Pediatric & Adolescent Lyme Disease Specialist
Tick-borne diseases are a 21st century epidemic in most geographical areas of the United States as well as Europe, China, Japan, Australia, South America, and Africa. Greater awareness regarding the spread of these diseases is gaining momentum as we enter the “Decade of the Microbe”. However, the multidimensional impact of Lyme Disease in particular on our most vulnerable population, children, is still under substantial scrutiny by the medical establishment despite numerous scientific articles demonstrating clear and contrary evidence.
Children are among the most vulnerable for tick-borne illness simply because they spend time outdoors, play low to the ground where ticks often reside, and are more likely to come into physical contact with these arthropods while they show affection to family pets.
The northeast United States in particular, was where Lyme Disease was first noted in 1975, among a population of children who demonstrated swollen sore knees, sore throats, fever, malaise, and debilitating fatigue. This observation was made by a housewife, Polly Murray, who to this day, is largely responsible for recognizing the first outbreak of Lyme Disease in Lyme, Connecticut. At the same time, Dr. Charles Ray Jones located in New Haven, Connecticut, not far from Lyme, Connecticut, who is now the world’s leading pediatric Lyme disease specialist, agreed with Mrs. Murray’s observations and began successfully treating many of these children with long term multiple antibiotics.
Dr. Jones was the first pediatrician to recognize the widespread prevalence of Lyme Disease in Connecticut, Rhode Island, Massachusetts, New York, New Hampshire and Maine. As of December 2010, Dr. Jones has treated over 20,000 children with various tick-borne diseases using long term antibiotics. Notably, most of these children recover and move on to do great things in the world.
As a mentor to Dr. Marra for 6 years, Dr. Jones taught her the detailed intricacies of diagnosing and treating multiple tick-borne infections in children. He encouraged her to look for the “subtle” nuances and the effects of tick-borne disease on developing bodies and brains. His unrelenting perseverance for the truth about the prevalence of Lyme Disease in children, has made him an international treasure and Dr. Marra is grateful to have had the opportunity to work with him.
As a result of working with Dr. Jones, she is well trained in pediatric Lyme Disease and co-infection treatment. She continues to foster her interest in this medical niche by attending annual ILADS (International Lyme and Associated Diseases Society) conferences, while discussing difficult cases with Dr. Jones and maintaining frequent professional dialogue with other Lyme Literate Doctors.
Dr. Marra feels privileged to know Dr. Jones and is thankful for his willingness to mentor her. She is fortunate enough to know someone with the kind of experience in the medical management of pediatric and adolescent Lyme disease. Dr. Marra utilizes his wisdom and insights on a daily basis in her own practice, and Pediatric/Adolescent Lyme Disease remains one of her greatest professional strengths. Dr. Marra intends on the continued practice of medicine for tick-borne illness with the skills that she has obtained in nearly 18 years of practice and over 7,300 patients with Dr. Jones’ principles at the core of her treatment plans. She remains a colleague and a friend of Dr. Jones, and hopes to continue his legacy with as much commitment to healing children as he does throughout his greater than 50 year medical career. Dr. Jones is without question an honorable man who dedicated his life to a most worthy cause, and for that, the world is no doubt a better place, despite the continued controversy over antibiotic treatment for chronic Lyme Disease.
Tick Bite Concerns
Ticks are considered arthropods and belong to the same family as spiders and mites, Ixodes. They have two body segments, 8 legs in the adult form and do not have wings or antennae. They have 4 life stages including: egg, 6 legged larvae, 8 legged nymph, and 8 legged adult. The larvae, nymph and adult stages can all carry and transmit infection. The life cycle of a tick is about two years barring the effects of global warming which may elongate their life cycle. Different ticks are maximally active at different times of the year, a convenient natural way of minimizing competition for host attachment. In general, May through August black-legged ticks and Lone Star ticks are active, and April through May, dog ticks are active. All of these species are potential carriers of the Borrelia bacteria.
The various ticks known to cause disease include Ixodes scapularis (deer tick) generally found in the northeast and upper Midwest and can carry Borrelia, Babesia, Anaplasma, Ehrlichia, Powassan Encephalitis, tick paralysis, Tularemia, Bartonella and Mycoplasma infections.
Ixodes pacificus is generally found on the West Coast and is known to carry all of the above mentioned tick-borne diseases.
Amblyomma americanum (lone star) is found throughout the United States and is generally known to transmit Ehrlichia, STARI (southern tick associated rash illness), Tularemia, tick paralysis, Rocky Mountain Spotted Fever and Q fever. Dermacentor variabilis (American dog tick) is found throughout the United States and is known to transmit tick paralysis, Rocky Mountain Spotted Fever, Tularemia, and Ehrlichia.
Dermacentor andersoni (wood tick) is found in the rocky mountain states and southwest Canada. This tick looks very similar to the American dog tick, and is known to transmit Rocky Mountain Spotted Fever, Tularemia, Colorado Tick Fever, Tick paralysis, and Q fever.
However, it should be noted that at this time (2011), migratory birds have been documented to carry these ticks and therefore geographic specificity of ticks is becoming less and less accurate.
There are about 850 known species of ticks worldwide and roughly 100 species are known to transmit disease. Parasitologists estimate that ticks evolved originally as feeding on amphibians and over evolutionary time, adapted to mammalian biology. Spirochetes (the bacteria that causes Lyme Disease) reside in the gut of the tick, and upon attachment to a host for a blood meal, the tick regurgitates the bacteria and deposits them into the hosts blood. This is the initial infection site, and may be the site of a “Bullseye Rash”.
Ticks rarely move more than three feet above the ground and cannot jump or fly. However, they can attach to birds, mice, deer, chipmunks, skunks, rabbits, humans and many other animals and this is precisely the way that infection spreads across states, countries and continents. Believe it or not, they have also been detected in the sea.
Ticks thrive in humidity and live in areas close to their potential hosts (i.e., leaf litter, ends of grass, attached to animals) and respond to exhaled carbon dioxide and body heat. They use chemosensors to actually locate a host. They attach to a host by a “stinger” and release an anesthetic compound to prevent the host from feeling the bite. As the tick feeds, a cement-like substance is secreted from the saliva to enhance its capacity to adhere to the skin and extract a blood meal. Ticks also secrete a substance at the site of attachment which functions as an “anesthetic” and allows their presence to go rather unnoticed by the host.
There are various opinions regarding the length of time that a tick can be attached in order for disease to be transmitted. However, Dr. Charles Ray Jones, a world leading authority on tick-borne illness in children with 50 years of clinical experience, feels that as few as 15 minutes of tick attachment is long enough for spirochetes to enter the hosts’ bloodstream. However, continued research in this area is necessary for proper documentation. Nonetheless, common sense suggests that other blood vectors need only to attach for a matter of minutes (i.e., mosquitoes, stinging flies, fleas, mites) to deposit their “venom” so the same should apply to ticks.
Babesiosis, often a co-infection of Lyme disease in humans, was first identified by Victor Babes in the late 19th century in Romanian cattle and the disease at that time was coined “Red Water Fever.” However, Babesia infection in humans was not confirmed until 1956 in a Yugoslavian farmer.
Babesia is a protozoan intracellular red blood cell parasite quite similar to malaria and is a worldwide emerging zoonotic disease. There are about 100 known species of Babesia that infect livestock animals and rodents. However, the three currently known species causing human disease, B. microtii, and B. duncani (formerly WA1 and first identified in Washington state but found throughout the United States), and Babesia divergens (found in Europe), are largely found in the northern hemisphere. The islands of Nantucket and Martha’s Vineyard on the eastern coast of Massachusetts, are considered endemic for Babesia species, however, migratory birds are likely transport vectors of all tick-borne illness, which may account for the bacteria’s presence on the west coast as well. Currently, scientists believe that there may be additional human pathogenic species such as B. bigemina and B. bovisbut further researcher is necessary in this area of infectious disease.
Babesia infection is transmitted through a tick bite or contaminated blood products, where sporozoites directly enter the bloodstream and infect red blood cells that contain a heme structure, where an iron molecule resides for oxygen binding purposes. Babesia interferes with red blood cell function, giving rise to common symptoms of: night sweats, air hunger, shortness of breath, severe headaches and often anemia of chronic disease. Serologically, low hemoglobin, hematocit and/or red blood cell count, as well as low ferritin and transferrin, may accompany this disease. Additionally, there are two confirmed human cases of maternal transplacental transmission in humans.
Laboratory testing for Babesia species can be difficult and serum antibodies as well as fluorescent in situ hybridization techniques and PCR (polymerase chain reaction) tests maximize the chances of documenting the presence of this bacteria. Additionally, infected hosts may have subclinical parasitemia which yields greater difficulty in laboratory detection. Babesia can also be observed in a Giemsa stain where the organism appears like a “Maltese cross.”
Since Babesia species are parasites, antiparasitic herbs and pharmacologics are required to treat fulminant disease. The presence of this bacteria in an already infected Lyme patient or an immunocompromised or splenectomized (spleen removal) patient, can complicate treatment substantially. However, antimalarial medications are typically used and shed light on a wider variety of treatment choices for this infection, especially when coupled with Lyme disease.
The last 20 years have been marked by global proliferation of human Babesia infections, and suspicion for this disease should be considered whenever a tick bite has been noted, even if a Bulls eye rash is not noted at the site of the bite. Babesia infection may be transmitted with or without Lyme disease and it is not known to be associated with a Bulls eye rash.
Consult your “Lyme Literate” physician, Dr. Susan L Marra, for more information regarding this global emerging zoonotic disease for proper diagnosis treatment.
Bartonellosis also known as “Cat Scratch Fever”, is an increasingly recognized and emerging bacterial zoonotic disease found all over the world. Bartonella species are fastidious haemotropic (blood loving) Gram-negative anaerobic (disliking oxygen) bacteria that are mainly transmitted by biting insects and arthropods such as fleas, sand flies, mosquitoes and ticks or a cat scratch. Species of Bartonella have been found in wild cats, rabbits, sheep, dogs, grey and red foxes, raccoons, coyotes and even sea otters in Alaska.
There are roughly 13 species of pathogenic Bartonella species including B. henselae, B. quintana, B. clarridgeriae, B. rochalimae, B. koehlerae, B. vinsonii berkhoffi, B. washoensis, and B. elizabethae, B. alsatica, B. melophagi, B. tamiae, and four of them have been isolated in cats, especially feral cats, giving rise to the name “Cat Scratch Fever.” Of note, cats appear to be a particular reservoir for Bartonella species however, it has also been found in dogs rendering question as to whether or not dogs are carriers of this bacteria as well. To date, reliable Bartonella serum antibody tests are limited to the species B. henselae and B. quintana. However, newly developed fluorescent in situ hybridization (FISH) testing is now able to detect Bartonella at the species level allowing better laboratory detection of bacterial presence.
Bartonellosis was first isolated in the early 1920’s, and prevalence of the infection varies geographically. Northern climates reportedly have less prevalence of the disease, although this trend is changing in conjunction with global climate change.
In immunocompetent patients, Bartonella infection is characterized by regional lymphadenopathy, low-grade fever, malaise, muscle aches, joint pain, and chronic fatigue. There have also been reported cases of hemolytic anemia, thrombocytopenic purpura, Henoch-Schonlein purpura Syndrome, retinitis, uveitis, neuroretinas, enlarged spleen, glomerulonephritis, endocarditis, and encephalitis due to infection.
Bartonella infection in immunocompromised patients with low natural killer cells (CD57 cells) low T helper cells (CD4 cells) and/or low T suppressor cells (CD8 cells) often present with “red streaks” resembling cat scratches, and this condition is known as bacillary angiomatosis or peliosis.
Electron microscopy studies of patients infected with Bartonella reveal that this bacteria has a particular affinity for the vascular endothelium (inside the blood vessel walls) where organisms are observed in clumps along the vessel wall. This appears to be an advantageous residence for bacteria that utilize nutrients in the host’s blood for their own benefit.
Clustering of Bartonella cases within families has been observed especially in families that have adopted feral cats. Ocular, neurologic, dermatologic, hematologic, orthopedic, cardiac, renal, and pulmonary presentations are typical for Bartonella infections but symptom presentation may vary among family members.
A combination of herbs, antibiotics, immune support, an alkalized diet, moderate exercise and nutritional support are highly recommended for successful treatment of a Bartonella infection.
Borrelia burgdorferi sensu stricto strains
Isolate Country Source Provided by 212 * France I. ricinus F. Milward 297 * USA Connecticut Human CSF R.C. Johnson 1352 * USA Texas A. americanum R. T. Marconi 19535 * USA New York Peromyscus leucopus J. F. Anderson 20006 * France I. ricinus J. F. Anderson 26816 * USA Rhode Island Microtus pennsylvanicus J. F. Anderson 27985 * USA Shelt. Isl I. scapularis J. F. Anderson 21305 * USA Connecticut Peromyscus leucopus J. F. Anderson 21343 * USA Wisconsin Peromyscus leucopus J. F. Anderson B31 * USA New York I. scapularis ATCC 35210 CA2-87 * USA California I. pacificus R. T. Marconi CA 5 * USA California I. pacificus R. Lane CA 6 * USA California I. pacificus R. Lane CA920953 * USA California Human skin L.M. Switalski Cat Flea * USA Texas Ctenocephalides felis D. Ralph Charlie tick * USA Wisconsin I. scapularis C. Kodner DK7 * Denmark Human skin M. Theisen ESP-1 * Spain I. ricinus R. C. Johnson GeHo * Germany Human skin (ECM) Vögel HB19 * USA Connecticut Human blood A. Barbour HII * Italy Human blood (arthritis) V. Sambri HUM 115 * USA California I. pacificus M. Janda HUM 3336 * USA California I. pacificus M. Janda HUM 7814 * USA California I. pacificus M. Janda IP1 * France (Poitiers) Human CSF G. Baranton IP2 * France (Tours) Human CSF G. Baranton IP3 * France (Pau) Human CSF G. Baranton IRS * Switzerland I. ricinus ATCC 35211 LAKE 339 * USA California I. pacificus M. Janda MEN 115 * USA California I. pacificus M. Janda MIL * Slovakia I. ricinus A. Livesley MUL * USA New York I. ricinus M. Theisen N40 * USA New York I. scapularis S. Norris NY1-86 * USA New York Human skin R. T. Marconi NY13-87 * USA New York Human skin R. T. Marconi PKa * Germany I. ricinus V. Preac Mursic Sh-2-82 * USA New York I. scapularis S. Bergström SON 188 * USA California I. pacificus M. Janda SON 328 * USA California I. pacificus M. Janda SON 335 * USA California I. pacificus M. Janda SON 2110 * USA California I. pacificus M. Janda SV1 * France (Rambouillet) I. ricinus C. Perez SV3 * France (Fontainebleau ) I. ricinus C. Perez SV4 * France (Pimpont) I. ricinus C. Perez Veery * USA Connecticut Veery bird R. T. Marconi VS 2 * USA Shelt. Isl I. scapularis O. Péter Z 118 * Germany I. ricinus A. Vogt Z 136 * Germany I. ricinus A. Vogt
courtesy of: NCBI
Ehrlichia chafeensis (HME), Ehrlichia ewengii and Anaplasma phagocytophilum (HGE), are emerging zoonotic diseases, especially in areas where human urban living encroaches on endemic tick areas. These bacteria are largely found in mammals residing in the southeastern, south central, and mid-Atlantic areas of the United States, and according to the CDC, most cases are reported in the states of Maryland, Arkansas, Missouri, Oklahoma and Tennessee. Ehrlichia and Anaplasma bacterias have also been noted in Brazil, the United Kingdom, France, Slovenia, Switzerland, Germany, the Netherlands, Spain, Russia and Japan. However, similar to other tick-borne diseases, migratory birds probably play a significant role in disease spread around the globe, and these bacteria (HGE and HME) are likely found in other areas of the world not yet identifying and reporting the disease. Of note, Ehrlichia in particular, is known to be a veterinary disease largely seen in horses and dogs.
Ehrlichia and Anaplasma are intracellular obligate bacteria that require a host for replication and a vector for transmission (i.e., ticks). Human signs and symptoms of these diseases are often not accompanied by a “Bullseye rash”, however, there may be redness and heat at the site of the tick bite. HME or HGE illness can occur quickly (depending on the number of bacteria delivered to the host at the bite site), or it can develop more slowly over time as the bacteria replicate and proliferate in the host. Generally, clinically presenting symptoms can include: fever, stiff neck, joint pain, muscle aches, headache, chills, malaise, nausea, and diarrhea. Elevated serum liver enzymes including ALT and AST may also occur, lending clues to the underlying bacterial infection in question.
HGE and HME are serologically diagnosed using antibody titer tests or by using PCR (polymerase chain reaction) which demonstrates the presence of bacterial DNA in the blood and therefore exposure to the bacterias that cause Ehrlichiosis. Careful determination of these bacterial infections is important because the presence of Rocky Mountain Spotted Fever, Brucella, Typhus, and Q fever (also zoonotic diseases) can cause false-positive serology for Ehrlichia.
Occasionally, these infections can require hospitalization, especially for pain management which results from the activation of acute and prolonged pro-inflammatory cytokine release and tissue damage due to the host’s immune system activation.
An integrated medicine treatment approach to Ehrlichia and Anaplasma infections, where a combination of immunosupportive herbs, anti-inflammitants and antibiotics in rotation, are recommended and generally yield favorable outcomes. However, not unlike the other tick-borne infections, when the infection(s) are diagnosed early (less than 12 months from the time of the tick bite) prior to dissemination throughout the body, a return to health is maximized.
In the next decade, cutting edge research on genomics, proteomics, and the cellular microbiology of these bacterial infections is likely to reveal additional therapeutic agents (i.e., herbal, nutritional and pharmacological). Future therapeutic intervention may focus on disengaging adhesin molecules that bind to white blood cells, which interfere with the replication and proliferation of these bacteria in the host. Around the world, more and more researchers are becoming interested in developing effective new therapeutics for eradicating these diseases.
Louse-borne relapsing fever (LBRF) is caused by the spirochete, Borrelia recurrentis, and is largely transmitted from person to person by lice. This bacteria is unique because it can alter the proteins expressed on its surface which causes the “relapsing” characteristic symptoms. It initially infects the mucus membranes and then moves into the bloodstream.
Symptoms can include:
- Cognitive Dysfunction
- Prolonged QT interval on EKG
Generally this is a more severe infection than tick-borne relapsing fever and is often found in poor, underdeveloped countries such as Ethiopia.
Tick-borne relapsing fever (TBRF) is a spirochetal infection cause by Borrelia hermseii, Borrelia miyamotoi, and several other less well known bacterial species. Tick-borne relapsing fever is found in Africa, Spain, Saudi Arabia, Asia, Canada, and the western United States. Rodents are the primary reservoir and ticks are the likely vector for this disease. TBRF is best diagnosed by PCR testing.
Symptoms of TBRF include:
- Cognitive Dysfunction
- Body Aches
- Other transient and nebulous symptoms vary from patient to patient
Brucellosis is a zoonotic and tick-borne disease caused by the bacteria Brucella melitensis, and is an ancient disease, dating back to the 5th plague of Egypt around 1600 BC. Archeological excavation of Egyptian human bones dating around 750 BC demonstrated evidence of osteoarticular abnormalities that are often symptom complications from a Brucellosis infection. Brucella is found all over the world, especially in countries that rely heavily on agriculture, livestock, and dairy products such as Australia, Canada, Denmark, Finland, the Netherlands, New Zealand, Norway, Sweden, the United Kingdom, the Middle East, and central Asia.
David Bruce was the first scientist to identify the bacteria Brucella melitensis in British soldiers stationed on Malta (an island in Italy) who developed severe fever leading to the name “Malta Fever” for this disease complex. In 1897, a Danish veterinarian, L.F. Bernhard Bang, discovered a bacillus bacteria in cattle and termed it “Bang’s Disease.” However, an American scientist, Alice Evans, famous for her work on pathogenic bacteria in dairy products, confirmed that Malta Fever and Bang’s Disease were caused by the same bacteria now known as Brucella melitensis. Alice Evans was largely responsible for instituting the pasteurization process of dairy products to prevent human disease in the United States.
To date, there are 9 species of Brucella, (5 are pathogenic to humans), and in 1990 it was discovered that Brucella was also found in marine mammals. Brucella species are facultative, intracellular, Gram-negative, coccobacilli, and nonmotile due to the lack of flagella. Sheep or goat's milk consumption is a significant source of Brucellosis infection, so minimizing the natural animal reservoirs for this disease is important for curbing disease outbreaks.
Symptoms of Brucellosis include fever, night sweats with a strange odor, chills, weakness, malaise, insomnia, anorexia, headache, joint pain, constipation, nervousness, depression, and impotence. Many organ systems can be affected by Brucella infection including the: brain (encephalitis), heart (endocarditis), joints (arthritis), testes (orchitis), and prostate gland (prostatitis).
Mothers who are breastfeeding may transmit the infection to their infants and sexual transmission has also been reported in the scientific literature.
Diagnosis of Brucellosis is confirmed using antibody titer tests, IgM, and IgG which demonstrates exposure to the Brucella bacteria.
Integrated medicine treatment for Brucellosis including herbal and nutrient immune support coupled with antimicrobial herbs and antibiotics generally yields very positive outcomes. However, Brucella can have varied effects on individuals so the length of treatment time is variable.
If you have additional questions or concerns please contact our office.