posted
I didn't want to take away from Polar's thread so I'm asking here.
Michelle, or anyone...if Babs or other protozoan diseases have an affinity for the brain vasculature it would account for unilateral headaches which I have. So this wouldn't necessarily show up on Ct scans or Mri's (which I had and were neg), right?? The spect scan would be a more appropriate diagnostic test? Also if it harbors in the vasculature...could this account for chronic nasal and sinus congestion? any articles you could cite for me would be appreciated. thank you again.
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CaliforniaLyme
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I can tell you that headaches= Babs big time. Here's some articles*)*)~!
1: Parasitol Today. 1999 Dec;15(12):492-7. Links Comment in: Parasitol Today. 2000 Jun;16(6):264-5. Can Babesia infections be used as a model for cerebral malaria? Schetters TP, Eling WM. Intervet International b.v., Parasitology R&D Department, PO Box 31, 5830 AA Boxmeer, The Netherlands. [email protected]
Infections with certain species of Plasmodium and Babesia induce, among other symptoms, cerebral pathology. The finding of heavily parasitized cerebral capillaries upon postmortem examination has led to the assumption that blockage of capillaries with infected red blood cells caused the cerebral symptoms and subsequent death. As this type of cerebrovascular pathology is found both in humans dying from malaria and in cattle dying from babesiosis, the latter could possibly be used as an animal model for the study of human cerebral malaria. However, before such a model system is adopted, the experimental data concerning cerebral pathology of babesiosis needs critical evaluation. Here, Theo Schetters and Wijnand Eling review the pathological mechanisms in cerebral babesiosis and relate these to cerebral malaria. Finally, they discuss the use of animal model systems for specific aspects of the pathological picture.
PMID: 10557150 [PubMed - indexed for MEDLINE] 1: Mem Inst Oswaldo Cruz. 1992;87 Suppl 3:297-301. Links A study on the pathogenesis of human cerebral malaria and cerebral babesiosis. Aikawa M, Pongponratn E, Tegoshi T, Nakamura K, Nagatake T, Cochrane A, Ozaki LS. Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106.
Cerebral complications are important, but poorly understood pathological features of infections caused by some species of Plasmodium and Babesia. Patients dying from P. falciparum were classified as cerebral or non-cerebral cases according to the cerebral malaria coma scale. Light microscopy revealed that cerebral microvessels of cerebral malaria patients were filled with a mixture of parasitized and unparasitized erythrocytes, with 94% of the vessels showing parasitized red blood cell (PRBC) sequestration. Some degree of PRBC sequestration was also found in non-cerebral malaria patients, but the percentage of microvessels with sequestered PRBC was only 13%. Electron microscopy demonstrated knobs on the membrane of PRBC that formed focal junctions with the capillary endothelium. A number of host cell molecules such as CD36, thrombospondin (TSP) and intercellular adhesion molecule I (ICAM-1) may function as endothelial cell surface receptors for P. falciparum-infected erythrocytes. Affinity labeling of CD36 and TSP to the PRBC surface showed these molecules specifically bind to the knobs. Babesia bovis infected erythrocytes produce projections of the erythrocyte membrane that are similar to knobs. When brain tissue from B. bovis-infected cattle was examined, cerebral capillaries were packed with PRBC. Infected erythrocytes formed focal attachments with cerebral endothelial cells at the site of these knob-like projections. These findings indicate that cerebral pathology caused by B. bovis is similar to human cerebral malaria. A search for cytoadherence proteins in the endothelial cells of cattle may lead to a better understanding of the pathogenesis of cerebral babesiosis.
PMID: 1343706 [PubMed - indexed for MEDLINE]
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CaliforniaLyme
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This is B. bovis the cow Babs, but since malaria has a similar pattern... ***************************** 1: Onderstepoort J Vet Res. 1979 Mar;46(1):41-9. Links An electron microscopic study of intra-erythrocytic stages of Babesia bovis in the brain capillaries of infected splenectomized calves. Potgieter FT, Els HJ. Splenectomized vaccine donor calves undergoing primary reactions to Babesia bovis infections may develop cerebral babesiosis which leads to death if not treated in time. A brain biopsy was performed on an artificially-infected animal showing nervous symptoms and the tissue was immediately processed for electron microscopic examination. Virtually every erythrocyte in the brain capillaries sectioned was infected with B. bovis. Intra-erythrocytic merozoites, trophozoites and dividing trophozoites were indentified. Important features of the piriform merozoites included a reduced apical complex consisting of the anterior polar ring, microtubules, rhoptries and micronemes. Unidentified membrane-bound bodies, mostly spherical in shape, were observed anterior to the nucleus. The trophozoites showed very little structural differentiation and no food vacuoles or micropores could be detected. Each trophozoite produced 2 identical merozoites and the parent cell became totally incorporated in the daughter merozoites in the multiplication process. Projections were seen radiating from the surface of infected erythrocytes which appeared to adhere to other surfaces on contact. This probably resulted in the sludging of infected erythrocytes in the capillaries. The latter observations coincide with those described for Babesia argentina.
PMID: 460822 [PubMed - indexed for MEDLINE]
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CaliforniaLyme
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1: Rev Electroencephalogr Neurophysiol Clin. 1978 Sep;8(3):315-20. Links [E.E.G. recordings during the course of a rare disease: piroplasmosis (author's transl)] [Article in French] Papy JJ, Philip F. Two E.E.G. recordings were made in a patient with human piroplasmosis (babesiosis). They showed signs of vigilance disturbances and generalized abnormalities, together with lateralization in the temporal region, on the right side in the first recording and on the left in the second one. These abnormal E.E.G. findings are reported, even though the clinical signs were not typical of babesiosis, as the biological diagnosis was certain (parasite definitely identified in the red blood cells, severe and progressive parasitic infestation), and it is impossible to evoke other aetiological elements. It is impossible to formulate a valid hypothesis, based on our present knowledge, to explain the mechanisms of this encephalic condition. We can only state the findings without prejudging its direct or indirect nature.
PMID: 571615 [PubMed - indexed for MEDLINE]
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CaliforniaLyme
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There are quite a few peopple on the LYME memorial page who died of anoxic encephalopathy which I really wonder if it was caused by Babs!!! And personally I tend to think that little Jamie Forshcner had cerebral Babs- that is my opinion based on what I have read & seen re pathology- *********************** 1: Lab Invest. 1996 May;74(5):853-9. Links Pathology of acute fatal babesiosis in hamsters experimentally infected with the WA-1 strain of Babesia. Dao AH, Eberhard ML. Department of Pathology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
A strain of Babesia (strain WA-1), recently isolated from a human in Washington State, was found to be unusually virulent for hamsters; it caused acute infection and death in a large proportion of animals 5 to 7 days after inoculation. To assess the basic pathologic lesions associated with this infection, 30 male Syrian hamsters (Mesocricetus auratus) were inoculated intraperitoneally with the WA-1 strain. Twelve animals (40%) died within 5 to 6 days. The other 18 animals, all infected and clinically ill, were killed on the sixth or seventh day for biochemical study. All 12 animals that died from the infection showed high parasitemia, heavy intravascular hemolysis, and pronounced vascular stasis with red-cell sequestration in the spleen, liver, lungs, kidneys, and brain. Serologic study revealed severe anemia (mean hematocrit, 29) with hemolyzed serum and marked elevation of the serum transaminases. The mechanism of death was thought to be diffuse anoxic tissue damage secondary to vascular stasis, which led to multiorgan failure.
PMID: 8642781 [PubMed - indexed for MEDLINE] 1: Onderstepoort J Vet Res. 1976 Jun;43(2):75-8. Links Cerebral babesiosis in a new-born calf. De Vos AJ, Imes GD, Cullen JS. A case of intra-uterine transmission of Babesia bovis is reported. The calf was born normally but showed signs of intravascular haemolysis and nervous involvement 24 h after birth. It died shortly afterwards from cerebral babesiosis. The dam was not clinically affected.
PMID: 1018892 [PubMed - indexed for MEDLINE]
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CaliforniaLyme
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Of course Lyme can cause that too- ************************************ 1: Neuropediatrics. 2005 Apr;36(2):104-7. Links Neuroborreliosis causing focal cerebral arteriopathy in a child. Cox MG, Wolfs TF, Lo TH, Kappelle LJ, Braun KP. Department of Child Neurology, University Medical Center, Utrecht, The Netherlands.
A 9-year-old girl presented with an acute right-sided hemiparesis. Initially, the clinical presentation and stable vasculopathic abnormalities on MR and conventional angiography were suspicious of a so-called "transient cerebral arteriopathy". Mild but persistent pleocytosis and an elevated CSF IgG index led to an extensive search for infectious and immunological causes of cerebral vasculitis, eventually revealing neuroborreliosis. Although rare, infectious and potentially treatable causes of arterial ischemic stroke should be considered in every child with a documented cerebral arteriopathy.
PMID: 15822023 [PubMed - indexed for MEDLINE]
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CaliforniaLyme
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ANd SO can EHRLICHIOSIS!!!!!! But ingeneral I think Babs with headache symptoms- still- it could be any of them which is why it is always important whatever the serology with TBDs to get treated for all the main bugs!! Those are the people I see get better/well- people who are treated for Lyme, Babs , Ehr, Bart and anti-virals regardless of serology- ************************** 1: Curr Treat Options Neurol. 2006 May;8(3):179-84. Links Ehrlichia infection of the central nervous system. Hongo I, Bloch KC. Division of Infectious Diseases, Vanderbilt University School of Medicine, A-2200 Medical Center North, 1161 21st Avenue South, Nashville, TN 37232, USA. [email protected]
Ehrlichiosis in the United States is caused by three closely related bacterial species (Ehrlichia chaffeensis, Ehrlichia ewingii, and Anaplasma phagocytophilum), all transmitted through tick bite. Although there is variation with respect to geography and tick vector, the clinical manifestations are similar, and treatment of these infections is identical. Ehrlichiosis can present with a spectrum of neurologic manifestations, ranging in severity from headache to meningoencephalitis. Treatment is straightforward if the diagnosis is suspected, but antibiotic therapy should not be delayed pending laboratory confirmation. Doxycycline, the treatment of choice for adults and children with suspected ehrlichiosis, has high bioavailability and can be administered orally in most cases. Therapy is typically continued at least 3 days after the last documented fever. Although there have been no studies specifically evaluating duration or dosing of doxycycline for Ehrlichia meningoencephalitis, anecdotal reports suggest 100 mg doxycycline administered twice daily is effective, despite limited penetration into the cerebrospinal fluid. Because doxycycline interacts with CYP3A4 enzymes, there is potential for drug interactions with a number of medications. In endemic areas, documentation of coinfection with Borrelia burgdorferi, the etiologic agent of Lyme disease, may require prolonging the duration of doxycycline therapy.
PMID: 16569376 [PubMed]
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treepatrol
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This is something Iam glad you brought up. I have had headaches ever since intermittent. {{{I had? Which my LLMD and I assume was assuming I had lyme induced encephilitis which this was terribly bad headache severe unrelenting headache lasted for over a month then took 6months to subside to where I actually forgot about it all the while I had to take ibuprophen to bring swelling down,these were so bad it hurt to blink or walk just the foot coming down was like a sledgehammer..}}
Now I wonder if these headaches I get are just from babsiosis? there not bad headaches there more like fluttering by sometimes in front of head sometimes side or the back this is curious to me now??? Because since taking mepron the last 17 days I have only had one.
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posted
thanks for the articles CL. Makes sense but I didnt think of it until I read Michelles comment. what could cause intermittant painful stabbing pain on one side of the head?? It enought to stop you in your tracks. Def. not migraines or normal characteristics of regular type headaches. It's always on the left temporal/frontal lobe too. HHMM...more I think of it, probably is attributed to issues with circulation. Nice thought...
so what tests?? Spect, EEG?
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Michelle M
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Go, California Lyme! Nice compendium of brainy research!
I don't have much to add to that. A lyme patient might get lucky on MRI, ha ha. Mine showed numerous (11) brain lesions, with differential diagnoses of cerebral vasculitis, lyme, MS. This is really not an unusual result for a brain MRI in late lyme disease.
However, I had (unbeknownst to me) not only lyme but babesia WA-1, and the sort of headaches to make a person start drafting a will.
I think you can have a lot of brain involvement with babesia without it showing up on an MRI. The diagnostic tool of choice is a SPECT, done by the right facility.
The study cited below indicates that even though there were five times as many babesia organisms found in the brain as elsewhere, there was no clumping or clustering observed in the brain vasculature.
This study looked at a post-mortem brain and relates to babesia microti, not babesia WA-1, which is a different animal.
Where an MRI has a low yield of positives, a SPECT has a really high yield for people with lyme - don't know the exact numbers but somewhere around 80% of lyme patients have SPECT scans showing areas of hypoperfusion. This won't absolutely nail down that it's from lyme or babesia but in conjunction with tests and symptoms sure makes it more certain. Also, a repeat SPECT after treatment will hopefully look much better.
Michelle --------------------------------------------- Malar J. 2006; 5: 69. Published online 2006 August 4. doi: 10.1186/1475-2875-5-69. Copyright � 2006 Clark et al; licensee BioMed Central Ltd.
Absence of erythrocyte sequestration in a case of babesiosis in a splenectomized human patient
Ian A Clark, et al.
Received March 3, 2006; Accepted August 4, 2006.
Background The importance of vascular occlusion in the pathogenesis of human haemoprotozoal disease is unresolved.
Methods Giemsa-stained tissue sections from a human case of Babesia microti infection in a splenectomized patient with chronic lymphocytic leukaemia and colon cancer were examined to ascertain the distribution of parasitized erythrocytes within the vascular lumen.
Results No evidence of sequestration was observed.
Conclusion This first report on the vascular location of B. microti in human tissue suggests that severe multi-organ failure due to babesiosis is independent of sequestration of parasitized erythrocytes. A similar pathogenesis may also cause multi-organ failure in other intraerythrocytic protozoal infections, including falciparum malaria.
Background
A central issue in the pathogenesis of the disease caused by falciparum malaria is whether vaso-occlusion by sequestered parasitized red cells is the necessary primary event in cerebral malaria and in multi-organ failure. The alternative view is that these changes are set in motion by the toxic effects of excessive release of inflammatory cytokines, with locally enhanced sequestration being a secondary event that sometimes focuses inflammatory mediators and exacerbates local pathology. The topic has recently been extensively reviewed [1,2].
Babesiosis is an emerging haemoprotozoan tick-borne disease often associated with symptoms that are similar to those of falciparum malaria [3,4]. Complications can include altered mental status, adult respiratory distress syndrome, renal insufficiency, disseminated intravascular coagulation (DIC), gastrointestinal bleeding and multi-organ failure [3,4].
The traditional view of these changes, when seen in falciparum malaria, is that they are precipitated by hypoxia secondary to obstructive sequestration [2,5]. Thus, the same constellation of pathologic events in human babesiosis could imply that sequestration also drives the pathophysiology of this disease. There is, however, no information on this crucial question. An answer was, therefore, sought through examining sequestration of Babesia microti-infected erythrocyte sequestration from a limited autopsy of a human fatality in which babesiosis was part of a complex diagnosis.
A sixty-seven year old male with chronic lymphocytic leukaemia and colon cancer, who had undergone splenectomy, experienced a B. microti infection that was confirmed by thin blood smear identification of B. microti DNA by PCR and a four-fold rise in anti-B. microti antibody titre. He received two courses of clindamycin and quinine over a two month period with clearing of parasitaemia each time.
Four months later he was admitted to hospital with fever, tachypnea and confusion. Confusion continued until coma supervened 19 days later. A diagnosis of babesiosis was made by identification of babesia on blood smears (2 to 3% parasitaemia), amplification of babesia DNA by PCR, and detection of anti-babesia antibody in serum.
The patient was treated with clindamycin and quinine, azithromycin and atovaquone and a second round of clindamycin and quinine over the course of three weeks with no improvement in parasitaemia. He developed DIC and became comatose after suffering a cerebellar brain haemorrhage. He expired two days later.
Immediately following death, tissue samples from brain (cortex, basal ganglia, pons, leptomeninges, cerebellum and spinal cord), lung, liver and kidney were collected into 10% formalin. Multiple sections from 3-6 paraffin blocks of each sampled tissue were stained with Giemsa and examined extensively by two independent operators to locate parasites.
In particular, information was sought to determine whether the parasitized erythrocytes were randomly located within the lumen of blood vessels or showed any tendency to attach to vascular endothelium. Sections were searched over several days until about three hundred parasitized erythrocytes were seen. None were close enough to vascular walls to suggest any degree of sequestration. In terms of sightings per unit time, parasites were about five times more commonly observed in the brain vasculature than elsewhere.
The cerebellum haemorrhage site and engorged meningeal vessels provided a much larger number of erythrocytes to peruse, and parasite density within the erythrocyte population in these tissues was equally low as elsewhere. Previously examined sections of B. microti-infected tissue of CBA/Ca mice were reviewed, confirming that even at very high parasite densities there was no tendency for parasitized red cells to sequester in this model.
Another haemoprotozoan parasite, Plasmodium falciparum, sequesters in Aotus sp. [6] as well as in man. Since late P. falciparum trophozoites and schizonts in peripheral smears are extremely rare, erythrocytes containing these stages evidently sequester in deeper vessels, even in mild human infections. Hence erythrocyte sequestration following parasite invasion appears to be a characteristic of the parasite rather than the host species, or the degree of host illness. This implies that the non-sequestration observed in this single splenectomised case of human B. microti infection will prove to be an equally constant feature of this parasite, as it is in mice, and irrespective of parasite density or its degree of contribution to the fatal outcome. Likewise, should the apparent absence of B. microti-infected red cell sequestration in this patient prove to be a general feature of all human babesial infections, a mechanism other than sequestration would be required to explain the multi-organ pathology that may occur during this disease.
Although a case of B. microti infection in a patient with an intact spleen has yet to be examined histologically for parasite location, this parasite is recorded as causing multi-organ pathology in both intact and splenectomized individuals [7,8]. Thus a difference between sequestration in intact and splenectomized hosts, as occurs in P. falciparum-infected Saimiri sciureus [9] (and to an extent in human cases [10]) is not required to infer from our case that non-sequestering B. microti can cause multi-organ pathology in man.
This first report on the vascular location of B. microti in human tissues suggests that severe multi-organ failure due to human infection by this parasite is independent of sequestration of parasitised erythrocytes. As reviewed in reference 1, vital organ sequestration can be vanishingly rare in fatal P. falciparum cases, even though adherence in some tissue is an inevitable characteristic of the later half of the erythrocytic cycle of this infection, irrespective of its contribution to death. Indeed, there is a report of two European adult deaths from fulminant untreated falciparum malaria, without discernible sequestration in the vital organs [11], that might plausibly have been due to systemic inflammatory causes. As reviewed for falciparum malaria [1], complications of human B. microti infection could, therefore, prove to be mediated by the same inflammatory processes as are accepted for bacterial sepsis and severe influenza [12].Posts: 3193 | From Northern California | Registered: Apr 2005
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Michelle M
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quote:Originally posted by Nimzovich76: Is not that Babesia has an affinity for brain vasculature, is that sequestration of the red blood cells in the brain has a greater impact since it diminishes brain flow inducing hipoxia and hence neurological symptoms. Sequestration of red blood cells occur in other organs as well.
Nimzovich, did you not read this part:
"In terms of sightings per unit time, parasites were about five times more commonly observed in the brain vasculature than elsewhere. " Yet you don't think babesia has an affinity for brain vasculature? Huh?
quote:I'll discuss that with my ID guy and get back to you on that.
Good luck with that.
Michelle
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