Babesia microti Treatments

             In a previous post I discussed the importance of studying Babesia microti.  One of the reasons is that it has the same vector, Ixodid ticks, as the parasite Borrelia burgdorferi, which causes Lyme disease.  Ten percent of patients, in the United States, infected with Borrelia burgdorferi are also co-infected with Babesia microti (Shoemaker et al., 2006).  The number of individuals with co-infections is still on the rise.  The double infection of the two parasites can cause more severe and persistent symptoms.  Patients with co-infections showed resistance to the drugs Azithromycin and Atovaquone, which are normally used to treat these parasitic infections (Shoemaker et al., 2006).  Other problems with the previous drugs of choice were that it did not relieve post Lyme disease syndrome (PLS) symptoms.  PLS is a set of symptoms that arise after Lyme disease has been treated.  It is most likely due to a neurotoxin released by the parasite B. burgdorferi.  It is believed that Babesia microti may also release a similar neurotoxin (Shoemaker et al., 2006).                                   

            An experiment was preformed in order to find the most effective drug for treating co-infections of B. microti and B. burgdorferi.  The results showed that a treatment of atovaquone  plus cholestyramine over a 9-week period is necessary to relieve the symptoms of both infections (Shoemaker et al., 2006).  The drug cholestyramine was also effective in relieving PLS symptoms in majority of the patients.  This is most likely due to the ability of cholestyramine to bind to the neurotoxins secreted by B. burgdorferi.  Once cholestyramine binds to the neurotoxin it can be excreted through the feces.  The reason previous drugs were less effective at relieving PSD symptoms is because although they would kill the parasites B. microti and B. burgdorferi they would leave the neurotoxins in the host’s blood stream (Shoemaker et al., 2006).  

            The reason I chose this article was because in my previous article I discussed methods of detecting Babesia microti.   I wanted to write a post about treatments for those who have been infected with the disease.  In my first blog post I also talked about how individuals can often be infected by Babesia microti and Borrelia burgdorferi at the same time.  This article discussed effective methods of individuals who have been co-infected with both parasites.  Since there has been an increase in the number of cases were the two parasites are being transmitted together, it is beneficial to have a drug that responds to both. 

References

Shoemaker, R.C., Hudnell, K.H., House, D.D., Kempen, A.D., Pakes, G.E. 2006.      Atovaquone    

          Plus Cholestrymine in Patients Coinfected With Babesia microti and Borrelia burgdorferi       

          Refractory to Other Treatment. Advances in Therapy.23 (1):1-11

Echidnophaga gallinacea is beginning to Threaten Wild Avian Hosts

            Echidnophaga gallinace, a generalist ectoparasite commonly known as the sticktight flea, was observed on a wild avian scrub-jay species, Aphelocoma coerulescens.  E. gallinacea are a common pest of poultry but are rarely seen on any free-living avian species.  Normally, E. gallinacea can cause ulcerations on any soft body parts and cause deadly infections from subcutaneously laying eggs on their hosts.  E. gallinaceas can live on their host for up to 19 days and use their host to supply them a blood meal.  While living on a host, E. gallinaceas lay their eggs, and eventually fall off onto soil ground.  Larvae develop in the soil for several weeks until they mature into adulthood.  Once larvae reach adulthood, a blood meal is necessary for them to reproduce.  The fleas search for a suitable host in areas of domesticated poultry. The effect E. gallinacea has on wild species is still largely unexplored.  However, a group of Florida avian species, A.coerulescens, has recently been reported as hosts for E. gallinacea. 

            In south central Florida, a study found that when scrub jays were sampled before the breeding season, 73% were infested with Echidnophaga gallinacea sticktight fleas with infestation numbers ranging from 1-57.  After four months, 46% of the sticktight flea-infested jays had died.  This number was relatively high compared to a death rate of only 5.9% for the non-infested jays.  E. gallinaceas infested scrub jays also showed signs of lower body mass, low hematocrit levels and high leukocyte counts when compared to non-infested scrub jays. Sticktight fleas are detrimental to Florida scrub-jays in terms of health and survival.  These ectoparasites can have profound effects on the survival of free-living avian species.  If this parasite is capable of having dire effects for one avian host like Aphelocoma coerulescens than it may have the ability to show its negative impacts on a plethora of other avian wildlife species. 

_{Boughton, R. K., J. W. Atwell, and S. J. Schoech. "An Introduced Generalist Parasite, The Sticktight Flea and Its Pathology in the Threatened Florida Scrub-Jay." Journal of Parasitology 92.5 (2006): 941-48.}

Leishmania and Sand Fly Saliva

In this study, Theodos et. al. (1991) looked at the effect of sand fly saliva on the effectiveness of Leishmania infections.  Researchers focused on the sand fly vectors Lutzomiya longipalpis and Phlebotomus papatasi and two species of Leishmania, Leishmania major and Leishmania Mexicana amazonensis.  Researchers suggest that the sand fly saliva contains calcitonin gene-related peptidss, or CGRP, which prevents the production of H₂0₂ by host macrophages.  They also suggest that the saliva could be preventing the macrophages from presenting antigens against Leishmania.

 In the first part of this study researchers tested the affect of the saliva on five different mice strains, one susceptible mouse strain, one mouse that is intermediately susceptible, and three strains that are genetically resistant.  The mice were injected with either L. major or with L. major and lysate of ½ of a salivary gland of L. longipalpis.  The disease was most pronounced in two of the resistant strains, which were then used for the other tests.  When the mice were injected with 1/10 of a salivary gland the lesion was significantly larger than the control.  Researchers then tested the effect of the saliva on L. Mexicana amazonensis and the results showed once again an increased infection in two of the mice strains.  The effect of P. papatasi saliva was also tested and showed similar results to the saliva from L. longipalpis.  The final part to this study tested whether or not the sand fly vectors introduces material that enhances infection when they are probing the skin while they are looking for blood.  The mice were anesthetized and shaved at their posterior end and were exposed to the bites of L. longipalpis.  The mice were then injected with L. major in the area they were bitten.  The results showed that the lesions developed quicker and the infection was more severe then in the mice that were not bitten by the sand fly.

I thought this was a very interesting article because it touches on something that I discussed in my first article about possibly finding a better cure for espundia caused by Leishmania braziliensis.  The article by Theodos et. al. (1991) suggests that it may be possible to vaccinate people against leishmaniasis by creating a vaccine against whatever is in the saliva that supports the survival of the parasite.  This would rid the need of using antimony compounds to try and kill off the parasite.  It would be interesting to see if the saliva is necessary for other strains of the parasite to survive.  It would also be interesting to know whether this occurs with other parasites and vectors, where a specific vector in some way enhances the survival and course of infection of a given parasite.  It’s hard to believe that something as simple as saliva can have such a large effect on the survival of this parasite.

Theodos, C. M., J. M. C. Ribeiro, and R. G. Titus.  1991.  Analysis of Enhancing Effect of Sand Fly Saliva on Leishmania Infection in Mice.  Infection and Immunity.  59(5):  1592-1598.            

Coccidiosis: Diagnosis and Precautions

Coccidiosis causes diarrhea in young or immune-compromised dogs.  In a study by Mitchell et. al (2007), 8 six to eight-week-old beagles were used to determine the role of I. canis in pathogenicity of diarrhea observed in infected dogs to rule out other causes, such as bacteria or viruses.  The puppies were infected orally with sporulated Isospora canis oocysts that had been extracted from the feces of two pitbull puppies.  The inoculum given was first treated with a bleach mixture to kill any bacteria before being exposed to the dogs.  Oocysts were mixed with Hill’s Science Diet dog food and fed to the experimental beagles. 
Fecal samples were examined by centrifugal flotation in Sheathers’ sugar solution the day before infection, day of infection, and days 1-29 post-infection.  When a dog first became positive in the study, quantitative oocyst counts were taken from the feces.  Upon becoming apparent, clinical signs of infected dogs were recorded daily and fecal samples were given a score of 1 to 4; 1 being normal and 4 being completely liquid.  It was also noted if blood or mucous was seen.  During the course of the study, five dogs were treated with 25mg/kg sulfadimethoxine, an anticoccidial drug, for two to three days due to severe diarrhea.

            Two dogs showing clinical signs of coccidiosis were necropsied ten days after the onset of infection.  Developmental stages of I. canis were detected in cells of the mucous membranes lining the small intestine in both dogs.  Microscopic lesions were observed due to swelling of the villi that line the small intestine (villous atrophy), expansion of lacteals (lymphatic capillary that absorbs dietary fats in the villi of the small intestine), and hyperplasia (enlargement) of lymph nodes (Montague, Watson & Herbert, 2005).  Bacterial and viral examinations were negative, proving that intestinal coccidiosis was the cause diarrhea.  All stages of the lifecycle of I. canis were present in the small intestine of these dogs.  Immunohistochemistry was done to determine whether developmental stages of I. canis contained cross-reactive antigens to similar parasites.  Developmental stages of I. canis did not react with antibodies of other parasites. 

            Results of the overall experiment demonstrated that clinical coccidiosis was induced in all dogs that had been infected.  Fecal scores of 3 or 4 were usually recorded, indicating severe diarrhea, and were usually seen two to three days before oocysts were passed with stool.  Clinical signs were consistent and included watery or bloody diarrhea, anorexia, weight loss, vomiting, and lethargy.  Increased rectal temperatures were also noted in most dogs.  All dogs excreted I. canis oocysts.  On average, infected dogs began releasing oocysts in their stool 9.8 days after infection by I. canis.  The time period in which the dogs released oocysts lasted on average 8.9 days.

To help prevent the spread of coccidiosis in kennels and catteries, it is important to use appropriate sanitation practices.  Because oocysts sporulate (asexually reproduce and release spores) immediately once in the environment and can survive for months, daily removal of feces can aid in preventing transmission of coccidiosis (Princeton University, n.d.).  After oocysts become infective, they are resistant to most commonly used disinfectants (CAPC, n.d.).  You should also regularly remove your dog’s and cat’s feces from your own yard to keep the yard free of potentially infectious feces or reinfection by ingestion of coccidia.  Predation should be discouraged to prevent infection caused by paratenic hosts (those that are not needed for the development of the parasite but aid in maintaining the lifecycle of the parasite (Roberts & Janovy Jr., 2005)).

Now that you know all about coccidiosis, especially isosporiasis, you can keep a closer watch on your pets, Kit Kat and Beau, for signs of infection.  As a precaution, you should bring a stool sample from your pet with you to his/her yearly appointment to have it checked for coccidia and other intestinal parasites.  As long as you are aware, you cannot stop your pets from becoming infected but you can try to avoid it, as well as get them treatment if needed to combat the infection early on before isosporiasis has a chance to cause major problems.

References

Companion Animal Parasite Council (CAPC). (n.d.). Current advice on parasite control: Intestinal parasites - coccidia. Retrieved from http://www.capcvet.org/capc-recommendations/coccidia/

Mitchell, S. M. et. al. (2007). Cystoisospora canis nemeseri, 1959 (syn. isospora canis), infections in dogs: Clinical signs, pathogenesis, and reproducible clinical disease in beagle dogs fed oocysts. Journal of Parasitology, 93(2), 345-352. Retrieved from http://0-ehis.ebscohost.com.www.consuls.org/ehost/pdfviewer/pdfviewer?vid=14&hid=2 3&sid=c1bb8c4a-33f9-401f-a4f3-67f863bef1c3@sessionmgr13

Montague, S. E., Watson, R., & Herbert, R. (2005). Physiology for nursing practice. (3 ed., p. 494). Elsevier. Retrieved from http://books.google.com/books?id=nddqAAAAMAAJ&dq=lacteal+chyle&q=lacteal+

Princeton University. (n.d.). Wordnet search - 3.1. Retrieved from http://wordnetweb.princeton.edu/perl/webwn?s=sporulation

Roberts, L. S., & Janovy Jr., J. (2005). Foundations of parasitology. (7th ed., p. 4). New York, NY: The McGraw-Hill Companies, Inc.

We're Not Fatal!

For our final installment we will review the work of Jamonneau et. al., (2012). Possibly, this is the most pertinent discovery of species of Trypanosoma we have come across thus far. As the title of this article implies, and as the authors have reviewed, it was previously assumed that if Human African Trypanosomiasis (HAT) was left untreated, it would result in 100% fatality. The authors attribute this previously assumed fatality rate to a few pieces of information which researchers have acquired in the past: sleeping sickness can have either chronic or more severe neurological symptoms, and the approximate one million deaths that the disease has already caused during three epidemic outbreaks on the African Continent. 

Previous reports of possible asymptomatic disease carriers and independent disease cures lead the researches to gather information through a longitudinal study on 50 patients who had been confirmed to be infected with Trypanosoma brucei gambiense in the past 5-15 years and either received treatment or refused treatment. Serological tests as well as parasite microscopy was used in order to detect the presence of parasites in individuals who had either been treated or refused treatment.  

Results showed that there were no neurological symptoms exhibited in any patients characteristic to the more severe second stage of infection, however 58% of patients who had been treated and 68% of patients who had not been treated exhibited symptoms such as headaches and fever which cannot be attributed to trypanosomiasis. 

Overall, the study provided information that supported the hypothesis that HAT was not 100% fatal when it was left untreated. Parasitological and serological tests supported the claim that self-cure can and did occur in some patients, while the same tests also argue that other patients can be asymptomatic carries of HAT but can control the disease at very low levels of parasitemia. Jomonneau et al., note however that chronically and experimentally infected pigs and cattle may possess undetectable levels of T. b. gambiense in the blood, but may still be able to infect the tsetse fly vectors and therefore humans may also present similar issues.  

All in all, the information presented is extremely valuable as it shows that the disease is not as fatal as it was previously thought. It may also even be possible for medical researchers to identify immune system defense mechanisms (Jamonneau et. al., 2012)! 

Jamonneau, V., H. Ilboudo, J. Kabore, D. Kaba, M. Koffi, P. Solano, A. Garcia, D. Courtin, C. Lavissiere, K. Lingue, P. Buscher, B. Bucheton. 2012. Untreated human infections by Trypanosoma brucei gambiense are not 100% fatal. PLOS Neglected Tropical Diseases. 6(6): pp. 1-8.

Passing the Parasite: Transmission from Painted Turtles to Snapping Turtles

            Siddall et al. (2001) conducted this experiment of transferring Haemogregarina balli from painted turtles, Chrysemys picta marginata, to snapping turtles, Chelydra serpentina, via the leech Placobdella ornata. Eleven painted turtles were collected from the Algonquin Park in Ontario, and six of them were determined to have hemogregarine in their peripheral circulation. Siddall et al. (2001) had hatchling leeches feed on the most heavily infected painted turtle and later had the leeches feed on two snapping turtles. The snapping turtles were uninfected before the leeches fed on them, and consequent blood films were taken periodically to determine when the hemogregarine would appear in the blood smears. The first hemogregarine merozoites were in the peripheral blood of the snapping turtles four months after they were infected by the leeches (Siddall et al., 2001).

            The ability of Haemogregarina to infect multiple vertebrates had never been tested before this experiment, although it has been known for a long time that hemogregarines can cross-infect a wide range of hosts (Siddall et al., 2001).  The authors determined that both parasite isolates from each separate species are likely to be H. balli as they are morphologically indistinguishable, not to mention that they personally passed the same H. balli amongst the turtles. However, that often isn’t the case and scientists may make the assumption that a speices of parasite is completely new because it is in a host that it has never been found in before. Many parasites have several species that they can utilize as intermediate or primary hosts, and that hasn’t always been discovered. The authors also mention that if there are no morphological differences between species of hemogregarines of turtle then they should be simply grouped under the oldest name that they are known by.

            Siddall et al. (2001) touch upon a very interesting point that has been mentioned before. Sometimes scientists make mistakes, or they categorize something inaccurately and it is important to keep that in consideration as taxonomic knowledge and species classification grows and develops. If two species of hemogregarine are essentially the same then they should be condensed under a single classification for greater simplicity and accureacy. However, I would want a genetic comparison between found parasites rather than basing species on morphological characteristics. Tkach et al. (2012) mentioned in their article about a new species of Trematode in the gall bladder of turtles. There was a species that was recorded to have the same unique morphological characteristic (the posteriorly extending cirrus sac beyond the ventral sucker). It was described so poorly that Tkach et al. (2012) had to base their decision on small morphological clues that identified their species as a newly discovered species. In both cases, it is important to recognize the significance of an analytical mind when discovering and identifying species of parasites.

Works Cited:

Siddall, M.E., and S.S. Desser. 2001. Transmission of Haemogregarina balli From Painted Turtles to Snapping Turtles Through the Leech Placobdella ornata. The Journal of Parasitology 87(5): 1217 – 1218.

Tkach, V.V., T.R., Platt and S.E. Greiman. 2012. A New Species of Opisthioglyphe (Trematoda: Telorchiidae) from Gall Bladder of Turtles in Malaysia. The Journal of Parasitology 98 (4): 863 – 868.