Archive for the ‘Malaria’ Category

Malaria Hides In People Without Symptoms

https://researchblog.duke.edu/2019/11/11/malaria-hides-in-people-without-symptoms/?

Malaria Hides In People Without Symptoms

It seems like the never-ending battle against Malaria just keeps getting tougher. In regions where Malaria is hyper-prevalent, anti-mosquito measures can only work so well due to the reservoir that has built up of infected humans who do not even know they carry the infection.

In high-transmission areas, asymptomatic malaria is more prevalent than symptomatic malaria. Twenty-four percent of the people in sub-Saharan Africa are estimated to harbor an asymptomatic infection, including 38 to 50 percent of the school-aged children in western Kenya. Out of the 219 million malaria cases in 2017 worldwide, over 90%  were in sub-Saharan Africa….(See link for full article)

__________________

**Comment**

I post this because Malaria is a protozoan similar to Babesia.  The question begging to be asked is, “Can people also have an asymptomatic Babesia infection that lies around for an opportune time to emerge?”

My educated guess is yes, it can.

Key quote:  “P. falciparum malaria is very diverse in the region,” she said. “It’s constantly mutating, which is why it’s so hard to treat….many study participants were infected with multiple, genetically-distinct malaria infections. Some carried up to fourteen strains of the parasite.

For more:  https://madisonarealymesupportgroup.com/category/babesia-treatment/

https://madisonarealymesupportgroup.com/2018/10/11/babesia-found-in-patient-with-persistent-symptoms-following-lyme-treatment/

https://madisonarealymesupportgroup.com/2019/09/05/babesia-subverts-adaptive-immunity-and-enhances-lyme-disease-severity/

We show that

  • burgdorferi infection attenuates parasitemia in mice while
  • B. microti subverts the splenic immune response, such that a marked decrease in splenic B and T cells, reduction in antibody levels and diminished functional humoral immunity, as determined by spirochete opsonophagocytosis, are observed in co-infected mice compared to only B. burgdorferi infected mice

Furthermore

  • immunosuppression by B. microti in coinfected mice showed an association with enhanced Lyme disease manifestations.
Due to the high prevalence of infection and the issues of congenital transmission and transmission through blood transfusion, the issue of concurrent infection and what it does to animal and human health is of paramount importance.

Variable Clinical Presentations of Babesiosis

https://journals.lww.com/tnpj/Pages/articleviewer.aspx?year=2018&issue=10000&article=00011&type=Fulltext

Variable clinical presentations of babesiosis

Paparone, Pamela, DNP, APN; Paparone, Philip W., DO

doi: 10.1097/01.NPR.0000545000.07640.11
Abstract: 
Human babesiosis continues to spread in multiple regions of the US. It is transmitted by Ixodes species ticks, as are Lyme disease and anaplasmosis. Its variable clinical presentations, together with serologic detection limitations, require that a high index of clinical suspicion be present for prompt diagnosis. This article discusses case examples showing the wide range of symptoms and presentations that are possible with babesiosis.
Human babesiosis is an infectious, malaria-like disease caused by intraerythrocytic protozoa of the genus Babesia, specifically Babesia microti and Babesia divergens.1-4 It is transmitted by Ixodes species ticks, as are Lyme disease and anaplasmosis (formerly known as ehrlichiosis). Babesia species are well-known pathogens in animals. During the past half century in the US, they have been increasingly recognized as pathogens in humans.1,5 Babesiosis may be acquired through the bite of an infected tick, a blood transfusion, or by transplacental transmission.2,6-8 (See Ixodes scapularis [blacklegged or deer ticks].)
Most infection passes undetected (because the patient may be unaware of the tick bite), especially in healthy adults.6,7 However, in immunocompromised patients—particularly those with hematologic disease and a history of splenectomy—Babesia infection may be severe and life-threatening.1

Epidemiology

The first reported case of babesiosis in the US was in 1968.9 It became a nationally notifiable disease in 2011, and among the 27 states where it was notifiable in 2013, there were 1,792 reported cases nationwide.5,10 Tick-borne and transfusion-associated cases of babesiosis occur in multiple parts of the country, including outside of areas of known endemicity.5 The number of reported cases is rising steadily in the US and worldwide, owing in part to increased medical awareness and improved diagnostic methods.1-3 (See Reported cases of babesiosis in the US.)

Health departments notify the CDC of babesiosis cases via the National Notifiable Diseases Surveillance System (NNDSS) using a standard case definition. In addition to basic demographic information (age, gender, and county of residence) provided via NNDSS, supplemental data (symptoms and history of transfusion) can be submitted to the CDC using a disease-specific case report form (CRF). Because babesiosis has been a reportable condition in some states for years, state-developed CRFs had already been in use to capture supplemental data.5

To promote standard data collection, the CDC developed a babesiosis CRF, which was approved by the Office of Management and Budget in August 2011 (www.cdc.gov/parasites/babesiosis/resources/50.153.pdf). Supplemental data, derived from the CDC’s or a state’s CRF, were merged manually with NNDSS records by matching a case ID number or demographic data. If case records had conflicting data, the more detailed record was considered correct.

As cases of babesiosis transmitted via tick bite or blood transfusion occur in multiple parts of the US, including outside of areas of known endemicity, ongoing national surveillance using the standard case definition will provide a foundation for developing evidence-based prevention and control measures to reduce the burden of the disease. In addition, mapping based on this surveillance allows for the identification of endemic areas, which aids the clinician in diagnosis.

Transmission and pathogenesis

The heightened recognition of tick-borne infection is derived largely from the increasing incidences of human babesiosis, anaplasmosis, and Lyme disease, both individually and together.11,12 Because these infections share the same rodent reservoir and tick vector hosts, they can be cotransmitted to human hosts.1,2,10,13-16 Coinfections involving various combinations of these pathogens are common and can be severe.12,14 The babesia parasite is suspected of causing proinflammatory cytokines that stimulate the production of nitric oxide, which may cause erythrocytic cellular damage when produced in excess.2

Diagnostic procedures and clinical management of the resulting disease syndrome are complicated by the diversity of pathogens involved and by the unusual diversity and duration of symptoms.

Clinical presentation

Common clinical features of babesiosis are similar to those of malaria and range in severity from asymptomatic to rapidly fatal. Most patients experience a viral infection-like illness with fever, chills, sweats, myalgia, arthralgia, anorexia, nausea, vomiting, or fatigue, and in some cases, patients may develop hemolytic anemia.1-4,10 Most symptomatic patients become ill 1 to 4 weeks after the bite of a B. microti-infected tick and 1 to 9 weeks (but up to 6 months in one reported case) after transfusion of contaminated blood products.6-8

A high index of clinical suspicion for babesiosis and the possible presence of other tick-borne infections are required for prompt diagnosis and proper treatment. Because the clinical findings are nonspecific, lab studies are necessary to confirm the diagnosis.

Diagnosis

Microscopic examination of blood smears is the current gold standard for detecting Babesia infection, while polymerase chain reaction testing has promising diagnostic value.1,2,16,17 Differentiating Babesia from malaria on peripheral smears can be difficult but rapidly resolved by the presence or absence of a history of travel.1 Peripheral smears for Babesia allow for same-day or, at the most, next-day confirmation of the diagnosis. The case examples described below demonstrate the range of symptoms and clinical presentations associated with babesiosis (with and without coinfection) that can challenge the NP.

Babesiosis is caused by parasites that infect red blood cells. Most US cases are caused by B. microti, which is transmitted by Ixodes scapularis ticks, primarily in the Northeast and Upper Midwest. Babesia parasites also can be transmitted via transfusion, anywhere, at any time of the year. In March 2018, the FDA approved the first B. microti blood donor screening tests. B. microti Arrayed Fluorescent Immunoassay detects antibodies to B. microti in human plasma, and B. microti Nucleic Acid Test detects B. microti DNA in human whole blood.18

Treatment

**Please see my comment at end of article**

Generally, treatment with atovaquone plus azithromycin is used for patients with mild-to-moderate babesiosis, whereas clindamycin plus quinine is recommended for patients with severe disease; both treatment regimens are given for 7 to 10 days.1-4 All four drugs are used FDA off-label for babesiosis; however, the dosage recommendations are supported by the clinical guidelines.1-4,19 The dosage regimen for atovaquone plus azithromycin for adult patients is atovaquone 750 mg orally every 12 hours, and azithromycin 500 to 1,000 mg orally on day 1 and 250 mg orally once daily for the subsequent days.1-4 Immunocompromised patients may require higher doses of azithromycin.2-4

The dosage regimen for clindamycin plus quinine for adult patients with severe disease is clindamycin 600 mg orally every 8 hours or clindamycin 300 to 600 mg I.V. infusion every 6 hours, and quinine 650 mg orally every 6 to 8 hours.1-4 Dose adjustments of quinine are needed for patients with severe chronic kidney disease.19,20 Of note, the only FDA-approved preparation of oral quinine currently available in the US is the 324 mg capsule.19,20 Previously, the dosage available in the US was a 325 mg capsule. The change in the quinine preparation from 325 mg to 324 mg may result in minor dose disparities between some guideline dosage recommendations that were published before the commercial preparation was changed.20,21

Although rare cases of resistance to atovaquone plus azithromycin have been reported, this combination is effective in most patients.2 Atovaquone is contraindicated in patients who develop or have a history of serious allergic or hypersensitivity reactions to the drug or any of the drug’s components. Azithromycin is contraindicated in patients with known hypersensitivity to azithromycin or any macrolide or ketolide antibiotic and also in patients with a history of cholestatic jaundice or hepatic dysfunction.19 Clindamycin is contraindicated in patients with a history of hypersensitivity to clindamycin or lincomycin. Quinine is contraindicated in patients with known hypersensitivity to quinine, mefloquine, or quinidine; prolonged QT interval; a glucose-6-phosphate dehydrogenase deficiency; or a history of myasthenia gravis or optic neuritis.19 Consult the manufacturer’s prescribing label for complete prescribing information for each drug.

Some patients, including those with severe illness, might require or benefit from supportive care, such as antipyretics, vasopressors (if the patient’s BP is low and unstable), blood transfusions, exchange transfusions (in which portions of a patient’s blood or blood cells are replaced with transfused blood components), mechanical ventilation, and dialysis. The NP should consider referral to an infectious-disease specialist for patients who are pregnant, have an underlying hematologic or oncologic problem, have had a splenectomy, are allergic to first-line antibiotic agents, or have had an unsatisfactory response to antibiotic therapy.

Red blood cell exchange transfusions are recommended for cases of severe babesiosis in patients with parasitemia of 10% or greater, severe anemia (hemoglobin less than 10 g/dL), or pulmonary, kidney, or liver impairment.2-4 Exchange transfusions are used to rapidly decrease parasitemia, correct anemia, and help remove toxic byproducts produced by the infection.2

Case examples

The case examples of patients with babesiosis show a wide range of symptoms and clinical presentations. The case examples below are cases that occurred in southeastern New Jersey, where the disease is endemic. All patients were hospitalized and treated in Atlantic County, New Jersey (see Summary of data from patients with babesiosis).

Case 1

Ms. A is a 78-year-old White female who was admitted with fever, chills, lethargy, fatigue, and marked changes in sensorium. She had a maximum temperature of 100.6° F (38.1° C); sepsis was considered for this patient. Multiple tick bites were found. Pertinent lab findings included lactate dehydrogenase (LDH), 528 units/L; aspartate aminotransferase (AST), 90 units/L; and alanine aminotransferase (ALT), 34 units/L. Her vitamin B12 and folate levels were normal.

Ms. A’s initial white blood cell (WBC) count was 5.0 × 109/L, but over the first 3 days of hospitalization, it gradually dropped to 2.6 × 109/L. Her hemoglobin dropped from 10.5 g/dL to a low of 8 g/dL, and her platelets were initially 39 × 109/L but gradually increased as she continued her course of treatment. Ms. A had 33% polymorphonuclear leukocytes, 2% bands, 49% lymphocytes, and 13% monocytes. Peripheral smear was positive for Babesia, and she had a Babesia immunoglobulin M (IgM) of 1:160 and Anaplasma (previously referred to as Ehrlichia) IgM of 1:320.

In view of Ms. A’s leukopenia and thrombocytopenia, anaplasmosis was suspected, and she was treated with doxycycline 100 mg I.V. infusion every 12 hours, atovaquone suspension 750 mg orally twice daily, and azithromycin 500 mg I.V. infusion every 24 hours. Doxycycline is the recommended treatment for anaplasmosis and was administered to cover the possibility of anaplasmosis in this patient. She was treated with that regimen for 5 days. She was then started on doxycycline twice daily, and azithromycin 500 mg daily (both oral) along with the atovaquone suspension of 750 mg twice daily for a 14-day course of therapy. Ms. A made a dramatic improvement in her mentation and resolution of her lethargy.

Case 2

Ms. C is a 90-year-old White female with a chief complaint of rectal bleeding. On admission, her lab studies revealed severe anemia with a hemoglobin of 7.6 g/dL and hematocrit of 22.6%. Her platelet count was 103 × 109/L and peripheral smear was positive for Babesia. Ms. C had spiking temperatures 100° F to 101° F (37.8° C to 38.3° C). Her rectal bleeding was controlled with an octreotide infusion to which she responded well (the bleeding ceased). Her peripheral smear was positive for Babesia, and she was placed on an oral dose of azithromycin 500 mg on day 1 and then 250 mg daily and atovaquone suspension 750 mg twice daily to complete a 10-day course.

Case 3

Mr. E is a 57-year-old White male admitted with fever, malaise, and chills. His temperature had risen to 101° F (38.3° C). His AST and ALT were 64 and 54 units/L, respectively, and gradually rose to a peak of 90 and 87 units/L, respectively, during his 5-day hospital stay. Mr. E’s WBC count decreased from his initial hospital results to 2.9 x 109/L with a hemoglobin of 9.2 g/dL. His platelets were initially 60 × 109/L but dropped to 34 × 109/L at their lowest level. In view of his elevated liver enzymes, leukopenia, and thrombocytopenia, anaplasmosis was highly suspected, and he was started on doxycycline 100 mg I.V. infusion every 12 hours.

Mr. E’s peripheral smear was positive for Babesia. He was started on oral clindamycin 600 mg every 8 hours and oral quinine 650 mg three times daily. Acute hearing deterioration occurred, and the quinine was discontinued. Mr. E’s regimen was then switched to oral azithromycin 500 mg on day 1 and then 250 mg daily and oral atovaquone 750 mg twice daily. He went on to complete only 7 days of therapy, and his elevated liver enzymes and thrombocytopenia resolved. The suspected anaplasmosis was not confirmed, as the Anaplasma IgM was negative. However, Mr. E’s leukopenia and thrombocytopenia resolved on the above regimens.

Case 4

Mr. J is an 81-year-old White male who was admitted with increasing lethargy, weakness, chills, and blurred vision. He had a history of coronary artery disease and hypertension. His hemoglobin on admission was 12.1 g/dL, and his hematocrit was 35.4%. His WBC count was 5.3 × 109/L. By day 2, his hemoglobin had dropped to 9.9 g/dL with a hematocrit of 29%. His platelets were initially 54 × 109/L and dropped to 46 × 109/L, but on therapy, rose to 191 × 109/L.

Mr. J had 82% polymorphonuclear leukocytes, 10% lymphocytes, and 6% monocytes. On the day of admission, a peripheral smear was positive for Babesia. Subsequently, serologic studies demonstrated an Anaplasma IgG of 1:256; the IgM was negative. Babesia serologies were greater than 1:320, both IgG and IgM. Anaplasmosis was suspected with Mr. J’s confirmed babesiosis, and he was started on azithromycin 500 mg I.V. infusion every 24 hours and doxycycline 100 mg twice daily.

At discharge on day 10, Mr. J was switched to clindamycin orally three times a day and quinine orally three times a day because of intolerance to azithromycin, and he completed a 14-day course of therapy. He convalesced satisfactorily. His hemoglobin at discharge was 12.5 g/dL and WBCs 7.4 × 109/L; platelets improved to 137 × 109/L.

Case 5

Mr. K is an 85-year-old White male who was admitted with fever and chills intermittently, recurring for several days prior to admission. He had a history of hairy cell leukemia, splenectomy, permanent pacemaker insertion for atrioventricular block, gouty arthritis, prostatic hypertrophy, and polymyalgia rheumatica. In the ED, Mr. K had an immediate peripheral smear for Babesia, and the intraerythrocytic parasite was demonstrated. He had been working on a golf course for the week prior to admission.

A second peripheral smear was positive for intraerythrocytic parasites with 10.4% of his red blood cells infected. Findings were also positive for Howell-Jolly bodies, which are erthrocytic nuclear remnants associated with asplenia or decreased splenic function. Mr. K was started on oral azithromycin 500 mg on day 1 and then 250 mg daily and atovaquone 750 mg suspension twice daily. Due to the possibility of concurrent tick-borne infection, he was also started on oral doxycycline 100 twice daily.

Over the course of day 1, Mr. K’s platelet count dropped from 25 to 23 × 109/L, with blood urea nitrogen of 29 mg/dL and creatinine of 1.2 mg/dL. His WBC count dropped from 4.1 to 2.5 × 109/L, and his hemoglobin dropped from 16 to 13 g/dL. He had 20% bands, 5% atypical lymphocytes, 47% polymorphonuclear leukocytes, and 23% lymphocytes. Mr. K remained on doxycycline, azithromycin, and atovaquone suspension for 8 days when he was discharged home.

Mr. K was readmitted the following day when he complained of the inability to ambulate and generalized weakness. He had peripheral smear positivity with babesiosis and was serologically positive for anaplasmosis with both IgM and IgG. Mr. K had continued on the prescribed antibiotic regimen up until his readmission that day. Due to the persistence of parasitemia despite adequate therapy, he was changed to clindamycin 600 mg I.V. infusion every 8 hours, and quinine was also being administered.

Unfortunately, Mr. K developed gastric distress and a generalized erythematous coalescing rash, which prompted the discontinuation of the clindamycin and quinine. His WBC count was 2.2 × 109/L, and his hemoglobin was 9.5 g/dL. Platelets had risen to 43 × 109/L, and he had 43% polymorphonuclear leukocytes, 10% bands, 42% lymphocytes, and 5% monocytes.

Because of the persistence of parasitemia, Mr. K underwent exchange transfusion. At that point, he had been restarted on azithromycin 500 mg I.V. infusion every 24 hours and atovaquone suspension 750 mg orally twice daily. Azithromycin and atovaquone were continued for 5.5 weeks, at which time he was parasite smear negative for Babesia. Subsequently, a Babesia peripheral smear remained negative.

Discussion of case examples

Case 1 shows the unusual effect of babesiosis on the sensorium in the older adult, as any infectious process can. The patient’s cognitive function was dramatically improved following treatment, despite the marked changes in mentation on admission. A coinfection with Anaplasma was suspected. In general, all cases of babesiosis need to be tested for late Lyme disease, via Western blot, although not immediately addressed.1,2,4

Patients with concurrent babesiosis and anaplasmosis—suspected or serologically positive—are treated with doxycycline, which is equally effective for Lyme disease, early or late. Generally, the greater number of concurrent tick-borne infections and the higher the parasitimia load, the more toxic the presentation.1,12

Case 2 shows the need to check the peripheral smear for Babesia despite the rectal bleeding issue on admission. This diagnostic test could have easily been omitted, causing a delay in the diagnosis. Such a delay in older adult patients that results in delayed treatment can put these patients at greater risk for severity of babesiosis. Generally, the combination of clindamycin and quinine has a much higher probability of intolerance and adverse reactions. This combination is not the treatment of first choice for babesiosis. Pertaining to anaplasmosis, the triad of leukopenia, transaminase elevation (mild or moderate), and thrombocytopenia demands empiric treatment with doxycycline prior to serologic confirmation.1,2,4

A peripheral smear for Babesia is rapidly interpreted, is inexpensive, and should be requested in evaluating all patients with any degree of anemia—especially during the spring and summer months in endemic areas. Serologic studies are variable in developing positivity and are generally less readily available.

Case 3 illustrates the importance of suspecting and investigating the possibility of babesiosis and anaplasmosis coinfection in a patient presenting with a tick-borne illness.

Case 4 demonstrates that no additional lab studies—other than peripheral smear for Babesia—are needed to confirm the diagnosis of babesiosis.

Case 5 exemplifies the therapeutic challenge and refractory response to treatment of babesiosis in patients with the comorbidities of a hematologic disease and/or splenectomy.

Patient education

Heightened awareness of babesiosis as well as prompt diagnosis and treatment are essential to prevention. Both patients and the general public need to become more aware of the existence of the disease and other tick-borne infections, especially individuals who live in or travel to regions where babesiosis is found. The NP can play an active and important role in providing patient education about the disease. The basic points of information to communicate include:

  • What babesiosis is and its potential to be a life-threatening illness
  • How individuals acquire babesiosis (tick bite, transfusion, or, rarely, vertical transmission)
  • Where in the world babesiosis is found
  • Signs and symptoms of babesiosis
  • Note that many individuals do not have any symptoms and do not get sick
  • Importance of seeing a healthcare provider if babesiosis is suspected
  • Treatability of babesiosis and need for prompt diagnosis and treatment.22,23

Individuals who live in or travel to endemic areas should avoid tick-infested areas; apply repellents and wear long pants and long-sleeved shirts when outdoors; shower soon after being outdoors; and check their entire body for ticks.3 When outdoors, they should walk on cleared trails, stay in the center of the trail, and minimize contact with leaf litter, brush, and overgrown grasses (where ticks are most likely to be found). If a tick is found attached to a person’s body, it should be properly removed as soon as possible.

The CDC offers a printable, one-page fact sheet for patients and the general public that details the basic information for babesiosis awareness in addition to the link for the CDC guide to proper removal of a tick attached to a person (www.cdc.gov/parasites/babesiosis/resources/babesiosis_fact_sheet.pdf).

Conclusion

This article illustrates the need for the NP to appreciate the variable clinical presentations of babesiosis to facilitate prompt diagnosis, provide proper therapeutic management, and avoid the poor outcomes associated with this disease. Staying knowledgeable of babesiosis is essential. It is important for the NP to understand that infected patients may not recall a tick bite and that clinical presentations may not only be variable but also nonspecific, ranging from subclinical to severe. The possibility of coinfection with other tick-borne illnesses (Lyme disease and anaplasmosis) must be considered. Furthermore, the NP needs to assume an active role in patient education to affect babesiosis awareness and prevention.

Ixodes scapularis (blacklegged or deer ticks)

The images below are of the Ixodes scapularis ticks, also known as blacklegged or deer ticks. From left to right, the male (M) with a dorsal scutum (also known as a shield on the hard-bodied tick) that covers the entire back on the male, the female (F) with only a portion of the back covered by the dorsal scutum, the nymph (N), and the larva (L).

Figure

Sourse: Procop GW, Church DL, Hall GS, et al. Koneman’s Color Atlas and Textbook of Diagnostic Microbiology. 7th edition. Philadelphia, PA: Wolters Kluwer Health, 2016.

Reported cases of babesiosis in the US1,2,22,23

Most cases of babesiosis in the US occur in seven states, five of which are located in the Northeast (MA, CT, RI, NY, and NJ) and two in the upper Midwest (MN and WI). The geographic range of babesiosis has expanded beyond these highly endemic areas and it is now reported all along the northeastern seaboard and inland, ranging from Maine to Maryland.

Sporadic cases of babesiosis have been reported in other areas of the US including the West Coast. Additionally, transfusion-associated cases of babesiosis can occur anywhere in the country. Congenital transmission of babesiosis has also been reported.

REFERENCES

1. Sanchez E, Vannier E, Wormser GP, Hu LT. Diagnosis, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: a review. JAMA. 2016;315(16):1767–1777.

2. Vannier EG, Diuk-Wasser MA, Ben Mamoun C, Krause PJ. Babesiosis. Infect Dis Clin North Am. 2015;29(2):357–370.

3. Vannier E, Krause PJ. Human babesiosis. N Engl J Med. 2012;366(25):2397–2407.

4. Wormser GP, Dattwyler RJ, Shapiro ED, et al 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;43(9):1089–1134.

5. Centers for Disease Control and Prevention. Babesiosis surveillance—18 States, 2011. MMWR Morb Mortal Wkly Rep. 2012;61(27):505–509.

6. Levin AE, Krause PJ. Transfusion-transmitted babesiosis: is it time to screen the blood supply. Curr Opin Hematol. 2016;23(6):573–580.

7. Leiby DA. Babesiosis and blood transfusion: flying under the radar. Vox Sang. 2006;90(3):157–165.

8. Herwaldt BL, Linden JV, Bosserman E, Young C, Olkowska D, Wilson M. Transfusion-associated babesiosis in the United States: a description of cases. Ann Intern Med. 2011;155(8):509–519.

9. Scholtens RG, Braff EH, Healey GA, Gleason N. A case of babesiosis in man in the United States. Am J Trop Med Hyg. 1968;17(6):810–813.

10. Centers for Disease Control and Prevention. Notice to readers: final 2013 reports of nationally notifiable infectious diseases. MMWR Morb Mortal Wkly Rep. 2014;63(32):702–715.

11. Western KA, Benson GD, Gleason NN, Healy GR, Schultz MG. Babesiosis in a Massachusetts resident. N Engl J Med. 1970;283(16):854–856.

12. Diuk-Wasser MA, Vannier E, Krause PJ. Coinfection by Ixodes tick-borne pathogens: ecological, epidemiological, and clinical consequences. Trends Parasitol. 2016;32(1):30–42.

13. Herwaldt BL, McGovern PC, Gerwel MP, Easton RM, MacGregor RR. Endemic babesiosis in another eastern state: New Jersey. Emerg Infect Dis. 2003;9(2):184–188.

14. Thompson C, Spielman A, Krause PJ. Coinfecting deer-associated zoonoses: Lyme disease, babesiosis, and ehrlichiosis. Clin Infect Dis. 2001;33(5):676–685.

15. Paparone PW, Glenn WB. Lyme disease with concurrent ehrlichiosis. J Am Osteopath Assoc. 1994;94(7):568–570, 573, 577.

16. Hildebrandt A, Gray JS, Hunfeld KP. Human babesiosis in Europe: what clinicians need to know. Infection. 2013;41(6):1057–1072.

17. Wang G, Wormser GP, Zhuge J, et al Utilization of a real-time PCR assay for diagnosis of Babesia microti infection in clinical practice. Ticks Tick Borne Dis. 2015;6(3):376–382.

18. U.S. Food & Drug Administration. FDA approves first tests to screen for tickborne parasite in whole blood and plasma to protect the U.S. blood supply. 2018. http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm599782.htm.

19. Facts and Comparisons. Drug. Facts and Comparisons 2013. St. Louis, MO: Wolters Kluwer Health; 2013.

21. Gelfand JA, Vannier EG. Clinical manifestations, diagnosis, treatment, and prevention of babesiosis. UptoDate. 2017. http://www.uptodate.com.

22. Joseph JT, Purtill K, Wong SJ, et al Vertical transmission of Babesia microti, United States. Emerg Infect Dis. 2012;18(8):1318–1321.

23. Centers for Disease Control and Prevention. Tickborne diseases of the United States. A reference manual for health care providers. 2017. http://www.cdc.gov/lyme/resources/TickborneDiseases.pdf.

____________________

**Comment**

According to Dr. Horowitz, an experienced LLMD (Lyme literate doctor), Babesia is a tenacious tick-borne infection that persists.  Experience has shown him patients often need 9-12 months of treatment, a far cry longer than what is suggested here.

For treatment options, please see:  https://madisonarealymesupportgroup.com/2016/01/16/babesia-treatment/

All patients of tick-borne infections need follow-up – years later from treatment.

While the research shows again and again the persistent symptoms of patients, the “powers that be” continue to treat this short-term and seemingly ignore the vast population out here struggling (and it’s far greater than the purported 5-10% of the patient population, I assure you).

The one drug, one disease paradigm also doesn’t work with most patients as we are often coinfected:  https://madisonarealymesupportgroup.com/2017/05/01/co-infection-of-ticks-the-rule-rather-than-the-exception/  This link shows that 45% of tested ticks were coinfected and carried up to 5 different pathogens. This directly translates to human infection and a survey substantiates this: https://madisonarealymesupportgroup.com/2014/11/14/studies-show-why-its-tough-to-treat-lyme-and-co/ The most common co-infections in the LDo study were Babesia (32%), Bartonella (28%), and Ehrlichia (15%) while a study by Dr. Janet Sperling in Canada found that the most common were Bartonella (36%), Babesia (19%), and Anaplasma (13%).

There is also the issue of tick bites igniting latent infections already within the human body such as Epstein Barr, numerous herpes viruses, and even Bartonella. Yet, patients are struggling with these – sometimes all at once.  Is it any wonder we are sicker than dogs?http://www.wildcondor.com/dr-horowitz-on-babesiosis.html Dr. Krause published in the New England Journal of Medicine that when a patient has Lyme and Babesia,Lyme is found three-times more frequently in the blood, proving Babesia suppresses the immune system. https://madisonarealymesupportgroup.com/2017/06/28/concurrent-babesiosis-and-lyme-in-patient/  Besides the fact it is a misnomer to think it novel that a patient has concurrent Lyme and Babesiosis, it is also a huge mistake to base treatment on geographical area as time and time again, entomologists are finding ticks in places they just shouldn’t be and ticks that shouldn’t be carrying pathogens, carrying them. Also, using logic, until every bird, fox, squirrel, lizard, deer, and every other rodent on the earth read the memo that they are not supposed to cross state and country boundaries, ticks are going to continue to defy the box “experts” put them into. And, there are other ways for pathogens to travel across state lines:https://doi.org/10.1111/tid.12741

Abstract
The potential for transmission of Babesia microti by blood transfusion is well recognized. Physicians may be unaware that products used for transfusion may be collected from geographically diverse regions. We describe a liver transplant recipient in South Carolina who likely acquired B. microti infection from a unit of blood collected in Minnesota.  Also, one must be careful of the “history of tick bite,” as well, as many never see the tick or subsequent bite, and fail to get a rash. A nymphal tick is nearly impossible to see. Lyme/MSIDS is a CLINICAL diagnosis.

So much research begging to be done.

 

 

It’s Time to Find the “Alzheimer’s Germ”

https://alzgerm.org/whitepaper

It’s Time to Find the “Alzheimer’s Germ”

Full White Paper

By Leslie C. Norins, M.D., Ph.D.

If a mystery disease is killing 303 people per day, and ¬there’s a chance it’s caused by an infection, aren’t all government germ detectives and labs in full investigative mode, 24/7? Of course—unless it’s Alzheimer’s disease (AD). Which it is.

U.S. deaths in 2015 (most recent year available) were 110,561. That’s 303 dying per day. It’s now the fifth leading cause of death. Cases are up 89 percent since 2000, says the Alzheimer’s Association. There’s no cure or preventive. And Congress says care of Alzheimer’s patients costs $153 billion a year.

 

What the Mystery of the Tick-Borne Meat Allergy Could Reveal

https://www.nytimes.com/2018/07/24/magazine/what-the-mystery-of-the-tick-borne-meat-allergy-could-reveal.html

Feature

His wife wasn’t home, so he drove himself to the university hospital emergency room near where he lived in Chapel Hill, N.C. As he explained his symptoms at the check-in counter, he began to feel faint, then fell to one knee. An orderly offered a wheelchair. He sat down — and promptly lost consciousness.

When he came to, he was on the floor. He had rolled out of the wheelchair and hit his head. A gaggle of worried-looking medical staff stood over him. They asked if he was on drugs. Did he have heart problems? His blood pressure was extremely low, probably the reason he had passed out. Niegelsky, who was 58, told them that he was healthy and drug-free and had no heart condition.

“I could see the concern on their faces in a way that did not help my confidence level at all,” Niegelsky says.

He felt as if insects were biting every inch of his hands, armpits and groin. A doctor asked if he had any food allergies. The hives and the low blood pressure suggested anaphylaxis, a severe allergic reaction. Again the answer was no, but Niegelsky did recall that he had a very bad allergic reaction a month earlier to a tick bite he got at a concert.

The E.R. doctor ordered two shots of epinephrine, a form of adrenaline that dampens the allergic reaction; the hives and itching began to subside about 25 minutes later. Now the doctor asked Niegelsky what he’d eaten that day. A hamburger for lunch, Niegelsky told him. In his recollection, the doctor’s eyes widened, and he said,

“I think we know what you have” — a condition called mammalian-meat allergy.

Meat allergy was first observed in the 1990s and formally described in 2009, which makes it a relatively recent arrival to the compendium of allergic conditions. Its most curious quality may be that it is seemingly triggered by a tick bite. In America, the culprit, called the lone-star tick — females have a distinctive white splotch on their backs — is common in the warm and humid Southeast, where most cases of meat allergy have been diagnosed. Niegelsky had in fact heard about the allergy from friends. He remembers shaking his head and thinking that it sounded “made up.” He understood now, in a visceral way, how real it was. That bite from a month ago had primed his body for today’s hives and plummeting blood pressure.

Until meat allergy was recognized, the prevailing medical wisdom held that an allergic reaction to meat from mammals was extremely unusual. Unlike that from shellfish, say, meat from mammals was thought by some allergists to be too similar to human flesh for the immune system to attack it with the full fury of the allergic arsenal. In this and other respects, meat allergy is upending longstanding assumptions about how allergies work. Its existence suggests that other allergies could be initiated by arthropod bites or unexpected exposures. It also raises the possibility that other symptoms often reported by patients that clinicians might dismiss because they don’t fit into established frameworks — gluten intolerance, for example, or mucus production after drinking milk — could, similarly, be conditions that scientists simply don’t understand yet.
Mammalian-meat allergy “really has the potential to revolutionize our understanding of food allergy, because it doesn’t fall under the umbrella of our paradigm,” Dr. Maya R. Jerath, a professor of medicine at Washington University School of Medicine, in St. Louis, told me. “Maybe our paradigm is wrong.”
The meat-allergy story begins somewhat obliquely, with a new drug for metastatic colon cancer called cetuximab. In 2006, Thomas Platts-Mills, an allergist at the University of Virginia School of Medicine, received a phone call from a colleague. Oncologists testing cetuximab were baffled to find that nearly one in four patients had severe anaphylactic reactions to the drug. A few patients even died. The caller urged Platts-Mills to look into the mystery. He agreed and began by comparing the blood from those who had an allergic response to cetuximab with the blood from those who didn’t. The patients who reacted, he discovered, had allergic antibodies to a complex sugar called galactose-alpha-1,3-galactose, or alpha-gal for short. Most mammals produce alpha-gal; it’s a component of their cell membranes. The exceptions are African and Asian apes and monkeys. As primates of African origin, we do not produce alpha-gal, either. That makes the human immune system unusual: It can learn to see alpha-gal, present in the beef and pork and other mammalian meat we eat, as foreign and threatening, thereby allowing for an allergic response. Cetuximab contained alpha-gal, it turned out; the sugar came from the genetically modified mice used to manufacture the drug.
While Platts-Mills had identified the molecule in the drug causing these severe allergic reactions, he didn’t yet know why those patients were allergic to it. How had their immune systems become sensitized to it? Humans aren’t born allergic to anything; allergy is like a bad habit the immune system needs to learn. Many scientists suspect that our allergic machinery — the swelling of tissues, mucus production, the coughing and sneezing — served an important purpose in our evolutionary past. It probably helped us to fight off parasites. But in allergic disorders, the body unleashes this ancient anti-parasite response inappropriately against molecules that aren’t obviously dangerous (beyond their role in causing a reaction) — against cat dander or pollens or peanuts. The mystery of any allergy is how and why the immune system is first led to make this mistake.
What had primed the patients to be allergic to the alpha-gal sugar? The oncologists did have one clue: They noticed that allergic patients tended to come from the Southeast. Initially Platts-Mills thought that maybe intestinal parasites or even a mold from the region was sensitizing patients to alpha-gal. But a technician in his lab pointed out that the geographical distribution of cases matched the reported distribution of a tick-borne disease called Rocky Mountain spotted fever.
That got Platts-Mills thinking about ticks.
At the same time, he was seeing a growing number of patients in his allergy clinic, many of them hunters and outdoorsy types, complaining about what was apparently a strange reaction to eating meat. They suffered stomach pains and rashes hours later. When Platts-Mills analyzed their blood, he found that, like the cancer patients who had an allergic reaction to cetuximab, they also had allergic antibodies for alpha-gal. And when he and his colleague Scott P. Commins surveyed the patients, they found that more than 80 percent of them reported having had strong reactions to tick bites.
Independent of the research Platts-Mills was doing, in 2007 an Australian allergist named Sheryl van Nunen described 24 cases of meat allergy associated with tick bites. Colleagues were skeptical of her claims, she told me. They didn’t think an allergy to meat from mammals was very likely. And she hadn’t identified what the immune system was specifically attacking, the molecule in meat that was attracting the onslaught. That discovery fell to Platts-Mills, Commins and their colleagues. They posited that alpha-gal was the allergen that made people sick hours after eating hamburgers (or, in Australia, kangaroo steaks). And they proposed tick bites as the trigger. Ticks could explain the two seemingly disparate phenomena: why people who reacted to cetuximab came from the Southeast and why most cases of meat allergy occurred in the same region. The Southeastern lone-star tick was exposing and thus sensitizing people to the sugar through its bites. Some subset of the ectoparasite’s victims would thereafter react to alpha-gal whenever they encountered it, including in meat and cetuximab.
Platts-Mills still lacked definitive proof that a tick bite initiated the allergy. He hadn’t conducted an experiment in which, for example, he deliberately induced meat allergy in human volunteers. But one day in August 2007, he took a hike in the nearby Blue Ridge Mountains. When he got home, he discovered hundreds of larval-stage ticks feeding on his ankles. (He spent the evening removing them with a knife and Scotch tape.) Platts-Mills doesn’t eat red meat often — he had a heart attack in 2005 — but a few months after that hike, on a trip to Europe, he ate two lamb chops and had a glass of red wine.
“Six hours later I was in a hotel, covered in hives, itching like crazy and laughing at myself,” he told me. By then, he thought he knew what was happening: The ticks had made him allergic to those chops.
In 2013, on a hike and a picnic with some friends in the Blue Ridge Mountains, Platts-Mills was again swarmed by larval ticks. By this time he was already monitoring his alpha-gal antibody levels, so he was able to compare how much antibody he had circulating before and after these ticks fed on him. Post-picnic, the allergic antibodies directed at alpha-gal in his bloodstream surged more than tenfold, direct evidence that tick bites had provoked the allergic response to alpha-gal. It seemed he had cracked the case, and others around the world took note. Sheryl van Nunen, now at the University of Sydney, told me this understanding of the precise cause of mammalian-meat allergy makes it unique.
“This is really allergy in a kit — how to get it and how to lose it,” van Nunen said. “There’s really nothing else like it.”
Until meat allergy was recognized, the prevailing medical wisdom held that an allergic reaction to meat from mammals was extremely unusual.  CreditPhoto Illustration by Daan Brand

Mammalian-meat allergy differs from most other food allergies in several important ways. One is the delayed reaction; it’s not uncommon for sufferers to wake up in the middle of the night, hours after a steak dinner, covered with hives and struggling to breathe. By contrast, those with food allergies to peanuts usually develop symptoms within minutes after ingesting the offending food. And whereas in most cases of allergy, the immune system pursues a protein, meat allergy is set off by a sugar.

Another unusual aspect of meat allergy is that it can emerge after a lifetime spent eating meat without problems. In other food allergies, scientists think that children’s immune systems may never learn to tolerate the food in the first place. But in meat allergy, the tick seems to break an already established tolerance, causing the immune system to attack what it previously ignored. One way to understand how the parasite pulls this off is to consider its bite as a kind of inadvertent vaccine. A vaccine teaches an immune system to pursue a pathogen it otherwise wouldn’t by exposing it to weakened versions of that pathogen — an attenuated measles virus, say — or bits and pieces of dead pathogen. Vaccines also often contain a substance called an adjuvant, which is designed to spur the immune system into action.

In similar fashion, when the lone-star tick feeds, alpha-gal leaks from its mouth into the wound, exposing the victim’s immune system to the sugar, prompting the immune system to remember and pursue alpha-gal. But exposure to alpha-gal alone probably doesn’t achieve this feat. Commins, who is at the University of North Carolina, at Chapel Hill, has identified a candidate, an enzyme in the tick’s saliva called dipeptidyl-peptidase that works as an adjuvant. It’s also common in bee and wasp venom. This enzyme, Commins argues, is what tells your immune system to see alpha-gal as the type of threat that warrants the itching and swelling of the allergic response.

Once sensitized, some victims find that they can no longer tolerate beef, pork, lamb — even milk or butter, foodstuffs with only very small amounts of alpha-gal. Several factors can also affect the severity of the allergic reaction, or if there is an allergic reaction at all. Grilled meat is less allergenic than other methods of preparation that preserve more of its fat. Fatty meat leads to more alpha-gal crossing a person’s gut barrier into his or her circulatory system, triggering a stronger immune reaction than leaner cuts. A study of German patients also found that alcohol imbibed with meat can push people toward an allergic reaction, as can exercise; both actions make the gut more permeable, exposing the immune system to more alpha-gal.

As it happens, an immune response to alpha-gal is also what drives, in part, the rejection of tissue transplanted from animals to people.

Scientists have developed genetically modified pigs meant to supply parts that can be grafted onto human bodies without eliciting an anti-alpha-gal immune reaction. Now, as awareness of the meat allergy spreads, there has been talk of using such alpha-gal-free pigs for food — pork chops your doctor can prescribe if you find yourself allergic to meat.

A recent study by scientists at the National Institutes of Health, which included Commins and Platts-Mills as co-authors, linked allergic sensitization to alpha-gal with a greater risk of arterial plaques, a hallmark of heart disease. It’s unclear whether having alpha-gal antibodies specifically increases your risk of developing plaques or whether some other factor increases a person’s risk of heart disease and sensitization to alpha-gal. But if it turns out that meat allergy pushes people toward cardiac arrest, it would imply that encounters with the lone-star tick contribute to the leading cause of death in the United States.

The big, unanswered question is why meat allergy is on the rise today. Commins estimates that at least 5,000 cases have been diagnosed in the United States, and many more probably remain undiagnosed. In some tick-heavy regions, the prevalence of meat allergy is estimated to be at least 1 percent of the population. Ticks are not new. Neither is the human consumption of meat. Why the sudden problem for so many? One possibility is that the ticks have changed somehow.

Maybe they’ve acquired a pathogen we don’t understand yet, and this infection is causing the allergy. Or perhaps, Commins says, changes to the insect’s microbiome, the collection of symbiotic microbes that it carries in its body, have somehow made its bites more allergenic.

The idea is plausible and could nicely explain how an arachnid that has been around for a long time could begin causing a new set of complications. Scientists have long debated where the alpha-gal in the tick originates: Does it come from the blood a tick sucks from other mammals and then regurgitates as it feeds on people, or does it come from the tick itself? Shahid Karim, a vector biologist at the University of Southern Mississippi, in Hattiesburg, told me that the answer might be neither; the sugar probably comes from the microbes that the tick carries within it. So it’s entirely possible, he said, that changes in its microbiome could, by increasing the amount of alpha-gal humans are exposed to in tick bites, make the lone-star tick more likely to induce meat allergy.

What such an account fails to address, however, is why the meat allergy has increased in other parts of the world, like Australia and Europe. (Van Nunen says that in the tick country around Sydney, people are now more likely to carry EpiPens, which contain a shot of adrenaline, for meat allergy than for better-known peanut allergies.) Other tick species are linked with meat allergy in those regions, not the lone-star tick. And it seems very unlikely that the microbiomes of all these ticks on different continents have changed in similar ways at the same time.

“I don’t for the life of me have a unifying hypothesis for why it’s happening everywhere,” Commins told me, although he added that pesticides could be one factor changing tick microbiomes globally.

It may simply be that an increase in the number of ticks has turned a problem once so rare that it went scientifically unnoticed into an observable epidemic.

“I think we’ve got far more tick bites today than people had as recently as 35 years ago,” Platts-Mills told me. He lays the blame for the growing spread of ticks on newly abundant deer.

In Virginia, he thinks new laws requiring dogs to remain on leashes have emboldened deer, which then bring ticks closer to people. People aren’t necessarily venturing deeper into the forests than in the past, he says. More than half the patients he sees with the allergy were bitten on their own lawns.

His leash theory is anecdotal, but it’s certainly true that the current ecological state of Eastern forests is probably encouraging ticks to multiply. After having been cleared in the Colonial era, the forests have partly grown back. Deer and turkey, which the lone-star tick likes to feed on, are abundant again. They thrive in the new-growth forests, now fragmented by roads and suburbs. Large predators are mostly absent. And the rise of tick-borne disease generally has been linked with the decline (or absence) of predators that eat the animals ticks feed on. In Australia, for example, van Nunen points to the eradication of foxes, an introduced species there, as one factor in the increase of ticks and the rise of meat allergy.

We might label this the disturbed ecosystem theory of meat allergy. Forests ecosystems have recovered partially — lots of animal hosts for ticks but not enough predators to keep those hosts in check — and this imbalance has fostered an exponential growth in the number of ticks. In some ways, this is the most probable explanation for the rise of meat allergy. Climate change may be aiding the lone-star tick’s move northward too, Rick Ostfeld, a disease ecologist at the Cary Institute of Ecosystem Studies, told me. Hundreds of cases of meat allergy have been diagnosed on Long Island in recent years, which wasn’t part of the tick’s range in recent history. The tick has been spotted as far north as Maine.

But what’s happening in the American East can’t account for the full extent of the phenomenon elsewhere in the world. In Northern Europe, ticks are proliferating as forests recover and the climate becomes warmer. But in Spain and Southern Europe, the rising incidence of meat allergy has not been accompanied by an increase in tick numbers, according to José de la Fuente, a professor at the Institute of Game and Wildlife Research in Ciudad Real, Spain. For him, the mystery of meat allergy is captured in one question: If a tick bites two genetically similar people, why might only one develop the meat allergy?

Onyinye Iweala, an assistant professor who works with Scott Commins’s lab at the University of North Carolina, echoes this uncertainty. Why are some people sensitized to alpha-gal — meaning they have allergic antibodies directed at the sugar in their blood stream — but never have an allergic reaction to it? This can happen in all allergies. You can have antibodies to, say, cat dander, yet never wheeze or sneeze around cats. Iweala suspects that sensitization to alpha-gal isn’t new. What’s changing is the proportion of people who, after sensitization, proceed to overt allergy. Something else in the environment, she told me, is likely pushing people toward full-blown meat allergy. Perhaps shifts in the microbes that live within us have somehow made us more easily sensitized by tick bite. As a model of how this might work, Iweala points to intriguing research on the interaction between malaria and the human microbiome that centers on alpha-gal.

OUR DISTANT ANCESTORS once made alpha-gal. Understanding why humans don’t could shed light on the meat-allergy mystery. Like other mammals, South American monkeys produce alpha-gal. Only Old World monkeys and apes (and humans) have lost the ability to make the sugar. Hence scientists deduce that the change most likely happened after New and Old World primates diverged from each other around 40 million years ago. One explanation for the disappearance of alpha-gal is that it was driven by some catastrophe, a deadly infection that afflicted Old World primates, perhaps, and as a result maybe these distant relatives of ours stopped being able to produce the sugar because doing so conferred an evolutionary advantage. The mutation that eliminated alpha-gal could have improved a primate’s ability to fight off an infection by enabling its immune system to more easily distinguish between its own body and some pathogen with alpha-gal.

What could this pathogen have been? In the late 2000s, Miguel Soares, a scientist at the Instituto Gulbenkian de Ciência in Oeiras, Portugal, began to suspect the plasmodium parasite that causes malaria. Because the protozoan is so deadly and has historically been so widespread in warmer climes, geneticists often say that malaria has been the single greatest force shaping the human genome in our recent evolutionary history. The parasite remains a leading cause of death in the developing world. And it’s coated in alpha-gal.

Soares and his colleagues investigated a rural Malian population that was naturally exposed to malaria. As it happens, humans produce some antibodies to alpha-gal all the time. They’re not allergic antibodies like those responsible for Lee Niegelsky’s anaphylactic experience, but antimicrobial ones that give rise to a different, less drastic immune response. Between 1 and 5 percent of all the antibodies circulating in any person, a remarkably large quantity, are directed at alpha-gal, Soares estimates. The target of these antibodies is not the alpha-gal in the steak you may have eaten for dinner but the alpha-gal that leaks into circulation from the microbes dwelling in your gut. There are natural variations in the amount of these antibodies any individual produces; some people make more, some less. Soares wanted to know if this variability influenced the villagers’ susceptibility to malaria.

What he discovered may yet change how malaria is combated. Villagers who produced the greatest quantity of alpha-gal antibodies, he found, weren’t immune to infection by the parasite, but they were less likely to be infected after exposure.

What was different about those with more alpha-gal antibodies? They had more gut microbes that produced the sugar, Soares speculated. By priming their immune response against alpha-gal, these individuals’ microbiomes probably helped shield them against malaria. Soares showed as much using mice. Rodents colonized by a strain of E. coli found in the human microbiome that contains alpha-gal produced antibodies to the sugar and were protected from malaria. Rodents that harbored an E. coli strain that didn’t produce the sugar, on the other hand, were not protected. (Other scientists later observed a connection between resistance to malaria and the composition of Malian villagers’ microbiomes.) This research highlights one reason we probably have a few pounds of microbes in us: Friendly microbes can help protect us against unfriendly ones.

Soares is currently working on a vaccine to spur the immune system to attack alpha-gal more actively, thereby conferring greater protection against malaria. His findings also raise the prospect, at least theoretically, of an antimalarial probiotic. In the context of meat allergy, his work underscores the fact that our microbes may affect how we respond to alpha-gal from other sources, including, perhaps, tick bites.

How might this work? You can envision antibodies as arrows that have Velcro on the front instead of arrowheads. Depending on their targets, that Velcro sticks only to a particular substance, like alpha-gal or peanut protein. The back end of the arrow displays a signal that tells the immune system what to do. Allergic antibodies, called immunoglobulin-E, or IgE for short, call for an allergic response. But the antibodies that humans typically have in circulation directed at alpha-gal are antimicrobial antibodies like IgM and IgG, not allergic ones.

A question central to the meat-allergy mystery is how, if we’re always exposed to alpha-gal from our gut microbes, and we’re constantly mounting a nonallergic response against it, the lone-star tick prompts what’s called “class switching,” spurring the immune system to pump out allergic antibodies instead of antimicrobial ones?

The microbes we host may, by stimulating the immune system and guiding its response to alpha-gal, make this class switching more or less likely, Onyinye Iweala told me. But scientists don’t yet know how the relationship works. Perhaps if your microbiota have more species that produce alpha-gal, these microbes stimulate your immune system in a way that protects you from allergic sensitization to the sugar when a tick bites. Or maybe the relationship works the other way around: If you host fewer alpha-gal-producing species and your immune system is less exposed to alpha-gal on a daily basis, that relative lack of stimulation might prevent alpha-gal allergy from developing when you’re bitten by a tick. These interactions can be tested — as Iweala is doing — with mice that, like humans, don’t produce alpha-gal.

What scientists do know is that if you treat a baboon with antibiotics, reducing the amount of alpha-gal-producing microbes in its gut, and thus lessening the stimulation they provide, the quantity of alpha-gal antibodies in its bloodstream also declines. This suggests that altering a primate’s gut microbes may change its immune response to alpha-gal. People living in developed countries, where most cases of meat allergy have been diagnosed, have been doing something very similar to themselves. “We keep changing the microbiome with antibiotics and what we eat,” Iweala says. By tweaking the microbes that live inside us, we may have inadvertently changed how our immune system responds to alpha-gal, making us more vulnerable to tick-induced meat allergy. It’s also possible, however, that the microbes that determine the general tone of our immune function have shifted, altering how we respond to all potential allergens, not just alpha-gal.

Since at least the late 20th century, and probably earlier, we’ve been living in the midst of what’s often called the allergy epidemic, an era that has seen an increase in the prevalence and severity of food allergies generally and, before that, a rise in the prevalence of respiratory allergies and asthma. The forces driving this trend may help account for meat allergy as well. A leading explanation holds that we develop more allergies now because our immune systems have become more sensitive to what they encounter, not because they are exposed to more pollens or allergenic foods than in the past. The reason the modern immune system errs this way, the thinking goes, is that it’s not receiving the right kind of education.

The news media have taken to calling this explanation the “hygiene hypothesis,” which is unfortunate and misleading; personal hygiene has little to do with what’s at issue. More accurate terms coined by researchers include the microbial-deprivation hypothesis, the disappearing-microbiota hypothesis and even the “old friends” hypothesis (the implication being that we’ve lost contact with once-ever-present friendly organisms).

Whatever you call it, the idea is that the rising tide of allergic diseases comes from changes to the type and quantity of microbes we encounter in our environment, particularly in our early life, as well as from changes to the microbes that live on and in us. Improved sanitation, antibiotics and the junk-food-ification of our diet, among other factors, may have shifted our microbial communities, giving us an immune system that’s overly jumpy, unable to reliably distinguish friend from foe and prone to diseases of overreaction, like allergies.

Studies on populations that have bucked the increase in allergies support the idea. Nearly 20 years of research on European children who grow up on farms with animals, for example, indicates that they are less likely to have respiratory allergies, asthma and eczema compared with other children in the same rural areas. The abundant microbial stimulation of the farm environment, scientists have proposed, tunes farming children’s immune system in a way that prevents allergic disease. The cowshed has thus become a stand-in for premodern conditions and the immune system that that environment produces — lightly stimulated but less likely to react to allergens — a model of how the human immune system might have worked in a more microbially enriched past.

So here is the question as it relates to meat allergy: If a lone-star tick bit a Bavarian farm-raised child, would she be less likely to develop an allergy to alpha-gal compared with her nonfarming counterparts? Put another way, if the tick bit someone 150 years ago when the whole world was more like a cowshed, would that person be less or more likely to develop a food allergy than someone from modern-day Chapel Hill?

It’s pure speculation at this point, but gradual, intergenerational changes to our microbes may have altered our immunological tenor, shifting it from cool, calm and collected toward restless and irritable and increasing the odds of developing allergy from a tick bite. Today we may encounter more ticks than in times past, but they may also be interacting with an immune system that’s more sensitive to their bites than ever before. “It’s the ‘perfect storm,’ as you would say in America,” Sheryl van Nunen told me.

For Lee Niegelsky, who had eaten hamburgers his entire life, the allergy forced him to constantly scrutinize his diet. You don’t realize how many foods have meat-derived products in them, he told me — especially in the South, where pork fat and bacon are widely used as flavoring — until you have to avoid meat for fear of passing out. Not long ago, for example, he fell ill after eating clam chowder, which he attributes to meat broth that he suspects was in the soup.

The good news is that, provided you’re not bitten by a tick again, sometimes the meat allergy fades on its own. A year after his visit to the emergency room, under Scott Commin’s supervision, Niegelsky began introducing small amounts of lean meat into his diet. The idea is to test the possibility that his allergic alpha-gal antibodies have subsided to the point that his immune system no longer attacks the sugar. It took Niegelsky about a week to muster the courage to take his first bite of pork tenderloin. He waited anxiously for six hours. When nothing happened, he moved on to steak.

Moises Velasquez-Manoff is a contributing Op-Ed writer for The Times and the author of ‘‘An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.’’ He last wrote for the magazine about carbon farming.

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**Comment**

I find it interesting that no one is mentioning the fact ticks have been tweaked in a lab for biowarfare purposes.  

https://madisonarealymesupportgroup.com/2018/03/07/hantavirus-tularemia-warnings-issued-in-san-diego-county/  Tularemia, brucella, certain Rickettsia’s, numerous viruses, some chlamydia’s, and of course mycoplasma have all been weaponized.  https://madisonarealymesupportgroup.com/2015/08/12/connecting-dots-mycoplasma/

http://www.immed.org/infectious%20disease%20reports/InfectDiseaseReport06.11.09update/PHA_Nicolson_0709_v4.07.pdf

“According to Dr. Nicolson, some of the experiments used Mycoplasma while others utilized various “cocktails of microbial agents” such as Mycoplasma, Brucella, and DNA viruses such as Parvovirus B19. This project later become the topic of a book by Dr. Nicolson entitled Project Day Lily.

Dr. Nicolson believes that Mycoplasma fermentans is a naturally occurring microbe. However, some of the strains that exist today have been weaponized. Dr. Nicolson’s research found unusual genes in M. fermentans incognitus that were consistent with a weaponized form of the organism. Weaponzing of an organism is done in an attempt to make a germ more pathogenic, immunosuppressive, resistant to heat and dryness, and to increase its survival rate such that the germ could be used in various types of weapons. Genes which were part of the HIV‐1 envelope gene were found in these Mycoplasma. This means that the infection may not give someone HIV, but that it may result in some of the debilitating symptoms of the HIV disease.”

Regarding the weaponization of tick pathogens:  https://www.lymedisease.org/lymepolicywonk-questioning-governments-role-lyme-disease-make-conspiracy-theorist/  (Go here to read excerpts of an interview with a biologist who acknowledged doing biowarfare work on ticks and mosquitoes.  He admits every time he has a strange illness his physician says it’s probably a rickettsia – an idiopathic condition that never tests positive but symptoms indicate it.)

‘The interview suggests to me that the reason we have such a large problem with our tick population today may be related to military experiments in the 50s. They were part of a biological warfare effort against the Russians. One goal was to figure out how to get ticks to reproduce quickly and abundantly, as well as how to distribute ticks to targeted areas.”

For a lengthy but informative read on the Lyme-Biowarfare connections:  CitizensAlert_Bob13  (Scroll to page 44 to see an executive summary.  Please notice the names of Steere, Barbour, Shapiro, Klempner, and Wormser, the first four are affiliated with the CDC Epidemic Intelligence Service (EIS).  Wormser, lead author of the fraudulent Lyme treatment guidelines, lectures as an expert on biowarefare agents and treatments).  The author of the pdf believes borrelia (Lyme) has been bioweaponized due to (excerpt from pdf footnote):

226 An article was put out by the Associated Press mentioning the study of Lyme disease at a new biowarfare lab at the University of Texas, San Antonio. The article was quickly retracted and mention of Lyme disease was scrubbed from the article. Here is the text of the original article: “A new research lab for bioterrorism opened Monday at the University of Texas at San Antonio. The $10.6 million Margaret Batts Tobin Laboratory Building will provide a 22,000-square-foot facility to study such diseases as anthrax, tularemia, cholera, lyme disease, desert valley fever and other parasitic and fungal diseases. The Centers for Disease Control and Prevention identified these diseases as potential bioterrorism agents.” MSNBC, 11/21/2005. For a comparison of the censored and uncensored articles, see: http://members.iconn.net/~marlae/lyme/featurearticle02.htm

So you tell me.  Could all this lab tweaking have something to do with tick borne illness and allergies?

Phase II Malaria Meds – 100% Cured – Good for Babesia?

https://www.sciencedaily.com/releases/2018/01/180119090342.htm

Promising malaria medication tested
New combination of drugs proves effective and well-tolerated; further studies planned

January 19, 2018

Universitaet Tübingen

Summary:
An international research team has conducted successful phase II clinical tests of a new anti-malaria medication. The treatment led to a cure in 83 cases.

FULL STORY

Researchers tested the efficacy, tolerability and safety of a combination of the drugs Fosmidomycin and Piperaquine. 

An international research team has conducted successful phase II clinical tests of a new anti-malaria medication. The treatment led to a cure in 83 cases. The new combination of drugs was developed by Professor Peter Kremsner of the Tübingen Institute of Tropical Medicine and the company DMG Deutschen Malaria GmbH. The study was recently published in Clinical Infectious Diseases and is freely accessible.

In the study, the researchers tested the efficacy, tolerability and safety of a combination of the drugs Fosmidomycin and Piperaquine. The twofold medication was administered for three days to patients aged one to thirty who were infected with malaria via the Plasmodium falciparum pathogen. In the 83 evaluable cases, there was a 100% cure rate. Patients tolerated the treatment well, and it led to a swift reduction of clinical symptoms. Safety issues were limited to changes in electrocardiogram readings, as had been described for Piperaquine.

The study was conducted at the Centre de Recherches Médicales de Lambaréné (CERMEL) in the African country of Gabon; CERMEL has close ties with the University of Tübingen. Financial support came from the nonprofit organisation Medicines for Malaria Venture (MMV).

“This study represents a milestone in the clinical research into Fosmidomycin,” says Tübingen Professor of Tropical Medicine Peter Kremsner. The substance was originally extracted from Streptomyces lavendulae and today can be produced synthetically. It blocks a metabolic pathway for the production of Isoprenoid in the malaria pathogen. This makes the malaria pathogen unable to metabolize or reproduce. Because Isoprenoids are formed via a different synthesis path in the human body, humans have no target structures for Fosmidomycin. For this reason humans tolerate the drug well and suffer barely any side effects. In addition, this unique mechanism excludes the possibility of cross-resistance to the drugs used in earlier malaria treatments.

The new combination meets WHO guidelines for combination therapies. The two drugs mechanisms against differing target structures means that they attack the parasite in the bloodstream independently of one another. This meets WHO requirements for a fast and effective treatment of the acute phase of infection, and for protection against relapse due to reappearance of the infection. The researchers say the effective mechanism helps to delay the formation of a possible resistance. Further studies are in planning to optimize dose.

Journal Reference:

Ghyslain Mombo-Ngoma, Jonathan Remppis, Moritz Sievers, Rella Zoleko Manego, Lilian Endamne, Lumeka Kabwende, Luzia Veletzky, The Trong Nguyen, Mirjam Groger, Felix Lötsch, Johannes Mischlinger, Lena Flohr, Johanna Kim, Chiara Cattaneo, David Hutchinson, Stephan Duparc, Moehrle Joerg, Thirumalaisamy P Velavan, Bertrand Lell, Michael Ramharter, Ayola Akim Adegnika, Benjamin Mordmüller, Peter G Kremsner. Efficacy and safety of fosmidomycin-piperaquine as non-artemisinin-based combination therapy for uncomplicated falciparum malaria – A single-arm, age-de-escalation proof of concept study in Gabon. Clinical Infectious Diseases, 2017; DOI: 10.1093/cid/cix1122

https://clinicaltrials.gov/ct2/show/NCT02198807    Evaluation of Fosmidomycin and Piperaquine in the Treatment of Acute Falciparum Malaria (FOSPIP)
Verified June 2015 by Jomaa Pharma GmbH.

Collaborator:
Centre de Recherche Médicale de Lambaréné

Brief Summary:
The objective of this study is to explore the role of fosmidomycin and piperaquine as non-artemisinin-based combination therapy for acute uncomplicated Plasmodium falciparum when administered over three days.
Together, fosmidomycin and piperaquine fulfil the WHO criteria for combination therapy by meeting the three key parameters of having different modes of action and different biochemical targets while exhibiting independent blood schizonticidal activity. Like the artemisinins, fosmidomycin is fast-acting, has an excellent safety record and is active against existing drug-resistant parasites. Piperaquine has a long half life protecting fosmidomycin as a much shorter lived molecule against selection of resistant parasites and will provide post-treatment prophylaxis.

Experimental: Fosmidomycin-Piperaquine
Fosmidomycin sodium capsules 450 mg, dosage: 30mg/kg twice daily for 3 days Piperaquine phosphate tablets 320 mg, dosage: 16 mg/kg once a day for 3 days

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**Comment**

It appears this works for Babesia as well:  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0019334&bw=1  Babesia divergens, a related parasite that also infects human erythrocytes and is also known to induce an increase in membrane permeability, displays a similar susceptibility and uptake behavior with regard to the drug. In contrast, Toxoplasma gondii-infected cells do apparently not take up the compounds, and the drugs are inactive against the liver stages of Plasmodium berghei, a mouse malaria parasite.

The big caveat; however, is that many Lyme/MSIDS patients are persistently infected with Babesia and need far more than 3 days for acute treatment:  https://madisonarealymesupportgroup.com/2016/01/16/babesia-treatment/  Dr. Krause published in the New England Journal of Medicine that when a patient has Lyme and Babesia, Lyme is found three-times more frequently in the blood, proving Babesia suppresses the immune system.

Testing which is poor as these organisms are not often found in high enough numbers in the blood, as well as people present subclinically. In other words, their Lyme case is more severe and they have malarial-type symptoms, but they can’t find Babesia in the blood in a Giemsa stain. It takes a trained eye to identify Babesia, which produces a Maltese Cross form, which may or may not be present in a particular smear. Also, doctors have been taught that besides the day and night sweats and chills, patients are supposed to get hemolytic anemia and their liver functions go up or their platelet count might go down (thrombocytopenia). The fly in the ointment is that only certain strains of Babesia do this. Many strains do not cause these symptoms – but doctors aren’t educated on these finer points. Also, to hide from the immune system, the various species produce offspring that have different exterior proteins, or genotypes. http://www.townsendletter.com/July2015/babesia0715_2.html According to Dr. Schaller, there is immense variation and pre-2015 treatments were “weak and showed ignorance of the power of Babesia – it is vastly harder to kill than malaria.”

 

Artesunate on Short Term Memory in Lyme Borreliosis

http://www.medical-hypotheses.com/article/S0306-9877(17)30288-8/fulltext

Lyme borreliosis is associated with memory deficits. While this may be related to cerebral infection by Borrelia bacteria, it may also be caused by concomitant co-infection by Babesia protozoa. The anti-malarial artemisinin-derivative artesunate has been shown to be effective against a number of Babesia species and to have efficacy against human cerebral malaria. We hypothesised that concomitant administration of artesunate in Lyme borreliosis patients would help alleviate the severity of self-reported short-term memory impairment. This hypothesis was tested in a small pilot study in which patients were treated with both an intravenous antibiotic and oral artesunate (20 mg four times per day); treatment was associated with a reduction in the severity of short-term memory difficulties (P ≃ 0.08). In light of these findings, we recommend that a formal randomised, placebo-controlled study be carried out.

 

For more on Babesia:  https://madisonarealymesupportgroup.com/2016/01/16/babesia-treatment/

More on Lyme:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/

Wolbachia – The Next Frankenstein?

Transmission electron micrograph of Wolachia within an insect cell

Credit:  Public Library of Science/Scott O’Neill

The latest in the effort for world domination over bugs and the diseases they carry is Wolbachia, a Gram-negative bacterium of the family Rickettsiales first found in 1924 and in 60% of all the insects, including some mosquitoes, crustaceans, and nematodes (worms). For those that like numbers, that’s over 1 million species of insects and other invertebrates. It is one of the most infectious bacterial genera on earth and was largely unknown until the 90’s due to its evasion tactics. It’s favorite hosts are filarial nematodes and arthropods.

Wolachia obtains nutrients through symbiotic relationships with its host. In arthropods it affects reproductive abilities by male killing, parthenogenesis, cytoplasmic incompatibility and feminization. However, if Wolbachia is removed from nematodes, the worms become infertile or die. These abilities are what make it so appealing for insect controlcytoplasmic incompatibility, which essentially means it results in sperm and eggs being unable to form viable offering.

http://www.slideserve.com/babu/wolbachia  (Nifty slide show here)

It also makes it appealing for use in human diseases such as elephantiasis and River Blindness caused by filarial nematodes, which are treated with antibiotics (doxycycline) targeting Wolbachia which in turn negatively impacts the worms. Traditional treatment for lymphatic Filariasis is Ivermectin but they also use chemotherapy to disrupt the interactions between Wolbachia and nematodes. This anti-Wolbachia strategy is a game-changer for treating onchocerciasis and lymphatic filariasis.  https://www.sciencedaily.com/releases/2017/03/170316120451.htm

Lyme/MSIDS patients often have nematode involvement.

https://microbewiki.kenyon.edu/index.php/Wolbachiahttps://www.psychologytoday.com/blog/emerging-diseases/200902/tick-menagerie-lyme-isnt-the-only-disease-you-can-get-tick  Both Willy Burgdorfer, the discoverer of the Lyme bacterium, as well as Richard Ostfeld, an animal ecologist found nematode worms in ticks. Since then, some provocative research involving nematodes, Lyme/MSIDS, dementia, and Alzheimer’s has been done.

https://madisonarealymesupportgroup.com/2016/06/03/borrelia-hiding-in-worms-causing-chronic-brain-diseases/https://madisonarealymesupportgroup.com/2016/08/09/dr-paul-duray-research-fellowship-foundation-some-great-research-being-done-on-lyme-disease/https://madisonarealymesupportgroup.com/2016/07/10/greg-lee-excellent-article-on-strategies-for-neurological-lyme/https://madisonarealymesupportgroup.com/2015/10/18/psychiatric-lymemsids/

https://www.scientificamerican.com/article/how-a-tiny-bacterium-called-wolbachia-could-defeat-dengue/  Yet, according to many, Wolbachia is the next eradicator of Dengue Fever and possibly Malaria, chikungunya, and yellow fever because it stops the virus from replicating inside mosquitoes that transmit the diseases. The approach is also believed to have potential for other vector-borne diseases like sleeping sickness transmitted by the tsetse fly.  Evidently, Wolbachia does not infect the Aedes aegypti mosquito naturally, so researchers have been infecting mosquitoes in the lab and releasing them into the wild since 2011. The article states it hopes that the method works and expects infection rates in people to drop and hopes that the mosquitoes will pass the bacterium to their offspring, despite it disappearing after a generation or two of breeding and needing to “condition” the microbes to get them used to living in mosquitoes before injecting them. They also state Wolbachia is

“largely benign for mosquitoes and the environment,” and “To humans, Wolbachia poses no apparent threat.”

Their work has shown that the bacterium resides only within the cells of insects and other arthropods. They also state that tests on spiders and geckos that have eaten Wolbachia mosquitoes are just fine and show no symptoms. An independent risk assessment by the Commonwealth Scientific and Industrial Research Organizatioin (CSIRO), Australia’s national science agency, concluded that,

“Release of Wolbachia mosquitoes would have negligible risk to people and the environment.”

Interestingly, trials are underway in Vietnam, Indonesia, and now Brazil.

They state that scaling up operations to rear enough Wolbachia mosquitoes is too labor-intensive and in Cairns they are going to put Wolbachia mosquito eggs right into the environment. Evidently, other researchers are wanting to release genetically modified (GMO) mosquitoes that carry a lethal gene, and they’ve done it, and it’s causing an uproar:   http://america.aljazeera.com/articles/2013/11/9/genetically-modifiedmosquitoessetoffuproarinfloridakeys.html

http://www.naturalnews.com/2017-07-25-googles-sister-company-releasing-20-million-mosquitoes-infected-with-fertility-destroying-bacteria-depopulation-experiment.html  As of July 14, 2017, Google’s bio-lab, Verily Life Sciences,  started releasing Wolbachia laced mosquitoes in California as part of project, Debug Fresno to reduce the mosquito population.

http://www.greenmedinfo.com/blog/research-exposes-new-health-risks-genetically-modified-mosquitoes-and-salmon  Numerous studies show unexpected insertions and deletions which can translate into possible toxins, allergens, carcinogens, and other changes.  Science can not predict the real-life consequences on global pattens of gene function.

Even the European count decides CRISPR plants are GMOS and should be subjected to the same controls:  https://www.technologyreview.com/the-download/611716/in-blow-to-new-tech-europe-court-decides-crispr-plants-are-gmos/

“It means for all the new inventions … you would need to go through the lengthy approval process of the European Union,” Kai Purnhagen, an expert at Wageningen University in the Netherlands, told Nature.

So, why question the use of Wolbachia as a bio-control?

For Lyme/MSIDS & chronically ill patients, 3 words: worms and inflammation.

Dogs treated for heart worm (D. immitis) have trouble due to the heart worm medication causing Wolbachia to be released into the blood and tissues causing severe Inflammation in pulmonary artery endothelium which may form thrombi and interstitial inflammation. Wolbachia also activates pro inflammatory cytokines. Pets treated with tetracycline a month prior to heart worm treatment will kill some D. immitis as well as suppress worm production. When given after heart worm medication, it may decrease the inflammation from Wolbachia kill off.
http://www.critterology.com/articles/wolbachia-and-their-role-heartworm-disease-and-treatment

The words worms and inflammation should cause every Lyme/MSIDS patient to pause. Many of us are put on expensive anthelmintics like albendazole, ivermectin, Pin X, and praziquantel to get rid of worms and are told to avoid anything causing inflammation due to the fact we have enough of it already. We go on special anti-inflammatory diets and take systemic enzymes and herbs to try and lower inflammation.   https://madisonarealymesupportgroup.com/2016/04/22/systemic-enzymes/

Seems to me, many MSIDS/LYME patients when treated with anthelmintics, will have Wolbachia released into their blood and tissues causing wide spread inflammation, similarly to dogs.

And that’s not all.

According to a study by Penn State, mosquitoes infected with Wolbachia are more likely to become infected with West Nile – which will then be transmitted to humans.

“This is the first study to demonstrate that Wolbachia can enhance a human pathogen in a mosquito, one researcher said.

“The results suggest that caution should be used when releasing Wolbachia-infected mosquitoes into nature to control vector-borne diseases of humans.” “Multiple studies suggest that Wolbachia may enhance some Plasmodium parasites in mosquitoes, thus increasing the frequency of malaria transmission to rodents and birds,” he said.

The study states that caution should be used when releasing Wolbachia-infected mosquitoes into nature. https://www.sciencedaily.com/releases/2014/07/140710141628.htm

So besides very probable wide spread inflammation, and that other diseases may become more prevalent due to Wolbachia laced mosquitoes, studies show Wolbachia enhances Malaria in mosquitos. Lyme/MSIDS patients are often co-infected with Babesia, a malarial-like parasite that requires similar treatment and has been found to make Lyme (borrelia) much worse. It is my contention that the reason many are not getting well is they are not being treated for the numerous co-infections.  Some Lyme/MSIDS patients have Malaria and/or Babesia as well as Lyme.

Regardless of what the CDC states, all the doxycycline in the world is not going to cure this complicated and complex illness.

Lastly, with Brazil’s recent explosion of microcephaly, the introduction of yet another man-made intervention (Wolbachia laced mosquitos) should be considered in evaluating potential causes and cofactors. And while the CDC is bound and determined to blame the benign virus, Zika, there are numerous other factors that few are considering – as well as the synergistic effect of all the variables combined. Microcephaly could very well be a perfect storm of events.
https://madisonarealymesupportgroup.com/2016/12/21/how-zika-got-the-blame/https://madisonarealymesupportgroup.com/2016/03/04/health-policy-recap/https://madisonarealymesupportgroup.com/2016/03/08/fixation-on-zikapolio/

I hate bugs as much as the next person, but careful long-term studies of Wolbachia are required here.

https://www.ncbi.nlm.nih.gov/pubmed/20394659  “Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.

In short, borrelia (as well as numerous pathogens associated with Lyme/MSIDS), is a smart survivor.

While borrelia have been around forever with 300 strains and counting worldwide, epidemics, such as what happened with Lyme Disease in Connecticut are not caused by genetics but by environmental toxins – in this case, bacteria, viruses, funguses, and stuff not even named yet.

Circling back to Wolbachia.

Hopefully it is evident that many man-made interventions have been introduced into the environment causing important health ramifications: Wolbachia laced mosquitoes and eggs, GMO mosquitoes including CRISPR, and in the case of Zika in Brazil, whole-cell pertussis vaccinations (DTap) for pregnant women up to 20 days prior to expected date of birth, a pyriproxyfen based pesticide applied by the State in Brazil on drinking water, as well as aerial sprays of the insect growth regulators Altosid and VectoBac (Aquabac, Teknar, and LarvX, along with 25 other Bti products registered for use in the U.S.) in New York (Brooklyn, Queens, Staten Island, and The Bronx) to combat Zika. “We feel it’s critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR, including single nucleotide mutations and mutations in non-coding regions of the genome … Researchers who aren’t using whole genome sequencing to find off-target effects may be missing potentially important mutations. Even a single nucleotide change can have a huge impact.”  http://articles.mercola.com/sites/articles/archive/2017/06/13/crispr-gene-editing-dangers.aspx?utm_source=dnl&utm_medium=email&utm_content=art3&utm_campaign=20170613Z1_UCM&et_cid=DM147520&et_rid=2042753642

All of this is big, BIG business.

Is the introduction of Wolbachia another puzzle piece in the perfect storm of events causing or exacerbating human health issues?

BTW:  Since 2017, ZAP Males® which are live male mosquitoes infected with the ZAP strain, a particular strain of the Wolbachia bacterium have a time-limited registration allowing them to be sold for five years in the District of Columbia and the following 20 states: California, Connecticut, Delaware, Illinois, Indiana, Kentucky, Massachusetts, Maine, Maryland, Missouri, New Hampshire, New Jersey, Nevada, New York, Ohio, Pennsylvania, Rhode Island, Tennessee, Vermont, and West Virginia.

Infected males mate with females, which then produce offspring that do not survive. (Male mosquitoes do not bite people.) https://www.ncipmc.org/connection/?p=4065

The jury’s still out, but it’s not looking good – particularly for the chronically ill.