Treating Lyme Disease (Jernigan)

Misfit Toy

Senior Member
If I do end up having lyme, I will try antibiotics. I am on zithromyacin right now due to bronchitis and not doing horrible. Shocker! This is the first time on this drug. My fear comes from having had mycoplasma. I was on 6 months of antibiotics, in which I became much worse. Much. Ever since then, I have been constipated, struggled with yeast etc. I take probiotics but they really do very little. I am not well enough to make kefir and I am allergic to milk and goat's milk. I have enough of a time just cooking myself a meal everyday. I get out almost everyday by way of walking or car.

Anyway, I would try anything to get better, but have seen horrible detox symptoms on youtube regarding lyme. It's awful. My friend suppossably has lyme, after having CFS for over 12 years. She is on antibiotics or was and almost died. Her heart was a total mess. It's a nightmare. I also have a friend who instantly felt better on antibiotics and has become so much better from them. She had classic lyme symptoms early including bells palsy. She is so much better! I just have a feeling I won't be one of those folks due to my history. Well, one who feels fabulous. Then there is the question of the LLMD. The lyme doctor who is a specialist who charges over $750 for an appointment because HE CAN. Because there are so many ill and desperate people out there who will spend that much out of pocket. My friend wants me to go to one in Manhattan. I am too sick to travel 2.5 hours a way and personally, I feel the whole thing is a racket. He is treating her the same way anyone does..."oh, ok...well let's put you on this antibiotic,....not working or making you worse...ok, now this one." Each additional appt. after the first one is between $485 and $285. She is broke. I think it's awful and she is more ill.

I think digesting all of this and knowing what to do is a process. I believe in emergency medicine. I do! But, I feel the foundation of the body needs to be built back up. That is so important.
If your positive for Babesia you probably have Lyme too. I think one of the reasons I didn't recover more then I did is that I have such a hard time being able to take any antibiotics. I never thought I could ever feel any worse then I did until I started antibiotics. It was scary.

Misfit Toy

Senior Member
How do you know if you have babesia? I had the blood work by Igenex that was $500. It was called The complete lyme panel, Western Blot. PCR Serum and whole panel. My doctor has been treating me for CFS for 10 years and I had to beg him to do this test. He just isn't wanting to do it. I don't get it. I think he would rather I just have CFS because he knows what a hard time I have with antibiotics.


Senior Member
Hi Spitfire

The test I had - Immunosciences panel C - included tests for Lyme 'co-infections' like babesia and bartonella. Have a look at one of the Lyme message boards (eg Eurolyme or Lymenet) - they talk about different tests all the time.

Hello- I' m new to this message board but been on prohealth for many years. I'm 48--originally dx'd with fibro in 1998. chemical sensitivies building before fibro diagnsis.I had a case of optic neuritis in 2006 followed by increasing neuro symptoms. MRIs have been normal -doctor's say no MS. Recent neuro is lumping be into CFS bucket. They don't know what to do with me I have so many symptoms now and MRI's are normal. Ive done every imaginable treatment- blood type diet, rolfing, acupuncture, reiki, massage, walked every day-thought I was building health until 2006. There is history of immune issues in my family since my mom has cfs/fms type issues, sister colitis, siser interstitial cystitis, nephew ASD. 2006 I started down the lyme path- did zhang protocol- no change- added bhuner herbs and had neuro explosion from hell in 2007- balance, extreme brain fog, jerking/wtiching, speaking, balance, numbness but went away, weak/shaky , sleep bad etc etc. i stopped all herbs and it took me 4 months to improve but not back t obaseline.
Went on LDN /did ashok's program- got better but not back to baseline before neuro explosion was stable 2008. Also did nystatin/candida diet extreme version since tested high for yeast according to great plains labs.
Also test high for oxalates.
Went off LDN since it was causing heavy menstrual cycles/did not think it was doing anything.
Declined in 2009/major decline this fall-more jerking, more brain fog, felt weaker , sleep disrupted etc.

Decided to try antibiotic protocol but chose to do autism doc Dr. McCandless fungal protocol since I always test high for yeast. Flagyl/diflucan combo- 1 week of flagyl- I got so sick I had to stop with really bad brain fog, tongue turned yellow,lost taste, smell,lost all appetitie-could not function-stopped sleeping continued diflcuan 3 weeks- addes a few herbs and have been crashing ever since- I went from having bad brain fog,some jerkinking and twitching, so dizzy somedays can't walk, feeling weak on left side/not strong but functional-driving , working/taking care of my kids-to know totally housebound on floor/couch.
Dizzy sick feeling in brain that won't go away, eye pressure/eyes hurt, head jerking/neck so weak I feel I can't hold my head up, body weak and shaky, total insomnia-some nights no sleep even on meds, nervous system in overdrive, body burning, night sweats, nubmness on left side now spreading to right, jproblems typing, coordination, spatial off, erking all over everything, whole body jerks forward, problems speaking/swallowing-you name it. The flagyl/diflucan pushed me over the cliff. And I keep declining 3 months later.

I'm seeing a big name lyme doc in NY first week of may -if can make it. Dealthly ill- feel like I'm losing all neur functtio- terrified/anxiety attacks daily- also dealthy afraid of abx treatement given how sick I am and where my first drug experience as well as herbs put me 2 years ago.

My genomics liver detox profile indicates my phaes I is too fast, phase II had medication detox problems-glucornidation.

I know there are no easy answers. I know the lyme doc will want to put me up to IV meds-I'm terrified I can't take that. Any sicker and I won't be able to walk and will be bedbound. I now someone who had similar issues but not as extreme as mind she's been on oral 18 months-better than crashed, IV 18 months with port- off port- now better, but has seizures and other issues. now on orals-she believes abx saved her life.

Does anyone have any advice? I don't know what to do. I wish I could have taken abx 12 years ago with original diagnosis-I could have handled it then. Now I' so sick. Losing neuro function is terrifing.


Daughters High School Graduation
Upstate SC, USA
Just FYI - A very good Lyme doctor from Fort Mill, SC just moved into the Washington, DC area and now has his clinic open - The Jemsek Specialty Clinic. He is very Lyme literate and have no doubt he saved 2 of my friends lives when other doctors would have killed both of them. North Carolina even pulled his medical license temporarily , but he vendicated himself.

There may be some links to some good info at the least. Hope it is of help!!


iherb code TAK122
Hi herbqueen - sounds like you have had an absolutely terrible time. We take these meds trustingly and then end up worse. Ijust wanted to say I was on a abx protocol through an enlightened UK doc. I was okayish on most but the Flagyl I just could not take, I had had it prescribed previously for a internal problem and had stopped then after 2 days as it affected my sight, the second time was no better and I stopped immediately, I do believe that some of these drugs just can't be tolerated by some of us, and its not de-toxing. I'm just so sorry the effects have been so bad for you, I do hope you get to see someone who can help you.
Have you thought about the herbal abx route? eg. cats claw/burbur/comanda(sp) I understand your fearful feelings about taking anything due to intolerances, I am the same, I am on a sorely restricted diet, I have B12 and mag injections several times a week, which I tolerate okay as well as Q10, EPA and Vit C, I have regular vit/mineral infusions as I can't take any of the oral B vits I've tried. Its an absolute pain and costs a fortune here. I started taking the Samento (cats claw) like this- 1 drop in a full glass of water (drink 1/4) for several days, I had built up to two drops but then got an activation of EBV and was out of it for a few months. Do I start again? you get so weary of it all. Good luck with everything and truly hope you feel a bit better soon.


Senior Member
Hi Maryb

FWIW I took Samento for about 6 months. It was one of the most powerful things I've ever taken. Like you I started on one drop and couldn't tolerate any more for weeks. I finally got up to 12 drops a day after 4 months, but I never felt any better.



Senior Member
Babesiosis - Emergency Medicine - INFECTIOUS DISEASES - Part I

A member recently asked me some questions about Babesia. I wasn't too familiar with it but since I work in a lab, I have access to things like Mayo Medical Labs guide to test interpretations and many other things. I came across a new journal article today and I've been trying to post it but have been unsuccessful so far.

I guess the full journal article is considered "too large"! I'm going to try and post it piecemeal on this thread since you all might benefit from it. The images do not upload. I do have it in a Word document but can't load it. Here goes:

Emergency Medicine - INFECTIOUS DISEASES

Last Updated: Jun 4, 2010

Synonyms, keywords, and related terms: babesiosis, Babesia species, Ixodes tick, parasitic infection, intraerythrocytic parasitic infection, tick bite, hemolytic anemia, thrombocytopenia, atypical lymphocyte formation, acute respiratory distress syndrome, ARDS, Lyme disease, Ixodes scapularis, white-tailed deer, white-footed mouse, Peromyscus leucopus, adult tick vector


Author: Tarlan Hedayati, MD, Assistant Professor of Emergency Medicine, Rush Medical College, John H Stroger Hospital of Cook County

Tarlan Hedayati is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Coauthor(s): Cameron Nima Nourani, MD, Resident Physician, Department of Emergency Medicine, John H Stroger Hospital of Cook County

Editors: Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Barry J Sheridan, DO, Chief, Department of Emergency Medical Services, Brooke Army Medical Center; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Author and Editor Disclosure

INTRODUCTION Section 2 of 13


Babesiosis is an intraerythrocytic parasitic infection caused by protozoa of the genus Babesia and transmitted through the bite of the Ixodes tick, the same vector responsible for transmission of Lyme disease. While most cases are tick-borne, transfusion and transplacental transmission have been reported. In the United States, babesiosis is usually an asymptomatic infection in healthy individuals. Several groups of patients become symptomatic, and, within these subpopulations, significant morbidity and mortality occur. The disease most severely affects patients who are elderly, immunocompromised, or asplenic. Among those symptomatically infected, the mortality rate is 10% in the United States and 50% in Europe.

Clinical Image Atlas
Click to view clinical images on the features, causes, epidemiology, diagnosis, and treatment of Lyme disease.


Babesiosis is a zoonotic disease maintained by the interaction of tick vectors, transport hosts, and animal reservoirs. The primary vectors of the parasite are ticks of the genus Ixodes. In the United States, the black-legged tick, Ixodes scapularis (also known as Ixodes dammini) is the primary vector for the parasite; in Europe, Ixodes ricinus appears to be the primary tick vector. In each location, the Ixodes tick vector for Babesia is the same vector that locally transmits Borrelia burgdorferi, the agent implicated in Lyme disease.

Ixodes scapularis, tick vector for babesiosis. Courtesy of the Centers for Disease Control and Prevention.

The primary US animal reservoir is the white-footed mouse, Peromyscus leucopus. Additionally, white-tailed deer serve as transport hosts for the adult tick vector, I scapularis. In Europe, the primary animal reservoir is cattle.

The Ixodid ticks ingest Babesia during feeding from the host, multiply the protozoa in their gut wall, and concentrate it in their salivary glands. The tick inoculates a new host when feeding again. The parasite then infects red blood cells (RBCs) and differentiated and undifferentiated trophozoites are produced. The former produce 2-4 merozoites that disrupt the RBC and go on to invade other RBCs. This leads to hemolytic anemia, thrombocytopenia, and atypical lymphocyte formation. Alterations in RBC membranes cause decreased conformability and increased red cell adherence, which can lead to development of noncardiac pulmonary edema and acute respiratory distress syndrome (ARDS) among those severely affected.1

Peripheral smear showing babesiosis.


United States

The first US case of babesiosis was reported on Nantucket Island in 1966. An increasing trend over the past 30 years may be the result of restocking of the deer population, curtailment of hunting, and an increase in outdoor recreational activities. Between 1968 and 1993, more than 450 cases of Babesia infections were confirmed in the United States. However, the actual prevalence of this disease is unknown because most infected patients are asymptomatic.


The first case of human babesiosis was reported in 1957 from the former Yugoslavia in an asplenic farmer. Approximately 40 cases have been reported since then, mostly in Ireland, the United Kingdom, and France. Sporadic case reports of babesiosis in Japan, Korea, China, Mexico, South Africa, and Egypt have also been documented.


Babesiosis exists as a spectrum of disease in 3 distinct groups: (1) asymptomatic infection, (2) a mild/moderate viral-like syndrome, and (3) severe disease with a fulminant course resulting in death or persistent relapsing course.1

The US mortality rate is significant.

 Twenty-five percent of adults and 50% of children infected with babesiosis are asymptomatic and/or improve spontaneously without treatment.
 Fewer than 10% of patients with babesiosis have died in the United States, mostly composed of elderly or asplenic patients.
 Deaths have been reported from transfusion-transmitted babesiosis within the immunocompromised population in areas where Babesia infection is not endemic.2
 Approximately 20% of patients with babesiosis are co-infected with Lyme disease. These patients experience more severe symptoms for a longer duration than those with either disease alone.
In Europe, babesiosis is a life-threatening disease.
 Fifty-three percent of infected patients become comatose and die.
 Eighty-three percent of infected patients are asplenic.


Babesiosis has no predilection for race.


The male-to-female ratio is about 1:1.


Babesiosis affects all age groups with similar frequency; however, patients older than 50 years are at increased risk for severe infection and death.


Senior Member
Babesiosis - Emergency Medicine - INFECTIOUS DISEASES - Part II

Just a note.... the formatting is lost when copying tables.... If someone can help me load this from Word, it will be much easier for everyone to read.

CLINICAL Section 3 of 13


Patients report a history of travel to an endemic area between the months of May and September. This is the period during which the Ixodes tick is in its infectious nymph stage; however, most do not recall the tick bite. The incubation period is between 1 and 4 weeks. The signs and symptoms mimic malaria and range in severity from asymptomatic to septic shock.
 Symptoms
 Generalized weakness
 Fatigue
 Depression
 Fever
 Anorexia and weight loss
 CNS - Headache, photophobia, neck stiffness, altered sensorium
 Pulmonary - Cough, shortness of breath
 GI - Nausea, vomiting, abdominal pain
 Musculoskeletal - Arthralgia and myalgia
 Renal - Dark urine


Physical examination findings of babesiosis can include the following:
 Fever
 Rigors
 Diaphoresis
 Altered mental status
 Renal insufficiency/failure
 Pulmonary edema
 Hepatosplenomegaly
 Spontaneous splenic rupture3
 Jaundice
 Shock


More than 100 species of Babesia exist, but only a small number of species are known to be responsible for the majority of symptomatic disease. The causative agent of babesiosis varies according to geographic region.
 In the United States, human infection with Babesia species is primarily due to Babesia microti, found mostly in northeastern and midwestern states. A few cases have been reported in Missouri, California, and Washington and are found to be caused by Babesia-like agents named after their geographic location, MO1 (Missouri), CA-1 (California), and WA-1 (Washington).
 In Europe, the causative agent of babesiosis is typically Babesia divergens, though B microti and B microti-like agents have been identified.
 Several reported cases of infection via blood transfusions from donors who lived in or traveled to an endemic area have been documented. All of these cases have occurred in the United States with the exception of one patient in Canada (acquired from a donor who became infected while in the United States) and one in Japan. The rate of acquiring B microti from a unit of packed red cells has been estimated to be 1 in 600-1800 in endemic areas.
 Case reports of transplacental/perinatal transmission have been documented.

DIFFERENTIALS Section 4 of 13

Anemia, Acute
Bites, Insects
Tick-Borne Diseases, Colorado
Tick-Borne Diseases, Ehrlichiosis
Tick-Borne Diseases, Introduction
Tick-Borne Diseases, Lyme
Tick-Borne Diseases, Q Fever
Tick-Borne Diseases, Relapsing Fever
Tick-Borne Diseases, Tularemia

WORKUP Section 5 of 13

|Lab Studies|
 In individuals who are asymptomatic, laboratory studies may be unremarkable.
 Wright- or Giemsa-stained peripheral blood smear
 This test reveals intraerythrocytic parasites (ring forms with a central pallor) and, rarely, pathognomonic tetrads of budding trophozoites, the so-called Maltese cross.
 The smear result may be negative in individuals with asymptomatic infection.
 Level of parasitemia does not correspond to severity of disease, although patients who are mildly ill may have less than 1% parasitemia and patients who are severely ill may have greater than 85% parasitemia. High parasite levels are especially seen in asplenic patients.
 Complete blood count (CBC) with differential may demonstrate mild-to-severe hemolytic anemia, thrombocytopenia, atypical lymphocytes, and leukopenia.
 Haptoglobin will be decreased.1
 Liver function test results often reveal mildly elevated hepatic transaminase levels, erythrocyte sedimentation rate (ESR), lactic dehydrogenase (LDH) level, alkaline phosphatase level, and serum bilirubin level.
 Urinalysis may reveal hemoglobinuria, proteinuria, and a dark color may be present.
 Direct Coombs test result may or may not be positive.
 Pulse oximetry results will be low in hypoxic patients with severe disease.
|Imaging Studies|
 Chest radiography may be indicated for patients with respiratory complications including suspected pneumonia or ARDS.
|Other Tests|
 Further testing specific for babesiosis takes place outside of the ED.
 Inoculation of a golden hamster or mouse with B microti-infected patient blood or a gerbil with B divergens-infected blood and subsequent antibody analysis of the animal's blood is used to confirm diagnosis when peripheral blood smear and laboratory results are equivocal. However, this test requires checking the animal periodically over 6-8 weeks, making the test time- and labor-intensive and impractical for rapid diagnosis.
 Polymerase chain reaction
 Polymerase chain reaction (PCR) is more sensitive and equally specific when compared with peripheral smear evaluation and hamster inoculation.
 PCR may be useful in monitoring the infection, although it cannot differentiate between acute/active forms and chronic forms of the disease.
 Immunofluorescence antibody testing
 Immunofluorescence antibody test (IFA) is considered the criterion standard for serologic detection of B microti infection.
 This test is used to confirm the diagnosis when the peripheral blood smear result is negative.
 A titer of greater than 1:64 is considered positive.
 A greater than 4-fold rise in titer or a single titer greater than 1:256 is suggestive of acute infection, with a gradual decline seen over weeks to months
 Correlation between severity of symptoms and titer levels is poor.
 Enzyme-linked immunosorbent assay immunoglobulin M Lyme titer
 Enzyme-linked immunosorbent assay (ELISA) immunoglobulin M (IgM) Lyme test is used because of the high percentage (25%) of patients co-infected with Lyme disease.
 Co-infection increases the severity of disease; therefore, diagnosing and treating both infections is important.
 Immunoblot antibody test
 This test has similar sensitivity and specificity for diagnosing babesiosis as that of IFA.
 Potential advantages over IFA include the lack of need for concentrated serum samples and ease of use, as immunoblot assays can be performed by generalist technicians versus trained microscopists.
 Because of the possibility of hemophagocytic syndrome, bone marrow biopsy is indicated in patients whose laboratory studies reveal pancytopenia and whose physical examination reveals hepatosplenomegaly, fever, coagulopathy, or lymphadenopathy.

TREATMENT Section 6 of 13

|Emergency Department Care|

 Suspicion of babesiosis in a patient with a history of exposure in an endemic area, tick bite, fever, chills, and fatigue is crucial.
 Peripheral blood smear or immunologic testing (see Workup) is necessary to make the diagnosis.
 If the patient is otherwise healthy and asymptomatic, no treatment is required.
 CBC with differential is important to determine the severity of infection.
 Immediately start elderly, immunocompromised, or asplenic patients on a combination treatment regimen of intravenous clindamycin and oral quinine or intravenous atovaquone and intravenous azithromycin to avoid acute renal failure.
 Intubation and mechanical ventilation may be required for patients who develop respiratory distress or failure.
 Consult an infectious disease specialist on all babesiosis-infected patients who require hospital admission.
 Consult a hematologist for whole-blood exchange transfusion in severe cases.

MEDICATION Section 7 of 13

Antibiotic and antimalarial therapy should begin immediately after diagnosis in symptomatic patients to reduce the level of parasitemia. The standard treatment has been clindamycin and quinine, but this regimen occasionally fails and patients report frequent side effects including tinnitus, decreased hearing, and diarrhea. Because of this, the drug regimen consisting of atovaquone and azithromycin is now the first line of treatment for mild/moderate disease and has been shown to be effective especially when clindamycin and quinine fail. For patients with severe symptoms, clindamycin and quinine are the first line of treatment.1 Parasitemia may persist despite treatment with either of the described drug regimens. In areas endemic for Lyme disease, physicians should consider treating for Lyme disease empirically.

Asymptomatic patients with positive smears and/or PCR results should have these studies repeated and a course of treatment started if parasitemia persists more than 3 months. Additionally, patients initially treated may require re-treatment if repeat smears or PCR are positive more than 3 months after initial therapy.

Partial or whole-blood exchange transfusion is indicated for patients with severe babesiosis, as demonstrated by high parasitemia (>10%); significant hemolysis; and/or renal, hepatic, or pulmonary dysfunction.

Drug Category: Antibiotics

Therapy should cover all likely pathogens in the context of this clinical setting.

Drug Name Clindamycin (Cleocin)
Description Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Administer in combination with quinine.
Adult Dose 1.2 g IV bid or 600 mg PO tid for 7-10 d
Pediatric Dose 20-40mg/kg/d IV or PO divided tid for 7-10 d; maximum of 600 mg/dose
Contraindications Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
Interactions Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

Drug Name Azithromycin (Zithromax)
Description Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Treats mild-to-moderate microbial infections. Administer in combination with atovaquone.
Adult Dose 600 mg PO qd for 7-10 d
Immunocompromised patients: Higher doses up to 1000 mg/d may be used
Pediatric Dose 12 mg/kg/d PO qd for 7-10 d
Contraindications Documented hypersensitivity; hepatic impairment; do not administer with pimozide
Interactions May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions Site reactions can occur with IV route; bacterial or fungal overgrowth may result from prolonged antibiotic use; may increase hepatic enzyme levels and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized patients, geriatric patients, or debilitated patients


Senior Member
Babesiosis - Emergency Medicine - INFECTIOUS DISEASES - Part III

Drug Category: Antiprotozoals

These agents may contribute to the eradication of the parasite.

Drug Name Atovaquone (Mepron)
Description May inhibit metabolic enzymes, which, in turn, inhibit growth of microorganisms. Administer in combination with azithromycin.
Adult Dose 750 mg PO q12h for 7-10 d
Pediatric Dose 40 mg/kg/d PO divided q12h for 7-10 d; maximum of 750 mg/dose
Contraindications Documented hypersensitivity
Interactions May increase zidovudine serum levels; coadministration with rifampin or rifabutin may decrease atovaquone levels; atovaquone may decrease levels of TMP-SMZ
Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions Caution in elderly patients and in hepatic and renal impairment

Drug Category: Anti-malarials
These agents are effective in eradicating the parasite.

Drug Name Quinine sulfate (Formula Q)
Description Inhibits growth of parasite by increasing the pH within intracellular organelles and possibly by intercalating into DNA of the parasites. Administer in combination with clindamycin.
Adult Dose 650 mg PO tid for 7-10 d
Pediatric Dose 30 mg/kg/d PO divided tid for 7-10 d; maximum of 650 mg/dose
Contraindications Documented hypersensitivity; optic neuritis; tinnitus; G-6-PD deficiency; history of black water fever
Interactions Aluminum-containing antacids may delay or decrease quinine bioavailability when administered concurrently; cimetidine increases quinine blood levels and creates the potential for toxicity; rifamycins decrease quinine concentrations by increasing hepatic clearance of quinine (effect can persist for several days after discontinuing rifamycins); concurrent administration of acetazolamide or sodium bicarbonate may increase toxicity by increasing quinine blood levels; quinine may enhance action of warfarin and other oral anticoagulants by decreasing synthesis of vitamin Kdependent clotting factors; digoxin serum concentrations may increase when digoxin administered concurrently with quinine; important to monitor digoxin levels periodically; quinidine may decrease plasma cholinesterase activity, causing a decrease in the metabolism of succinylcholine
Pregnancy X - Contraindicated; benefit does not outweigh risk
Precautions Caution in G-6-PD deficiency and tendency to develop granulocytopenia; prolonged treatment or overdosing with quinine may cause cinchonism; quinine has quinidinelike activity, and thus can cause cardiac arrhythmias

FOLLOW-UP Section 8 of 13

|Further Inpatient Care|

 Monitor level of oxygenation and watch for development of respiratory complications after initiation of treatment in patients who present with respiratory complaints. Respiratory distress may be due to endotoxin sensitivity; endotoxin release often results from medication-induced intraerythrocytic death of the parasites.
 In severe cases of babesiosis, exchange transfusion may be the only means of reducing the level of parasitemia.
 Mechanical ventilation may be necessary in patients with severe disease.
 Monitor CBC for development of hemophagocytic syndrome.
 If the patient does not respond to or cannot tolerate treatment with clindamycin and quinine, commence alternative treatment with atovaquone and azithromycin.
 Exposure to endemic areas
 Persons at risk of severe infection should avoid endemic areas between the months of May and September.
 Skin should be covered with appropriate clothing, including tucking long pants inside socks.
 Early removal of ticks from humans and pets should prevent transmission of disease; a tick must remain attached for at least 24 hours for transmission of the parasite.
 Tick repellent, such as products with 10-35% diethyltoluamide (DEET), should be applied on skin and clothes.
 People from endemic areas who report a fever within the last 2 months or a history of tick bite are not allowed to donate blood.
 Respiratory
 Patients who have undergone splenectomy are unable to clear infected RBCs, thereby leading to higher levels of parasitemia, eventually leading to hypoxemia and subsequent risk of cardiopulmonary arrest.
 In severe cases, damage to RBC membranes, decreased deformability, and cytoadherence to capillaries and venules lead to pulmonary edema and respiratory failure.
 These respiratory problems begin after treatment has been initiated when intraerythrocytic death of parasites has been postulated to cause sensitivity to endotoxin.
 ARDS may be due to mechanisms such as endotoxemia, complement activation, immune complex deposition, cytoadherence, microemboli, and disseminated intravascular coagulation.
 Cardiac
 Myocardial infarction
 Congestive heart failure
 Renal
 Renal insufficiency
 Renal failure
 Postsplenectomy patients may develop hemophagocytic syndrome, acute renal failure, and generalized seizure.
 Coma can occur, possibly due to severe sepsis, ARDS, or multisystem organ failure.
 Co-infection with Lyme disease is a possible complication.


 In the United States, the prognosis for babesiosis is excellent; most patients recover spontaneously. Patients who have had their spleen removed are at the greatest risk for severe complications and death.
 In Europe, most symptomatic patients are asplenic, which contributes to a poor prognosis. More than 50% of patients become comatose and die.
 Babesiosis may continue for more than 2 months after treatment; asymptomatic infections can persist silently for months to years. Patients with positive smears or PCR more than 3 months after initial treatment should be re-treated, regardless of the presence or absence of seizures.
|Patient Education|
 For excellent patient education resources, visit eMedicine's Bites and Stings Center. Also, see eMedicine's patient education article Ticks.

MISCELLANEOUS Section 9 of 13

|Medical/Legal Pitfalls|

 Failure to consider diagnosis in children
 Failure to initiate immediate therapy in individuals considered at high risk (ie, asplenic, elderly, immunocompromised)
 Administration of quinine therapy to a patient who is pregnant

|Special Concerns|

 Pregnancy
 Do not give quinine to pregnant patients.
 If the infection is subclinical, drug therapy is not indicated.
 Combination therapy with clindamycin and quinine or atovaquone and azithromycin is more effective than either atovaquone or azithromycin alone.
 Geriatric patients: Initiate therapy with clindamycin and quinine immediately.
 In patients with fever of unknown origin (FUO), consider babesiosis as a diagnosis if the patient lives in or has traveled to an endemic area or received a blood transfusion in the past.4

FURTHER READING Section 10 of 13

Clinical guidelines

Infectious Diseases Society of America practice guidelines for clinical assessment, treatment and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis. Wormser GP, Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC, Klempner MS, Krause PJ, Bakken JS, Strle F, Stanek G, Bockenstedt L, Fish D, Dumler JS, Nadelman RB. The clinical assessment, treatment, and prevention of lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2006 Nov 1;43(9):1089-134. PubMed

MULTIMEDIA Section 11 of 13

Media file 1: Peripheral smear showing babesiosis.
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Media file 2: Ixodes scapularis, tick vector for babesiosis. Courtesy of the Centers for Disease Control and Prevention.
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REFERENCES Section 12 of 13

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