Archive for the ‘Ticks’ Category

Genomic Confirmation of Borrelia garinii, United States

https://wwwnc.cdc.gov/eid/article/29/1/22-0930_article

Volume 29, Number 1—January 2023
Natalie RudenkoComments to Author , Maryna Golovchenko, Ales Horak, Libor Grubhoffer, Emmanuel F. Mongodin1, Claire M. Fraser, Weigang Qiu, Benjamin J. Luft, Richard G. Morgan, Sherwood R. Casjens, and Steven E. Schutzer
 
 

Abstract

Lyme disease is a multisystem disorder primarily caused by Borrelia burgdorferi sensu lato. However, B. garinii, which has been identified on islands off the coast of Newfoundland and Labrador, Canada, is a cause of Lyme disease in Eurasia. We report isolation and whole-genome nucleotide sequencing of a B. garinii isolate from a cotton mouse (Peromyscus gossypinus) in South Carolina, USA. We identified a second B. garinii isolate from the same repository. Phylogenetic analysis does not associate these isolates with the previously described isolates of B. garinii from Canada.

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Important excerpt:

How and when B. garinii arrived in South Carolina remains unknown. There were no reported Lyme disease outbreaks in the southeastern United States in humans at the time the strains were deposited in the repository or during the subsequent 2 decades. This finding minimizes the urgency for an immediate new search for B. garinii in this region. Nonetheless, clinical vigilance for B. garinii in humans in this region seems warranted.

 

True to form, the CDC downplays the finding of a new strain which very well could explain why sick patients continue to be mis or undiagnosed due to faulty testing and strain diversity, which will never be picked up using current 2-tiered CDC testing because it doesn’t look for other strains.

But, truth be damned.  It just doesn’t matter to corrupt public health.

Chlamydia & Alzheimer’s

https://iv.iiarjournals.org/content/36/6/2650

Circulating Chlamydia Trachomatis Antigens in Subjects With Alzheimer’s Disease

STEVEN LEHRER and PETER H. RHEINSTEIN

Abstract

Background/Aim: Chlamydia pneumoniae (C. pneumoniae) is implicated in the pathogenesis of Alzheimer’s disease (AD). Chlamydial elementary and reticulate bodies have been identified in tissues from afflicted AD brain regions by electron and immunoelectron microscopy, whereas similar tests of non-AD brains were negative for the bacterium. Studies in mice have shown that C. pneumoniae can rapidly penetrate the central nervous system by entering glia and causing beta amyloid deposition via the nerves between the nasal cavity and the brain, which serve as invasion pathways.

Materials and Methods: We used data from the UK Biobank (UKBB) to assess the relationship of chlamydia and AD. Circulating C. pneumoniae antigen measurements were not available, but UKBB data field 23037 held measurements of PorB antigen for Chlamydia trachomatis (C. trachomatis). We used C. trachomatis as a surrogate for C. pneumoniae since serum cross-reactivity to C. trachomatis and C. pneumoniae antigens occurs in patients with documented infection and in healthy children as revealed by microimmunofluorescence and immunoblotting techniques. Single nucleotide polymorphism (SNP) data for rs429358 and rs7412 were used to impute ApoE genotypes.

Results: PorB antigen levels for C. trachomatis were significantly higher in subjects with AD (p=0.007). PorB antigen levels were not related to ApoE genotype (e3e3, e3e4, e4e4) p=0.783. To control for the effects of age, sex, educational level, and apoE genotype, logistic regression analysis was performed. AD was the dependent variable. Independent variables were sqrt PorB antigen for C. trachomatis, age, sex, educational level, apoE genotype. AD odds ratio (OR) increased 1.156 for each unit increase of sqrt PorB antigen for C. trachomatis and the effect was significant (p=0.004).

Conclusion: PorB antigens for C. trachomatis being significantly higher in subjects with AD, corroborates previous studies demonstrating that C. pneumoniae inflammation appears to play a role in AD development. AD may result from the reactivation of embryologic processes and pathways silenced at birth. A trigger for the reactivation may be bacterial or viral infections. Further studies are warranted.

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https://www.nature.com/articles/s41598-022-06749-9

Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk

Abstract

Chlamydia pneumoniae is a respiratory tract pathogen but can also infect the central nervous system (CNS). Recently, the link between C. pneumoniae CNS infection and late-onset dementia has become increasingly evident. In mice, CNS infection has been shown to occur weeks to months after intranasal inoculation. By isolating live C. pneumoniae from tissues and using immunohistochemistry, we show that C. pneumoniae can infect the olfactory and trigeminal nerves, olfactory bulb and brain within 72 h in mice. C. pneumoniae infection also resulted in dysregulation of key pathways involved in Alzheimer’s disease pathogenesis at 7 and 28 days after inoculation. Interestingly, amyloid beta accumulations were also detected adjacent to the C. pneumoniae inclusions in the olfactory system. Furthermore, injury to the nasal epithelium resulted in increased peripheral nerve and olfactory bulb infection, but did not alter general CNS infection. In vitro, C. pneumoniae was able to infect peripheral nerve and CNS glia.

In summary, the nerves extending between the nasal cavity and the brain constitute invasion paths by which C. pneumoniae can rapidly invade the CNS likely by surviving in glia and leading to Aβ deposition.

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For more:

Acrodermatitis Chronica Atrophicans

https://pubmed.ncbi.nlm.nih.gov/33085436/

Acrodermatitis Chronica Atrophicans

In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan.
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Excerpt:

Acrodermatitis chronica atrophicans (ACA) is a late and chronic manifestation of Lyme borreliosis (LB). ACA predominantly involves the distal portions of extremities and is characterized by chronic cutaneous atrophy. Unlike other skin manifestations of Lyme disease, including erythema migrans (EM) and borrelial lymphocytoma (BL), ACA does not spontaneously resolve. If untreated, ACA may progress from bluish-red discoloration and inflammation to chronic atrophy and fibrosis, with the late-stage being more treatment-resistant.

ACA was first described in 1883 by Buchwald in Germany, and cases were later reported in 1895 in North America. The diagnosis of ACA is based on clinical presentation, as well as serologic testing and histopathologic confirmation. Recognizing ACA is often challenging due to variable latency in disease onset following the primary borrelial infection, and lack of symptoms leading to delay in seeking treatment.

Lyme borreliosis is the most common vector-borne disease in the northeastern United States. It is a multisystem disease caused by the spirochete Borrelia burgdorferi.It is transmitted to humans via an Ixodes tick bite. There are 3 skin manifestations of LB: Erythema migrans (stage 1) with a characteristic “bull’s eye rash,” which, if untreated, can be followed by early disseminated infection, borrelial lymphocytoma (stage 2) along with neurologic and cardiac abnormalities, and late infection, especially arthritis in North America or acrodermatitis chronica atrophicans (stage 3) in Europe. Acrodermatitis chronica atrophicans is the most common late and chronic manifestation of LB. Approximately 20% of patients with ACA have a history of spontaneously healed EM, usually on an extremity where the ACA lesion developed 6 months to 8 years later.

Sections

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**Comment**

While ‘the powers that be’ continue to want to confine this complex illness within numerical stages and a “one size fits all” box, please know that patients have jumped from stage to stage in no particular order, with some requiring much longer courses of antibiotics/treatments.

For more:

Lyme Disease & Herxheimer Reaction in Newborn

https://danielcameronmd.com/lyme-disease-herxheimer-reaction-newborn/

LYME DISEASE AND HERXHEIMER REACTION IN NEWBORN

Newborn with lyme disease and herxheimer reaction being examined by doctor.

The Herxheimer reaction, also referred to as a Jarisch-Herxheimer reaction, is “a transient clinical phenomenon that occurs in patients infected by spirochetes who undergo antibiotic treatment.”¹ It was first described in patients with syphilis but has also been associated with other spirochetal infections including leptospirosis, Lyme disease, and relapsing fever. The reaction is associated with the onset of new symptoms or a worsening of existing symptoms in patients receiving antibiotic treatment.

In 2020, investigators published a case involving a 13-year-old boy with Lyme arthritis, a common manifestation of Lyme disease, who developed a Herxheimer reaction when treated with doxycycline. On the 7th day of treatment, the boy developed a low-grade fever and severe arthralgias with intense hip, ankle and cervical spine pain and myalgias.

You can read more about the 13-year-old boy’s case in an earlier blog “Herxheimer reaction in a 13-year-old boy with Lyme disease.” 

Newborn with herxheimer reaction

In their article “Lyme disease in a neonate complicated by the Jarisch–Herxheimer reaction,” Prodanuk and colleagues² describe the case of a 21-day-old infant who was admitted to the hospital with decreased activity, poor feeding and abdominal distension.

The parents removed an engorged tick from the infant’s forearm 5 days earlier. An EM rash was present at the site of the tick bite.

“Given the erythema migrans lesion at the site from which the engorged tick was removed, we made a presumptive diagnosis of Lyme disease and administered IV ceftriaxone,” the authors write.

Two hours after treatment began, the infant developed a fever, tachycardia and other symptoms consistent with the Jarisch–Herxheimer reaction.

Testing for Lyme disease was negative.

Clinicians should also “be aware of the possibility of the Jarisch–Herxheimer reaction during the initial phase of treatment.”²

Several studies, they warn, indicate “newborns with findings consistent with early localized disease may also be at higher risk for disseminated disease.”

“Given the limited data for neonates and the possible predisposition of this population to disseminated Lyme disease, clinicians should strongly consider administering IV antibiotics to target Lyme disease,” the authors suggest.

Patients can experience a broad range of symptoms resulting from a herxheimer reaction, explains Nykytyuk and colleagues, including fever, severe polyarthralgias, myalgias, chills, hypotension, nonpruritic, nonpalpable rash, tachycardia, nausea, headache, strengthening of existing or occurrence of new symptoms of the underlying disease.¹

The exact cause of Jarisch-Herxheimer reactions is still unknown. “At first, the role of an endotoxin in the development of JHR was suggested, but later experimental studies showed that spirochetes do not have biologically active endotoxins,” the authors explained.¹

References:
  1. Dhakal A, Sbar E. Jarisch Herxheimer Reaction. [Updated 2022 Apr 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557820/
  2. Prodanuk M, Groves H, Arje D, Bitnun A. Lyme disease in a neonate complicated by the Jarisch-Herxheimer reaction. CMAJ. 2022 Jul 18;194(27):E939-E941. doi: 10.1503/cmaj.220112. PMID: 35851530; PMCID: PMC9299745.

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**Comment**

This infant won the lotto by having astute parents, a noticable tick bite, and EM rash.  Many are not so fortunate to have these clear signs.  Many also test negative.  Without the signs and positive test, many are misdiagnosed and miss this opportunity for early treatment which is imperative.

For more:

Patients Want Canadians to Know About Lesser-Known Tick-Borne Diseases

https://www.ctvnews.ca/health/be-vigilant-patients-want-canadians-to-know-about-lesser-known-tick-borne-diseases

‘Be vigilant’: Patients want Canadians to know about lesser-known tick-borne diseases

While these infections are indeed spreading, it has nothing to do with the climate.  Faulty climate change maps which have been used to push a ‘climate change’ agenda have been debunked, with many experts finally coming forth and denying that man has anything to do with the climate at all.
Important to note: neither of these spreading pathogens are listed as a nationally notifiable disease in Canada, which simply means nobody has a clue as to their prevalence.  This is true for many of the “lesser  known” tick-borne diseases as well, and is a real problem.  You can’t state how big a problem is if you aren’t even looking for it.
One of the patients sent her tick to a private lab and paid out of pocket for tests that look for a wide range of pathogens. 
This is another real problem that needs to be addressed.  Since everyone and their brother knows ticks are spreading everywhere and are often infected with pathogens transmitted to animals and humans, tick testing should be widely available and FREE.  There is no tick testing for the public right here in Wisconsin, an epicenter for Lyme, Powassan, and other infections.  This simply shouldn’t be.
Rather than fund more faulty, erroneous climate change research, how about we fund labs for something practical like testing ticks and all the pathogens they carry?
Since so many patients slip through the cracks, testing ticks directly would help us know what pathogens are in an area and an idea about prevalence.

This information; however, should never be used against patients, which has happened historically.  The lunacy of telling someone they can’t have Lyme disease because certain ticks don’t exist there or “there aren’t any recorded cases,” is shear madness and defies all sound logic.  Ticks travel everywhere due to migrating birds and other animals that don’t understand borders.

For more:

To be clear, a test only picks up what it is created to pick up.  To this day, many strains of of the pathogens infecting humans do not have testing, and those that do aren’t accurate.