Tickborne diseases in the United States are a significant public health problem, and in the past 50 years scientists have detected at least a dozen new such infections. With more than 30,000 cases diagnosed each year, Lyme disease is the most commonly reported vector-borne illness in the United States, and in 2015 it was the sixth most common nationally notifiable disease.1
Due to increased education and recognition, most practitioners are familiar with the symptomatic presentation of Lyme disease. In stage 1, patients usually exhibit the classic erythematous expanding annular “bulls-eye” rash known as erythema migrans, and approximately 50% experience constitutional flu-like symptoms. In stages 2 and 3, or disseminated Lyme disease, patients may present with Bell’s palsy or other cranial nerve deficits, arthritis, peripheral neuropathies, and cardiac manifestations such as transient heart block and carditis.
Borrelia burgdorferi, the spirochete that causes Lyme disease, is not the only pathogen spread by the deer tick Ixodes scapularis in the northeastern United States:
- Babesia microti, the agent of babesiosis, and
- Anaplasma phagocytophilum, the agent of human granulocytic anaplasmosis (HGA; formerly human granulocytic ehrlichiosis) are asserting a presence in similar geographic regions. Coinfection with these organisms is possible.
- Human monocytic ehrlichiosis (HME), caused by Ehrlichia chaffeensis, is another emerging tickborne disease with similar geography to HGA.
The incidence of babesiosis, HGA, and HME is increasing, and the geographic areas for their tick vectors are expanding. HME and HGA can be serious infections with high rates of hospitalization and complications, particularly when diagnosis or treatment is delayed.
Babesia microti is the predominant protozoan cause of babesiosis in the United States; occasional sporadic cases of babesiosis caused by other species have been reported. Babesiosis is transmitted by the bite of an infected I scapularis (commonly known as the black-legged or deer tick) (Figure 1), usually in the nymphal or adult stage. The primary carrier of Babesia are white-footed mice, although it is found in other small mammals. Although white-tailed deer are the most important food source for the adult stage of the tick, deer are not infected with B microti.2 Babesia is rarely transmitted by blood transfusion, organ transplant, or vertically during pregnancy. The incidence of transfusion-transmitted babesiosis in the United States is 1.1 cases per million red blood cell units distributed.3
HME is caused by Ehrlichia chaffeensis, anobligate intracellular gram-negative species of rickettsial bacteria that grows within membrane-bound vacuoles in human and animal leukocytes.4,5 Less commonly, human disease is caused by E ewingii, the organism responsible for canine granulocytic ehrlichiosis. The principal vector of E chaffeensis is the lone star tick (Amblyomma americanum) (Figure 2). Other ticks occasionally have been found to contain DNA of E chaffeensis, but their role in transmission is unlikely.4 The white-tailed deer is the main competent reservoir for E chaffeensis, although domestic goats, dogs, raccoons, and coyotes may also carry the bacterium.
HGA is caused by the gram-negative bacterium Anaplasma phagocytophilum, which is transmitted byI scapularis, the same vector of Lyme disease and babesiosis. I pacificus, the western black-legged tick, is the primary vector of HGA in the western United States. Also similar to Lyme disease, deer and the white-footed mouse are the principal animal hosts for HGA.
Glad word is getting out about the prevalence of other diseases spread by ticks as most of us are infected with numerous things making our cases more severe, of longer duration, and necessitating numerous medications.
What I am concerned about is the continued effort to put all of this into a 2 minute sound bite.
Nothing about treating this is easy or simple. It takes education, savvy, experience, and most of all – an open mind.
Having listened to ILADS trained doctors for hours on end I learned that we are extremely complex cases with vast individuality. Some struggle with Mast Cell disorders, some have severe psychiatric issues, and on and on. There is no way a singular treatment plan will cover the wide and varied presentations of this plague.
A few considerations of the article:
- Most doctors are NOT aware of the symptoms of Lyme disease which mimics over 300 different diseases: https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/. They keep misdiagnosing patients every single day. Doctors are afraid to even treat this and would rather diagnose you with ANTHING other than Lyme/MSIDS. Even if they diagnose you they will treat you with the antiquated and unscientific CDC “Lyme guidelines” which have produced treatment failures since the beginning. https://madisonarealymesupportgroup.com/2018/12/15/everything-about-lyme-disease-is-steeped-in-controversy-now-some-doctors-are-too-afraid-to-treat-patients/
- The three stages of Lyme they present is outdated. Many never experience some stages or they can jump straight to third stage. This article tells the story of a little girl that within 4-6 hours of tick bite developed facial palsy and couldn’t walk or talk. That’s fast. I guarantee you, she isn’t the only case like this. In my own case all my initial symptoms were gynecological. Mainstream medicine would consider Lyme/MSIDS in a million years – yet, that’s exactly what it was: https://madisonarealymesupportgroup.com/2017/02/24/pcos-lyme-my-story/ If doctors fixate on a set prescribed stage order they will miss many people – which they already are. This is not Simple Simon met a pie-man.
- Again, many never get a rash and I never had flu-like symptoms. I had raging ovarian pain and a swollen knee.
For more on the coinfections listed:
If you also are infected with Lyme as well as other pathogens, you are one sick dog and need a trained ILADS professional. Contact your local support group for these professionals.