Archive for the ‘Transmission’ Category

LDA President Pat Smith on Contagion Live

Patricia Smith, President of the Lyme disease Association, discusses Lyme disease has spread throughout the United States in the past decade. Part 1

Lyme Disease: What Makes Diagnosis & Treatment Difficult? Part 2

How Have Tick-Borne Diseases Grown in the United States? Part 3

What Do I Need to Know About Lyme Transmission Time? Part 4

Are Patients Facing Difficulties in Accessing Treatment for Lyme? Part 5

Why is May Lyme Disease Awareness Month? Part 6

How Does Government Acknowledgement of Lyme Affect Patient Care? Part 7

The Current State of Lyme Disease Prevention. Part 8

Lyme Disease Legislation May Advance Patient-Centered Research. Part 9

Review of Tick Attachment Time For Different Pathogens

Stephanie L. Richards, Ricky Langley, Charles S. Apperson and Elizabeth Watson 


Improvements to risk assessments are needed to enhance our understanding of tick-borne disease epidemiology.

We review tick vectors and duration of tick attachment required for pathogen transmission for the following pathogens/toxins and diseases: (1) Anaplasma phagocytophilum (anaplasmosis); (2) Babesia microti (babesiosis); (3) Borrelia burgdorferi (Lyme disease); (4) Southern tick-associated rash illness; (5) Borrelia hermsii (tick-borne relapsing fever); (6) Borrelia parkeri (tick-borne relapsing fever); (7) Borrelia turicatae (tick-borne relapsing fever); (8) Borrelia mayonii; (9) Borrelia miyamotoi; (10) Coxiella burnetii (Query fever); (11) Ehrlichia chaffeensis (ehrlichiosis); (12) Ehrlichia ewingii (ehrlichiosis); (13) Ehrlichia muris; (14) Francisella tularensis (tularemia); (15) Rickettsia 364D; (16) Rickettsia montanensis; (17) Rickettsia parkeri (American boutonneuse fever, American tick bite fever); (18) Rickettsia ricketsii (Rocky Mountain spotted fever); (19) Colorado tick fever virus (Colorado tick fever); (20) Heartland virus; (21) Powassan virus (Powassan disease); (22) tick paralysis neurotoxin; and (23) Galactose-α-1,3-galactose (Mammalian Meat Allergy-alpha-gal syndrome).

Published studies for 12 of the 23 pathogens/diseases showed tick attachment times. Reported tick attachment times varied (<1 h to seven days) between pathogen/toxin type and tick vector. Not all studies were designed to detect the duration of attachment required for transmission. Knowledge of this important aspect of vector competence is lacking and impairs risk assessment for some tick-borne pathogens.


The researchers point out that unlike mosquitoes which rely on saliva for transmission, ticks can transmit via saliva, regurgitation of gut contents, and also via the cement-like secretion used to secure itself to the host (hard ticks).  Published data on transmission times relies upon rodent studies showing 15–30 min for Powassan, anywhere from 4-96 hours for bacteria, 7–18 days for the protozoan Babesia microti, and 5-7 days for neurotoxin (Tick Paralysis). For soft ticks, attachment time of 15 sec–30 min was required for transmission of Borrelia turicata (Tick Relapsing Fever).

The challenge with these studies, and there are many, is that most placed multiple ticks on multiple rodents.  Multiple ticks may be transmitting different pathogens.  It has also been shown that ticks feeding on mice coinfected with B. microti and B. burgdorferi were twice as likely to become infected with Bb compared to B. microti, suggesting that coinfection can amplify certain pathogens – which is another reason to only use one rodent and one pathogen to separate out multiplying factors to muddy the waters.  Also, rarely do studies record the titer of both tick and host – again, making it nearly impossible to determine what’s what.  It was also noted that transmission times are unknown for many pathogens.

**And as always:  if you are the ONE person who contracted Lyme Disease in 10 minutes, all these numbers are essentially meaningless.  The frightening truth is that these numbers, along with geographical information regarding tick habitats, are often used against patients.  It is beyond time for doctors to listen, educate themselves, and treat patients with the respect they deserve – not to mention it’s time for them to treat patients clinically and not based on tests that are wrong over half the time and with the knowledge that ticks are spreading everywhere and bringing the pathogens with them. (In other words, throw the maps away!)

The review essentially gives the following transmission times for various pathogens. Again, please know these numbers are not definitive and many, many cases have proven this fact.

Take each and every tick bite seriously and don’t mess around and take a “wait and see approach.”  There is too much at stake.

Transmission Times noted in review:

Anaplasmosis: 24 hours and increased dramatically after 48-50 hours.  It is possible for it to be transmitted transovarially (from mom to baby tick) and it inhabit’s the salivary glands more frequently than the mid-gut.

Babesiosis:  Greater than 36 hours, 17% after 48 hours, and 50% after 54 hours.  Can be transmitted transovarially and transstadially (pathogen stays with tick from one stage to the next).  Ticks feeding on mice coinfected with B. microti and B. burgdorferi were twice as likely to become infected with Bb compared to B. microti.

Lyme Disease (Borrelia burgdorferi):  24 hours; however, the researchers comment that there are questions regarding previous transmission studies.  They also commented that there may be a difference in attachment time between nymphs and adult females. Transovarian transmission is unknown.

Tick Relapsing Fever (Borrelia turnicatae, B. hermsii):  15 and 30 seconds respectively.  Transovarian transmission is unknown.

Borreliosis (Borrelia mayonii):  24 hours.  Transovarian transmission is unknown.

Borrelia myamotoi Disease:  24 hours.  Transovarial transmission occurs.

Tularemia (Francisella tularensis):  Not assessed.  Can be transmitted mechanically by deer flies, horse flies, mosquitoes, aerosol/ingestion when processing/eating infected animal tissues.  Can be transmitted transtadially and transovarially.

Rocky Mountain Spotted Fever (Rickettsia rickettsii):  10-20 hours.  Can be transmitted transovarially.

Heartland Virus:  Not assessed.  Can be transmitted transovarially and transstadially.

Powassan Virus:  15 Minutes; however, it is possible it was sooner since the first they checked for transmission was 15 minutes.  Can be transmitted transovarially.

Tick Paralysis (Neurotoxin):  2-6 days.

Alpha Gal/Mammalian Meat Allergy (Galactose-a-1,3-Galactose):  Not assessed.  Transovarian transmission is unknown.

For more on transmission times, please read:



Powassan and Bb Infection in Wisconsin and U.S. Tick Populations

Powassan/Deer Tick Virus and Borrelia Burgdorferi Infection in Wisconsin Tick Populations

Knox Konstance K., Thomm Angela M., Harrington Yvette A., Ketter Ellen, Patitucci Jacob M., and Carrigan Donald R. Vector-Borne and Zoonotic Diseases. May 2017 Online Ahead of Print

Powassan/Deer Tick Virus (POWV/DTV) is an emerging cause of arboviral neuroinvasive disease in the upper Midwest. These studies describe the prevalence and geographic distribution of Wisconsin ticks carrying POWV/DTV as well as the high frequency of Ixodes scapularis ticks coinfected with both POWV/DTV and Borrelia burgdorferi, the causative agent of Lyme disease. These findings suggest that concurrent transmission of POWV/DTV and B. Burgdorferi from coinfected ticks is likely to occur in humans.

Results (see link for maps and graphs of locations and results)

The distribution of I. scapularis and D. variabilis tick collection sites are categorized by geographic quadrant (QNW, QNE, QSW, & QSE) of the state (Fig. 1, Table 1). Nearly 80% of adult female I. scapularis ticks analyzed were collected from the northern half of the state (QNW and QNE) and accounted for 85% of POWV-positive ticks. While only 90 I. scapularis ticks were collected from the southern two quadrants, POWV-positive ticks were identified in both QSE and QSW. QNW I. scapularis ticks revealed the highest MLE of infection for both POWV and B. burgdorferi (4.67% and 23.42%, respectively). A separate analysis of I. scapularis collections from Harvest One endemic zone (Spooner/Hayward) QNW demonstrated a frequency of infection for both POWV (4.65%) and B. burgdorferi (27.91%) that is comparable to the total QNW (Fisher’s exact, p = 1.00 and p = 0.35, respectively). QSE contained the lowest MLE for POWV (1.53%), but B. burgdorferi-infected ticks were high with a MLE of 15.69%. Of the 295 D. variabilis ticks analyzed from both harvests, none (0%) had evidence of POWV infection; however, B. burgdorferi infection in D. variabilis ticks was seen in both QNW (3.1%) and QSW (2.86%), consistent with the high B. burgdorferi infection rate observed in I. scapularis ticks in these same quadrants.

Powassan Virus: An Emerging Arbovirus of Public Health Concern in North America

Hermance Meghan E. and Thangamani Saravanan. Vector-Borne and Zoonotic Diseases. May 2017 Online Ahead of Print

Powassan virus (POWV, Flaviviridae) is the only North American member of the tick-borne encephalitis serogroup of flaviviruses. It is transmitted to small- and medium-sized mammals by Ixodes scapularis, Ixodes cookei, and several other Ixodes tick species. Humans become infected with POWV during spillover transmission from the natural transmission cycles. In humans, POWV is the causative agent of a severe neuroinvasive illness with 50% of survivors displaying long-term neurological sequelae. POWV was recognized as a human pathogen in 1958 when a young boy died of severe encephalitis in Powassan, Ontario, and POWV was isolated from the brain autopsy of this case. Two distinct genetic lineages of POWV are now recognized: POWV (lineage I) and deer tick virus (lineage II). Since the index case in 1958, over 100 human cases of POWV have been reported, with an apparent rise in disease incidence in the past 16 years. This recent increase in cases may represent a true emergence of POWV in regions where the tick vector species are prevalent, or it could represent an increase in POWV surveillance and diagnosis. In the past 5 years, both basic and applied research for POWV disease has intensified, including phylogenetic studies, field surveillance, case studies, and animal model development. This review provides an overview of POWV, including the epidemiology, transmission, clinical disease, and diagnosis of POWV infection. Recent research developments and future priorities with regard to the disease are emphasized.

Early timeline of POWV transmission
The duration of I. scapularis attachment required for successful transmission of DTV to a host was found to be as little as 15 min (Ebel and Kramer 2004). This finding was particularly striking because unlike other tick-borne pathogens (Borrelia burgdorferi, Babesia microti, and Anaplasma phagocytophilum), very little time between tick attachment and virus transmission is needed for POWV. The reactivation period required for some nonviral tick-borne pathogens provides a grace period of approximately 24 h, where a minimal risk of transmission occurs if humans remove the attached tick within this timeline; however, there is no such grace period for POWV due to its very short timeline of transmission. These differences underscore why the timeline of POWV transmission must be carefully considered when analyzing the early immunomodulatory events that occur at the feeding site of the tick.

**My comment**
The idea of a “grace period” is ludicrous. Ticks do not understand grace, trust me. For accurate information about transmission times of Lyme see:  In short, it can happen in hours for sure – not requiring the oft repeated dogma of 24-48 or more hours.  Ticks often feed partially and then drop off.  These partially fed ticks have spirochetes in their saliva and can transmit much more quickly.

Every single tick bite should be taken seriously!

Bartonella Vectors

  Published on Jul 14, 2016
Dr. Tom Mather and Dr. Ed Breitschwerdt on the growing risks of tick and flea exposure from “Healthy Body, Healthy Minds” with special thanks to ITV productions.

Bartonella is a formidable coinfection for many Lyme/MSIDS patients.  Symptoms are largely associated with where blood flow is compromised:

Skin rashes (stretch-mark-like), cysts, heartburn, abdominal pain, chest pain, gastritis, duodentis, mesenteric adenitis, psychological issues (anxiety, anger, suicidal thoughts, depression, irritability), pain in the soles of the feet, skin tags and red papules, endocarditis, acute encephalopathy, seizures, visual and auditory hallucinations, ocular floaters, fatigue, partial paralysis, laryngitis, severe confusion, difficulty swallowing, muscle weakness, and vasculitis that occurs anywhere in the body which can destroy blood vessels.  For a longer list of symptoms see:

Since it exists in very low amounts in human blood, blood tests are unreliable. It also has a long division time between 22-24 hours and requires a special growth environment. There is a Triple Draw through Galaxy which collects blood over 8 days to maximize the test, stating a 90% reduction in false negatives.   Vectors include fleas and flea feces, biting flies such as sand flies and horn flies, the human body louse, mosquitoes, mites, and ticks; through bites and scratches of reservoir hosts; and potentially from needles and syringes in the drug addicted. Needle stick transmission to veterinarians has been reported. There is documentation that cats have received it through blood transfusion.

Bartonella has recently been found in winged adult deer keds in Finland:

Moose as reservoirs, deer keds as vectors in Norway:

Bartonella infection in southern Finnish moose was 90.6% (inside the deer ked zone), while northern Finnish moose was 55.9% (outside the deer ked zone). At least two species of bartonellae were identified.

Just what are deer keds?  In the fly family (6 legs), they will chuck their wings as soon as they land on a host to suck blood more easily.

For more on Bartonella:

Transmission Time For Lyme/MSIDS Infection

An oft quoted dogma currently exists that states you can not get infected with Lyme or the various coinfections that typically come with it if you get the tick off within a window of  24-48 hours.


Transmission Time:  Only one study done on Mice. At 24 hours every tick had transmitted borrelia to the mice; however, animal studies have proven that transmission can occur in under 16 hours and it occurs frequently in under 24 hours.  No human studies have been done and  no studies have determined the minimum time it takes for transmission.

There’s also the issue of partially fed ticks transmitting more quickly:  Ticks can spontaneously detach – and the authors of this study found that they did so 15% of the time in mice.  They also state that about a tenth of questing nymphs appear distended with partially fed sub-adult ticks being common.  This quicker transmission is due to spirochetes presiding in the salivary glands rather than the mid-gut.

It’s important to note that ticks typically carry more than just borrelia and transmission times have not been studied for many of these pathogens. and  Transmission with more than one pathogen is associated with more severe illness and renders antibiotics less effective.  The longer a tick is attached the greater the risk of transmission.  Tick Borne Viruses can be transmitted in minutes.

In the following video microbiologist Holly Ahern explains how the 24-48 window myth has been inappropriately used and is keeping people from getting diagnosed and treated.  Bob Giguere of IGeneX states a case of a little girl who went outside to play about 8:30a.m. and came inside at 10:30 with an attached tick above her right eye. By 2 o’clock, she had developed the facial palsy. At the hospital she was told it couldn’t be Lyme as the tick hadn’t been attached long enough. They offered a neuro-consult…..

By 4pm she couldn’t walk or talk.

A Lyme literate doctor trained by ILADS met the family in his office on a Saturday, gave her an intramuscular injection of antibiotics and within 2 hours the palsy was gone. He continued her treatment for approximately 4 weeks.


Ocular Bartonellosis
J Trop Med. 2017; 2017: 7946123.
Published online 2017 Feb 7. doi:  10.1155/2017/7946123
PMCID: PMC5318637

Clinical Profile and Visual Outcome of Ocular Bartonellosis in Malaysia
Chai Lee Tan, Lai Chan Fhun,  Evelyn Li Min Tai, Nor Hasnida Abdul Gani, Julieana Muhammed, Tengku Norina Tuan Jaafar, Liza Sharmini Ahmad Tajudin, and Wan-Hazabbah Wan Hitam 


Background. Ocular bartonellosis can present in various ways, with variable visual outcome. There is limited data on ocular bartonellosis in Malaysia. Objective. We aim to describe the clinical presentation and visual outcome of ocular bartonellosis in Malaysia. Materials and Methods. This was a retrospective review of patients treated for ocular bartonellosis in two ophthalmology centers in Malaysia between January 2013 and December 2015. The diagnosis was based on clinical features, supported by a positive Bartonella spp. serology. Results. Of the 19 patients in our series, females were predominant (63.2%). The mean age was 29.3 years. The majority (63.2%) had unilateral involvement. Five patients (26.3%) had a history of contact with cats. Neuroretinitis was the most common presentation (62.5%). Azithromycin was the antibiotic of choice (42.1%). Concurrent systemic corticosteroids were used in approximately 60% of cases. The presenting visual acuity was worse than 6/18 in approximately 60% of eyes; on final review, 76.9% of eyes had a visual acuity better than 6/18. Conclusion. Ocular bartonellosis tends to present with neuroretinitis. Azithromycin is a viable option for treatment. Systemic corticosteroids may be considered in those with poor visual acuity on presentation.

In the results section we learn that 19 patients with ocular bartonellosis were followed from 3-68 weeks. Neuroretinitis is an inflammation of the neural retina and optic nerve which can be caused by viruses, autoimmune disease, or bacteria including: syphilis, Rocky Mountain Spotted Fever, toxoplasmosis, toxocariasis, histoplasmosis, leptospirosis, and Lyme Disease. Tuberculosis and Tularemia can also present similarly. The most common ocular complaint was blurred vision with around 60% reporting headaches as their initial symptom.

We also learn that the treatment of choice was Azithromycin followed by Doxycyline, ciprofloxacin, ceftazidime, and cotrimoxazole, with 60% receiving systemic corticosteroid therapy. The discussion section states that the treatment of Bartonellosis is still controversial and that they had to resort of isolated case reports for information. In this case study a 44 year old woman had non-specific blurriness of vision in her left eye. After they went through about every other possibility, they asked about pets at which she showed multiple cat scratches on her arms.

Laboratory results showed:
*White blood cell count: 18,200 with left shift (12,194 segmented neutrophils and 3276 bands)
*Bartonella Henselae IgG 1:1024 (strongly positive)

According to this study, a literature review suggested that a one month course of doxycycline or erythromycin (with or without rifampin) is adequate to treat the organism and hasten recovery. They chose a one month course of doxycycline 100 mg twice daily. The patient returned for follow-up appointments one and two months after this initial diagnosis. Vision improved to 20/60 in the affected eye, improving visual fields, decreased optic disc edema, and resolving sub-retinal fluid.

The case study also states that diagnosis officially requires 3 out of 4 criteria:
• Lymphadenopathy in the absence of other reason (can be missed because it is not present yet or subclinical)
• Positive Bartonella H. titer or skin test
• Known cat contact, preferably with pustule or papule at the site
• Lymph node biopsy with bacilli present, necrosis

They admit this woman met only 2 of the criteria. They also state it is well documented patients will almost always get better on their own but that hundreds of reports give various treatment regimens including doxycycline, erythromycin, rifampin, azithromycin, ciprofloxacin, later addition of steroid drop, and many others.

The unfortunate thing about both of these reports is they make Bartonellosis out to be a benign pathogen, which for Lyme/MSIDS patients couldn’t be further from the truth.

As to the criteria to diagnose:

Thankfully, this woman didn’t present with swollen lymph nodes so they had to find a reason and state it was either subclinical or hadn’t presented yet.

*Hardly anyone I know with Bartonella has swollen lymph nodes.

*The testing for Lyme and every coinfection, including Bartonella, is abysmal.

*They emphasize the cat’s role but don’t even mention ticks, mites, biting flies, other arachnids, sand flies, mosquitoes, fleas and flea feces, the human body louse, potentially from needles and syringes in the drug addicted, as well as bites and scratches from other reservoir hosts.

*As to node biopsy, even this NIH study shows a lack of specificity and lack of typical micro abscesses in almost half of the cases and may mimic other lymphadenopathies.

* This CDC article states that Bartonella spp. may be the cause of unclear and undiagnosed chronic illness in humans previously bitten by ticks.

*They also fail to mention there are 15 species and counting of Bartonella known to infect humans and that Dr. Ricardo Maggi states, “This case reinforces the hypothesis that any Bartonella species can cause human infection.”  Besides the cat (including bobcats, mountain lions, and other large cats), rats, dogs, rabbits, deer, cattle, small woodland animals, rodents, coyotes, foxes, and elk were found to harbor Bart. The question really should be, “What doesn’t carry Bartonella?”  Here, Dr. Mozayeni states about 60% of Lyme patients tested positive for Bartonella and that it is one of the major coinfections. This link also has treatments, explanation of Bartonella including what it does and how it can present, along with a link for a checklist you can print out and take to your doctor to discuss.

I appreciate Dr. Breitschwert’s and Dorsey Kordick’s comment in the concluding remarks,

“Not too long ago, many were taught during microbiology courses (or medical school training) that blood is generally a sterile medium. Increasingly, this assertion must be qualified with regard to Bartonella spp. as well as other intracellular pathogens that have coevolved with humans and animals to persist in circulating blood cells such as erythrocytes or macrophages for months to years and perhaps longer.”

I wish more researchers were this transparent, then perhaps patients would be taken more seriously.   And, don’t kid yourself, Bartonella is a formidable foe to the immunocompromised.

Possible Transfusion-Transmitted Babesia divergens-like/MO-1 in Arkansas Patient  Mary J. Burgess, MD Eric R. Rosenbaum, MD, MPH Bobbi S. Pritt, MD, MSc Dirk T. Haselow, MD, PhD Katie M. Ferren, MD Bashar N. Alzghoul, MD Juan Carlos Rico, MD Lynne M. Sloan, BS Poornima Ramanan, MD Raghunandan Purushothaman, MD Robert W. Bradsher, MD    Published March 13, 2017

A patient with asplenia and multiple red blood cell transfusions acquired babesiosis infection with Babesia divergens-like/MO-1 and not Babesia microti, the common United States species. He had no known tick exposure. This is believed to be the first transfusion-transmitted case and the fifth documented case of Babesia divergens-like/MO-1.