors seen in North America.  Recently, however, Rhipicephalus saguineus was found to be the vector involved in an outbreak of RMSF in Arizona.  The cayenne tick (Amblyomma cajennense) is a common vector for Rocky Mountain spotted fever from Texas through South America.

Ticks capable of transmitting Rocky Mountain spotted fever are all three host ticks.  With the three host ticks the larval and nymphal stages of the tick will feed on small- or medium-sized mammals such as mice.  The adult ticks feed on larger mammals such as raccoons, dogs, deer, and people.  Infected Dermacentor ticks will pass the organism to their offspring, thereby transmitting to succeeding generations a higher pathogen load in a process known as transstadial transmission.

Most cases of Rocky Mountain spotted fever occur between the months of April through October when ticks are most active.  There appears to be a 10-year cycle of activity relative to peak occurrences regarding the incidence of RMSF in man.  The reasons for the cyclic pattern in human infection is currently unknown.  Young dogs and purebred dogs appear to be more susceptible to infection, especially the German Shepherd and English Springer Spaniel.  

Clinical signs of infection with Rocky Mountain Spotted Fever are non-specific and are quite diverse.  Common presenting clinical signs that are non-specific include lethargy, anorexia, vomiting, diarrhea, and a rapid and dramatic weight loss.  Clinical signs of respiratory disease may also be seen, such as nasal discharge, tachypnea, and dyspnea (difficulty breathing).  In addition there may be a mucopurulent discharge from the eyes and injection of the sclera (prominent blood vessels on the eye and redness).  

More specific clinical signs of Rocky Mountain spotted fever infection include muscle pain (myalgia), a neutrophilic polyarthritis (arthralgia), and hemorrhaging.  Bleeding may occur from the nose (epistaxis), in the stool (melena), in the urine (hematuria), and on the skin and mucous membranes petechia and ecchymotic hemorrhages (small and medium sized hemorrhages) may be seen.  A hemorrhage in the retina (back of the eye) is a consistent finding and may be helpful in getting a provisional diagnosis.  

Non-altered, or intact male dogs may suffer from orchitis (inflammation of the testicles) and scrotal edema, hyperemia, and epididymal pain.  Edema may also be seen in dependent body areas such as the lower legs and abdomen, the pinna (ear), and the muzzle.

Central nervous system abnormalities may occur and can include hyperesthesia (increased sensitivity of the skin), ataxia (imbalance), vestibular signs, stupor, seizures, and coma.  Gangrene may affect the distal extremities due to vascular obstruction and may necessitate reconstructive surgery or amputation.  Terminal signs of disease may be associated with cardiovascular collapse including hypotension, oliguric renal failure (no urine being produced), or brain death. 

The most consistent hematologic finding on a blood sample is thrombocytopenia, or a lack of platelets.  Other changes in the blood may include an initial leukopenia, or lack of white blood cells, followed by a leukocytosis, or an increase in the white blood cell numbers.  A mild to severe non-regenerative anemia (lack of red blood cells) is often seen.

Blood chemistry changes, which are common, include hypoalbuminemia (low blood albumin levels) and an elevated serum alkaline phosphatase.  Other changes that will occur less frequently include hyponatremia (low sodium levels), and hyperbilirubinemia (high levels of bilirubin in the blood).  

Commonly seen abnormalities in blood clotting include a prolonged activated partial thromboplastin time and elevated levels of fibrinogen.  Occasionally there is a prolonged prothrombin time and an elevation of fibrinogen degradation products.  In rare instances disseminated intravascular coagulation (DIC) can occur.  

In urine samples the pet may demonstrate the presence of protein (proteinuria), blood (hematuria), or bilirubin (bilirubinuria). 

A fourfold increase in a serologic titer between acute and convalescent blood samples is considered to be diagnostic.  The onset of clinical signs may precede seroconversion, therefore necessitating the use of two samples spread weeks apart.   

Treatment consists of administration of doxycycline, tetracycline, or chloramphenicol.  Any delay in therapy may increase the risk of complications or even death.  When an infection is suspected, treatment should be started even before the infection can be confirmed.  Response to antibiotic therapy is rapid and dramatic 24 to 48 hours following the onset of treatment.  

In situations where response to treatment is slow, or the severity of clinical signs is severe, coinfection with Babesia, Bartonella or Ehrlichia should be considered.  

It is believed that natural immunity probably develops subsequent to subclinical infection with Rocky Mountain spotted fever.  

There is currently no vaccine available for prevention of RMSF.  The best way to prevent infection is to limit exposure to ticks, and when exposed to ticks, remove them before attachment occurs. 

References:

Comer, Karen.  “Rocky Mountain Spotted Fever.”  Pp. 27-43.

Ettinger, Stephen and Edward C. Feldman.  Veterinary Internal Medicine. Elsevier/Saunders.  6th Edition. Vol. 1. 2005.  P. 631-632.

Kidd, Linda.  “Spotted Fever Rickettsiosis in Dogs:  An Update.  NAVC Clinician’s Brief.  April 2009. PP. 9-12.

Rosenthal, Marie.  “Vector-Borne Disease Important area of Research; Ticks most common Vector.”  Veterinary Forum.  December 2008. Pp. 8-9.

Wetzel, Linda Marie.  “Vector-Transmitted Diseases in Companion Animals:  Trends, Risks, Controls.” DVM Newsmagazine.  April 2007.  Pp. 10-11.