Rickettsiosis, Ehrlichiosis, Anaplasmosis, and Neorickettsiosis

Chapter 17 Rickettsiosis, Ehrlichiosis, Anaplasmosis, and Neorickettsiosis



Robert G. Sherding


Microbial genetic analyses have recently led to the extensive taxonomic reclassification and renaming of several animal pathogens that are now found in the genera of Rickettsia, Ehrlichia, Anaplasma, and Neorickettsia. Pathogens in these four genera are obligate intracellular bacteria that are vector-transmitted by tick bites (Rickettsia, Ehrlichia, Anaplasma) or parasitized trematodes and aquatic insects that are ingested (Neorickettsia). The geographic distribution of vectors determines regional prevalence of each infectious agent. In general, serologic cross reactivity is common among organisms within each genus, but minimal between genera.


The full scope of disease caused by many of these agents is still being defined. In high-prevalence areas with a heavy tick population, such as the southeastern United States, dogs are frequently infected with multiple tick-transmitted pathogens simultaneously; for example, dogs infected with Ehrlichia spp. and Anaplasma spp. may be co-infected with Bartonella vinsonii (berkhoffii), Borrelia burgdorferi, or Babesia spp. Breitschwerdt has observed that the synergistic effects of these polymicrobial infections may lead to an unpredictable variety of chronic disease manifestations not seen with single-agent infections.



ROCKY MOUNTAIN SPOTTED FEVER


(Rickettsia rickettsiae)


Rocky Mountain spotted fever (RMSF) is a tickborne rickettsial disease of dogs and humans that is most prevalent in the Southeast, Midwest, and Great Plains regions of the United States. Because of its acute nature, most cases of canine RMSF occur during tick season, between April and October.




Etiology


Canine RMSF is a tick-transmitted infection caused by R. rickettsii, one of several rickettsial species included in the spotted fever group.



Transmission



• The main vectors for R. rickettsii are the American dog tick (Dermacentor variabilis), found primarily east of the Great Plains and in parts of the west coast, and the wood tick (Dermacentor andersoni), found in an area from the Rocky Mountains to the Cascades. These are three-host ticks; the permanent hosts are humans, dogs, and cats, and the reservoirs are rodents.

• Ticks usually acquire the organism through feeding on infected animals, although vertical transmission in tick populations also can occur.

• Ticks usually do not infect the hosts until they have been attached for a minimum of 5 to 20 hours. This infection also can be transmitted iatrogenically through blood transfusions.


Pathogenesis



• Once inoculated into the host via a tick bite, the organism quickly invades and replicates in vascular endothelial cells, resulting in widespread necrotizing vasculitis, altered vascular permeability, edema, platelet aggregation, and multi-organ damage (e.g., skin, brain, heart, lung, liver, and kidneys). The incubation period varies from 2 to 14 days.

• Only an acute form of clinical disease is recognized in dogs. The clinical illness lasts 7 to 14 days, with high mortality rate in untreated animals. In contrast to most other tickborne infections in dogs, R. rickettsii has not been associated with chronic or recurrent disease, and it does not persist in a chronic carrier form.


Clinical Signs


Exposure to R. Rickettsii can lead to either subclinical infection or an acute, rapidly progressive disease of short duration. Most dogs with acute RMSF present between April and October, coinciding with the tick season. The clinical signs and laboratory abnormalities are highly variable. Because of the acute course, ticks may still be found on the dog (or may have been recently removed by the owner); however, a negative tick history by no means excludes RMSF.


Clinical findings in dogs with acute RMSF can include any of the following:


• General signs: Fever, anorexia, lethargy, vomiting/diarrhea, weight loss, and generalized lymphadenopathy.

• Polyarthritis: Poorly localized joint and muscle pain and lameness.

• Ocular signs: Schleral and conjunctival hyperemia and petechiae; retinal vasculitis and hemorrhages; and anterior uveitis and hyphema.

• Neurologic signs: Hyperaesthesia, tetraparesis, ataxia, vestibular signs, stupor, and seizures.

• Cutaneous vasculitis: Hyperemia, edema, and petechial-to-ecchymotic hemorrhages (face, distal extremities, scrotum, ventral abdomen); and skin necrosis and gangrene in severe cases.

• Pneumonitis: Cough, tachypnea, dyspnea, and exercise intolerance.

• Myocarditis: Cardiac arrhythmias or sudden death.

• Other signs: Icterus, orchitis, bleeding (epistaxis, melena, and hematuria), or oliguric renal failure.


Laboratory Findings



• Frequent hematologic findings include mild-to-moderate thrombocytopenia (>80% of cases), leukocytosis with a left shift, toxic granulation of neutrophils, monocytosis, and mild anemia. Rare findings are transient leukopenia (early) and overt disseminated intravascular coagulation (DIC) (late). Anti-platelet antibodies have been demonstrated in natural and experimental canine RMSF infections.

• Biochemical abnormalities, which reflect vascular injury and organ damage, can include hypoalbuminemia, increased serum liver enzymes, hyperbilirubinemia, azotemia, hyponatremia, hypochloremia, hypercholesterolemia, and metabolic acidosis.

• Synovial fluid is typical of neutrophilic polyarthritis, and cerebrospinal fluid has a mild increase in protein and cells (neutrophils).


Diagnosis


Suspect RMSF in dogs residing in endemic areas that present with an acute, rapidly progressive febrile illness and a recent history of tick infestation. The diagnosis of RMSF can be confirmed by serum antibody titers and polymerase chain reaction (PCR) assays that are readily available to practicing veterinarians through the Vector Borne Disease Diagnostic Lab at North Carolina State University. Submission requirements and forms are available at www.cvm.ncsu.edu/docs/tickbornediseaselab.html.


• Using the indirect fluorescent antibody (IFA) serologic test, a serum titer of >1:128 is presumptive evidence of RMSF; however, dogs often have a negative titer when tested early in the disease (first 5 days). A definitive diagnosis is established by a fourfold rise in paired titers (2-3 weeks apart); or based on a single titer of >1:1024 at 7 days or more after the onset of clinical signs.

• The prevalence of seropositivity is higher than the prevalence of the clinical disease and must be considered when interpreting titers. This is due in part to cross reactivity with nonpathogenic tickborne Rickettsia spp. High titers can persist for up to 1 year after successful treatment or recovery from the disease, which also must be considered.

• Rapid confirmation of the diagnosis can be established by PCR identification of rickettsial DNA in an EDTA blood sample or in tissues. Prior antibiotics can cause a false-negative PCR result.

• The direct immunofluorescence test can confirm the diagnosis by detecting rickettsial antigens in fresh or paraffin-embedded tissues, especially skin, as early as 3 to 4 days post-inoculation. Skin biopsies obtained with local anesthetic and a biopsy punch can be used. A positive result is highly specific for RMSF; however, false-negative results occur in up to 30% to 40% of cases (low sensitivity).


Treatment



• Doxycycline (5-10 mg/kg, PO or IV, q12h) for 14 days is the drug of choice for treating dogs with RMSF. Tetracycline (22 mg/kg PO q8h), enrofloxacin (3 mg/kg, SC or PO, q12h), or chloramphenicol (15-25 mg/kg, PO, IM, or IV, q8h) given for 14 days have also been effective for treating dogs with RMSF.

• Initiate supportive therapy as needed, but use extreme caution with fluid therapy because vascular damage predisposes the patient to severe edema.



Key Point


Do not delay treatment of dogs suspected of having RMSF. Initiate doxycycline while awaiting confirmatory diagnostic tests to prevent development of complications such as fatal central nervous system (CNS) disease, cardiovascular collapse, oliguric renal failure, or gangrene.



Prognosis


The prognosis is good when treatment is instituted promptly. Clinical response should occur within hours of initiating appropriate drug administration. The mortality rate is high if an ineffective antibiotic is used or treatment is delayed until the disease is advanced. Dogs with severe CNS signs may die within hours, before treatment takes effect.



Prevention



• Prevention of RMSF in dogs depends on minimizing tick exposure, using an effective tick preventative product on a regular basis, and routinely checking dogs for ticks and removing them promptly. Dogs that recover from RMSF are immune to re-infection.

• RMSF is one of the most important rickettsial diseases in humans. Dogs are not reservoirs or chronic carriers for R. rickettsiae, and thus dogs are considered minimal zoonotic risk. However, take precautions (i.e., wear gloves) when removing ticks or handling blood from a potentially infected dog.

• A confirmed diagnosis of RMSF in a dog is an indication that R. rickettsiae is endemic in the local tick population. Dogs can thus serve as sentinels for the potential risk of human exposure in a geographic area.


CANINE EHRLICHIOSIS


Canine ehrlichiosis is a tick-transmitted infectious disease of dogs caused by various species of Ehrlichia, a genus comprised of obligate intracellular gram-negative cocci that have a tropism for leukocytes. This intracellular location facilitates chronic persistence and resistance to antimicrobial therapy. Feline ehrlichiosis is discussed at the end of this chapter under Feline Ehrlichia-Like Diseases.




Etiology and Transmission


Ehrlichia organisms are transmitted to dogs through the saliva of an attached tick, and ticks become infected when they feed on the blood of an infected host. Ehrlichia species are distributed worldwide according to the geographic distribution of specific vector ticks. Ehrlichia organisms can also be transmitted iatrogenically through transfusion of contaminated blood.


• Ehrlichia canis is transmitted primarily by Rhipicephalus sanguineous, the common brown dog tick, and infection occurs worldwide in tropical and temperate climates. E. canis infections have been reported year-round throughout the United States, most frequently in the Southeast.

• Ehrlichia ewingii is transmitted by Amblyomma americanum, the lone-star tick, and probably other ticks (e.g., Dermacentor variabilis, Rhipicephalus sanguineous). Infection occurs predominantly in the Southern and Central United States, including Missouri, during tick season (spring and summer).

• Ehrlichia chaffeensis is transmitted by Amblyomma americanum, and infection occurs in the Southern United States.


Clinical Signs and Laboratory Findings


E. canis and E. chaffeensis most frequently infect circulating monocytes and mononuclear phagocytic cells in lymph nodes, spleen, liver, and bone marrow, resulting in widespread lymphoreticular hyperplasia, organomegaly (lymphadenomegaly, splenomegaly, and hepatomegaly), and hematologic abnormalities. E. ewingii infects granulocytes.


After a transient acute phase of infection, dogs either clear the infection, or in the case of E. canis infection, they enter a prolonged subclinical phase that can extend for months to years until they finally develop clinical signs of chronic-phase disease. Most dogs with E. canis infection are diagnosed in the chronic phase.



Acute Phase of Infection


The acute phase of canine ehrlichiosis begins 1 to 3 weeks after the bite of an infected tick. The clinical signs vary from mild to severe and last 2 to 4 weeks. The clinical presentation of acute ehrlichiosis can resemble RMSF (see previous section).


• Acute-phase infection causes transient fever, anorexia, lethargy, oculonasal discharge, generalized lymphadenopathy, splenomegaly, hepatomegaly, and moderate-to-severe thrombocytopenia.

• Less frequent manifestations that are seen in severe cases include neurologic signs due to meningoencephalitis (ataxia, paresis, hyperaesthesia, twitching, cranial nerve deficits); anterior uveitis and chorioretinitis; dyspnea or exercise intolerance due to pneumonitis; edema of the limbs and scrotum; and petechial and ecchymotic hemorrhages due to thrombocytopenia or platelet dysfunction.

• E. ewingii most frequently causes acute neutrophilic polyarthritis with lameness, stiffness, and joint pain and swelling. It also can cause acute meningoencephalitis and a variety of neurologic signs (ataxia, paresis, etc.).

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Rickettsiosis, Ehrlichiosis, Anaplasmosis, and Neorickettsiosis

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