Tickborne Zoonotic Infections

Tickborne zoonoses deserve special consideration. More zoonotic diseases are transmitted by ticks then by any other vector. 9 Tickborne infections include bacterial, rickettsial, viral, and protozoan infections. As a subset of zoonotic infection, these diseases often go unrecognized in the initial evaluation of febrile patients. Because a high proportion of physicians in the United States know little about tickborne disease, they do not consider this diagnosis in febrile patients. 8 Additionally, not all patients who acquire a tickborne zoonotic infection recall a history of a tick bite. 10 Nevertheless, tickborne zoonoses represent a significant source of mortality and morbidity in the United States—approximately 13,000 cases each year.11 An understanding of the geographic distribution of tickborne zoonoses is important in diagnosing this zoonotic subset (Table 1..45.-3.). The seasonal variation in tickborne zoonoses follows that of other zoonotic infections in North America, the highest incidence being incurred during spring and summer. Rocky Mountain spotted fever (RMSF), Lyme disease, relapsing fever, Colorado tick fever, tularemia, babesiosis, and ehrlichiosis often present with an undifferentiated febrile illness most characteristic of a viral infection, though often accompanied with a rash ( Table 1.4.5:4).

TABLE 145-3 Tickborne Zoonotic Infections: Geographic Distribution

RMSF is the one of the most frequently reported rickettsial infections in the United States.12 The causative organism is Rickettsia rickettsii, a pleomorphic, obligate intracellular parasite, and the vector is the Dermacentor sp. tick. Deer, rodents, horses, cattle, cats, and dogs can serve as zoonotic hosts. RMSF is classically described as a triad of fever, rash, and tick exposure in a majority of infected patients; but a history of tick exposure can only be recalled in approximately 50 percent of these patients. Additionally, RMSF is often misdiagnosed.13 Other presenting signs and symptoms include malaise, myalgias, lymphadenopathy, abdominal pain, nausea, vomiting, diarrhea, hepatosplenomegaly, cephalgia, conjunctivitis, confusion, meningismus, renal failure, respiratory failure, and myocarditis. The rash of RMSF occurs on days 1 to 15 of the illness but is absent in up to 17 percent of patients. 14 Characteristically, this rash appears maculopapular, occurring on the extremities and around the wrist and ankles. The rash spreads centripetally up the trunk, involves the palms and soles, and can become petechial and, rarely, necrotic. The characteristic presentation of this rash may aid in the diagnosis of RMSF. Laboratory abnormalities are nonspecific and consist of a normal or decreased leukocyte count, thrombocytopenia, elevated liver function studies, and hyponatremia. Laboratory diagnosis is unreliable in the early course of RMSF. Diagnosis can be confirmed with a rise in antibody titer between acute and convalescent serum. Skin biopsy with immunofluorescent testing can also confirm diagnosis, but a negative skin test does not exclude infection.15 Additionally, a culture of R. rickettsii may confirm diagnosis. Treatment is with a tetracycline or chloramphenicol (doxycycline 100 mg PO bid for 14 days or chloramphenicol 500 mg qid for 10 days).

Lyme disease is the leading vector-borne zoonotic infection in the United States. 16 Though most prevalent in the Northeast, all continental 48 states have reported Lyme disease. The responsible organism is Borrelia burgdorferi, a spirochete, and the vector is the Ixodes spp. tick. Small mammals and deer serve as the principal zoonotic hosts. Typically described in three distinct stages, the initial stage of illness often presents with a macular dermatitis: erythema migrans. This rash associated with early Lyme disease occurs 2 to 20 days at the site of the tick bite and is a result of a vasculitis. Erythema migrans, which is an erythematous plaque with central clearing, may persist for up to 1 month and recur in the secondary stage of Lyme disease.17 Erythema migrans, though, occurs in only 60 to 80 percent of cases.18 Untreated erythema migrans resolves spontaneously in 3 to 4 weeks. Nevertheless, erythema migrans may aid in the diagnosis of Lyme disease. 1 18 With the dissemination of the Borrelia spirochete, the secondary stage of illness—fever, adenopathy, and flulike symptoms—along with multiple annular dermatologic lesions may occur. The most common neurologic symptom is the development of cranial neuritis, and often facial nerve palsy that can be unilateral or bilateral. This palsy can occur concomitantly with the initial rash of erythema migrans. Other peripheral neuropathies can occur in addition to an asymmetric oligoarticular arthritis of the large joints, with a particular predilection to the knees. Chronic manifestations, the tertiary stage of illness, occur years after the initial infection and consist of chronic arthritis, myocarditis, subacute encephalopathy, axonal polyneuropathy, and leukoencephalopathy. These manifestations account for the tertiary stage of illness. 19 Diagnosis is principally a clinical one, though a two-step serologic test—enzyme immunoassay and Western immunoblot—may help to confirm it. Borrelia burgdorferi has been cultured, but that is extremely difficult. Treatment is with doxycycline (100 mg PO bid for 10 to 21 days) in the initial stage of illness. 9 Alternative antibiotic therapy includes amoxicillin, (500 mg PO tid for 10 to 21 days), cefuroxime (500 mg PO bid for 21 days), and clarithromycin (500 mg PO bid for 21 days). 16 Prophylactic treatment is not recommended, since fewer than 10 percent of the bites transmit the disease, and because prophylactic antibiotic administration may depress the immune response to the disease. A vaccine against Lyme disease is now available for high-risk individuals. This vaccine is made from the outer surface protein of B. burgdorferi using recombinant technology. As the tick feeds on an immunized host, antibodies are ingested destroying spirochetes in the gut of the engorging tick prior to the transmission to the host. A course of three injections of vaccine are required for maximal effectiveness in preventing asymptomatic infections.

Relapsing fever is frequently misdiagnosed and underreported.20 The responsible organisms are Borrelia spirochetes, which can alter their surface antigens. The vectors are Ornithodoros ticks, and the principle zoonotic reservoirs are wild rodents. Often the initial presentation is that of a rash or pruritic eschar at the site of a tick bite. An average incubation period of 7 days precedes the onset of fever, chills, cephalgia, myalgia, arthralgia, abdominal pain, and general malaise. Characteristically, the febrile episodes are interspersed with afebrile periods. Leukocytosis, thrombocytopenia, and an elevated erythrocyte sedimentation rate are the typical laboratory findings. Diagnosis is confirmed with the appearance of spirochetes on Wrights- or Giemsa-stained peripheral blood smears. Treatment is with doxycycline or erythromycin (doxycycline 100 mg PO bid for 14 days or erythromycin 500 mg qid for 10 to 14 days). 2 ,22

Colorado tick fever has an RNA virus as etiology. Endemic to the western mountainous regions of the United States, approximately 300 cases are reported annually. The principal vector is the tick of the Dermacentor sp., and the zoonotic reservoirs are deer, marmots, and porcupines. With an incubation period of 3 to 7 days, the onset of illness is characterized by fever, chills, cephalgia, myalgia, and photophobia. Often following the initial presentation is a macular or petechial rash. Rarely, complications occur. Diagnosis is most often clinical, with associated epidemiologic factors, but the virus can be isolated from blood or cerebrospinal fluid (CSF) by inoculating suckling mice.23 Treatment is supportive care, with infrequently, a long convalescence.

Tularemia, which has been characterized as "a plague-like disease of rodents,"24 is caused by a gram-negative, nonmotile coccobacillus: Francisella tularensis. The zoonotic vectors are ticks of the Dermacentor sp. and the Amblyomma sp., and the principal zoonotic reservoirs are rabbits, hares, and deer. 11 However, tularemia can be contracted through open wounds while dressing an infected zoonotic host. The clinical presentation depends on the method of inoculation, with the ulceroglandular form being the most common. This particular form is often an ulcer at the site of the tick bite, with painful regional adenopathy. Other forms are a glandular form without ulcerations, and a typhoidal form consisting of fever, chills, cephalgia, and abdominal pain. The oropharyngeal form and pneumonic form are the result of deposition into the eyes or inhalation of F. tularensis bacterium. Laboratory findings are nonspecific, and the diagnosis can be determined by culture and enzyme-linked immunosorbent assay (ELISA). Treatment is with streptomycin [15 mg/kg intramuscularly (IM) daily for 10 to 14 days] or gentamicin (3 mg/kg/day in three divided doses daily for 10 to 14 days). A live attenuated vaccine is available for research workers and laboratory personnel. 25

Babesiosis is a malaria-like disease with the etiologic agents being protozoan parasites: Babesia microti and Babesia equi.26 The major zoonotic reservoirs are domesticated mammals, rodents, and deer. Ixodes ticks functions as the principal vector. Blood transfusions have been implicated in the transmission of babesiosis. Clinically, the presentation is of generalized malaise, anorexia, fever, and chills often progressing to intermittent sweats, myalgia, and cephalgia. Splenectomy and immunologic impairment are thought to be risk factors for this zoonosis. Additionally, babesiosis can progress, resulting in hemolytic anemia. Laboratory tests often show evidence of hemolysis, liver dysfunction, anemia, thrombocytopenia, and renal failure. Interestingly, approximately 20 percent of the patients with babesiosis have a concurrent infection with Lyme disease. Diagnosis is made by finding intraerythrocytic ring forms on a Giemsa-stained peripheral blood smear, though false-negative results can occur when the level of parasitism is low. Treatment is with oral quinine (650 mg tid for 7 days) plus intravenous or oral clindamycin (600 mg tid for 7 days).26

Ehrlichiosis is a zoonotic disease with two principal presentations of human granulocytic ehrlichiosis and human monocytic ehrlichiosis. The etiologic agent responsible for the granulocytic form is thought be be similar to Ehrlichia phagocytophila and Ehrlichia equi.2 28 The predominant form in the United States is the monocytic form caused by Erlichia chaffeensis. The ehrlichia bacteria are gram-negative pleomorphic coccobacilli that infect circulating leukocytes. 28 The zoonotic reservoirs are thought to be deer, dogs, and other mammals, with the vectors being Ixodes sp. and Amblyomma sp. ticks. Characteristic clinical presentation is that of fever, cephalgia, malaise, nausea, vomiting, abdominal pain, anorexia, and myalgia. In a minority of cases, a maculopapular or petechial rash is present involving the soles and palms. Renal failure, respiratory failure, and encephalitis can develop. Diagnosis is with serologic testing. Laboratory studies can demonstrate leukocytopenia, thrombocytopenia, and liver dysfunction. Treatment is with doxycycline, 100 mg PO bid for 7 to 14 days. 28

Tick removal can present a vexing challenge to the emergency physician. The use of a burning match or any action resulting in crushing the tick should be avoided. These attempts at removal result in the tick regurgitating into the wound site. Additionally, they have the potential for incomplete removal of the tick. The most effective way to remove an imbedded tick is a two-step approach. First, viscous lidocaine is applied to kill the tick and anesthetize the bite site. Second, careful and gentle traction is applied to the tick's head with fine forceps. It is imperative that all parts of the tick be removed. Residual tick body parts can stimulate a granulomatous reaction and persistent infection.

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