hi there. i'm zzozzez and i post parasites, either information long text posts i've written from self-study and undergrad work, or just interesting things i run across. if you also love all things parasitic and worm-like, maybe we can chat?
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Oh CDC, how you amuse me. I was looking through the cdc website, studying morphology of certain parasites for my practical tomorrow and then I saw this which funny enough looks a lot like how suspects would line up in front of a white wall with height marks, except instead of people it’s the parasite. And someone stands behind a one wall mirror to see which one he thinks is the killer lol. I’m weird. Anyway, ok back to studying.
Leucochloridium [is] a parasitic worm that invades a snail’s eyestalks, where it pulsates to imitate a caterpillar (in biology circles this is known as aggressive mimicry — an organism pretending to be another to lure prey or get itself eaten). The worm then mind-controls its host out into the open for hungry birds to pluck out its eyes. The worm breeds in the bird’s guts, releasing its eggs in the bird’s feces, which are happily eaten up by another snail to complete the whole bizarre life cycle.
Oh my goodness. There are suddenly quite a lot of you. That happened rather suddenly, so hello.
Here’s some pictures I’ve taken recently, enjoy.
From top to bottom that’s: Schistosoma mansoni, a male and female mated pair, a nurse cell larva complex holding Trichinella spiralis, and a hatching Hymenolepis diminuta egg that looks like Pacman! (I grew that little bugger myself, feed a beetle feces, fed a rat the beetle guts, and dissected it to produce this little beauty.)
Mucocutaneous Leishmaniasis without graphic images.
I just got a massive jump in folks following this blog, so hi! I’m excited to talk parasites with y’all. :D
Mucocutaneous Leishmaniasis caused by one species, L. braziliensis. It is a zoonotic parasite that causes cutaneous lesions. In rare cases, however, (around 2-3%) parasitic infection with this species can result in invasion and erosion of soft tissue in mucocutaneous cavities (oral, genital, nasal, anal). This condition is known as Mucocutaneous Leishmaniasis (MCL), it is rare but devastating.
Above is a picture of a severe mucocutaneous erosion of the nasal cavity, it takes a long time without treatment for the infection to progress to this stage, and the primary concern at this point is: reducing scarring and reconstructing lost tissue, and more importantly, secondary infections. Below is a case that has not progressed as far, if caught this early it can be contained and stopped.
The lifecycle is much the same as in the previous 2 posts, however, to migrate to mucocutaneous tissue an ulcer must have time to develop, and from there early during the infection, amastigotes must be transported to the tissue. Lesions are slow to appear, and can “smolder” for months to years before developing into an obvious lesion. Person to person transmission is incredibly unlikely, but can transfer from reservoir hosts (tropical mammals, dogs, rodents) is possible.
MCL infection of the nose is the most common, and if left untreated (for an incredibly long period of time, I’m talking years here) can spread to the lung tissue and result in death. Parasites are uncommonly found in wound scrapings, but can be detected with PCR. Ulcers will heal over leaving behind some serious scar tissue, and again, the biggest concern when treating this is secondary infections.
The drug of choice is still sodium stibogluconate with all of it’s awful side effects in tow, and in difficult cases where infection persists after initial treatment, Liposomal amphotericin-B can be used. Other possible drugs include: Pentamidine and Allopurinol.
To prevent this parasitic infection similar precautions to avoid many vector based parasites can be used. Interestingly, deforestation for oil exploration, logging, development, and farming has led to increased numbers of cities at the edge of forested regions, and this leads to the mammals (possible reservoir hosts of Leishmania) living closely and perhaps in urbanized areas. Which leads to more exposure to the disease. This is a common issue with many zoonotic diseases.
Avoiding vectors is great advice, but too simple to really make sense as advice for people in endemic areas due to lack of awareness to them and living in such close proximity to them. For those traveling, avoid excursions at night. Due to the effectiveness of reducing malaria infections in Africa by using insecticide soaked clothing and bed netting, similar measures are being used to try and prevent Leishmania infections as well. City development construction teams should attempt to maintain a wide uninhabited zone between the forests and city edges. Prevention and education should be focused on in relief efforts, as vaccines are still in development.
Warning! There are graphic images of infection following! There are pictures of open wounds and lesions. I will repost this without images as well.
Also, I just got a massive jump in folks following this blog, so hi! I’m excited to talk parasites with y’all. :D
Mucocutaneous Leishmaniasis is caused by one species, L. braziliensis. It is a zoonotic parasite that causes cutaneous lesions. In rare cases, however, (around 2-3%) parasitic infection with this species can result in invasion and erosion of soft tissue in mucocutaneous cavities (oral, genital, nasal, anal). This condition is known as Mucocutaneous Leishmaniasis (MCL), it is rare but devastating.
Above is a picture of a severe mucocutaneous erosion of the nasal cavity, it takes a long time without treatment for the infection to progress to this stage, and the primary concern at this point is: reducing scarring and reconstructing lost tissue, and more importantly, secondary infections. Below is a case that has not progressed as far, if caught this early it can be contained and stopped.
The lifecycle is much the same as in the previous 2 posts, however, to migrate to mucocutaneous tissue an ulcer must have time to develop, and from there early during the infection, amastigotes must be transported to the tissue. Lesions are slow to appear, and can “smolder” for months to years before developing into an obvious lesion. Person to person transmission is incredibly unlikely, but can transfer from reservoir hosts (tropical mammals, dogs, rodents) is possible.
MCL infection of the nose is the most common, and if left untreated (for an incredibly long period of time, I’m talking years here) can spread to the lung tissue and result in death. Parasites are uncommonly found in wound scrapings, but can be detected with PCR. Ulcers will heal over leaving behind some serious scar tissue, and again, the biggest concern when treating this is secondary infections.
The drug of choice is still sodium stibogluconate with all of it’s awful side effects in tow, and in difficult cases where infection persists after initial treatment, Liposomal amphotericin-B can be used. Other possible drugs include: Pentamidine and Allopurinol.
To prevent this parasitic infection similar precautions to avoid many vector based parasites can be used. Interestingly, deforestation for oil exploration, logging, development, and farming has led to increased numbers of cities at the edge of forested regions, and this leads to the mammals (possible reservoir hosts of Leishmania) living closely and perhaps in urbanized areas. Which leads to more exposure to the disease. This is a common issue with many zoonotic diseases.
Avoiding vectors is great advice, but too simple to really make sense as advice for people in endemic areas due to lack of awareness to them and living in such close proximity to them. For those traveling, avoid excursions at night. Due to the effectiveness of reducing malaria infections in Africa by using insecticide soaked clothing and bed netting, similar measures are being used to try and prevent Leishmania infections as well. City development construction teams should attempt to maintain a wide uninhabited zone between the forests and city edges. Prevention and education should be focused on in relief efforts, as vaccines are still in development.
Cutaneous Leishmaniasis (CL) is caused by four species of Leishmania, but we’re only going to cover three of the most common ones.
- L. major
- L. tropica
- L. mexicana
Several million people suffer from CL every year, and is difficult to eradicate due to having two reservoir hosts: wild dogs and rodents. It is however the easiest to treat when caught early on. In the Middle East doctors discovered inoculation with scrapings from an open lesion could result in permanent immunity to further infections, if you have carried these parasites once they will not infect you twice.
We’ve already gone over the basic lifecycle in the previous post, so I won’t repeat myself. The special result in CL is the development of an open lesion at the site of infection after amastigotes invade macrophages.
Above are examples of a recent infection and a healing one. They can develop into ulcers if not treated. The infection is first noticed by a red papule at the bite site 2-8 weeks after the bite, and progresses to a painless 1cm nodule, before finally ulcerating and depressing the skin as seen above. After the wound heals over and scars, permanent immunity against other CL infections is achieved, this is after treatment! Should not progress this far, and should be treated if lesion develops! Live specimens of amastigotes will only be found at the edges of wounds. CL can cause a wide spectrum of lesion producing diseases, and open wounds should be covered and monitored for secondary infections.
CL should always be expected in soldiers after returning home and travelers to endemic areas, endemic areas include: Saudi Arabia, Kenya, Ethiopia.
Diagnosis depends on PCR exclusively as it can otherwise be confused with other lesion producing diseases. For quicker diagnosis, examination of scrapings from lesions can also be useful, as PCR is slow.
A picture of a few histological stains of amastigotes inside macropahges is above.
Treatment can be kind of rough as the drug of choice is sodium stibogluconate which has serious side effects including: rashes, headaches, pancreatitis, joint pain, muscle pain, and liver damage. Cure rates average out at 85%-95%, 100% cure rate results from retreatment. Ketoconazole is an anti-fungal medication and is effective but not as good as sodium stibogluconate. A drug called fluconazole is showing promising results right now as well!
As transmission from person to person cannot occur, prevention is possible. Dogs can be fitted with pyrethoid-covered collars, and sleeping under insecticide covered bed netting are good measures. Limiting outside activity early in the day and late at night, when sand flies are most active, is another good preventative measure. A vaccine may also soon be available!
Warning! There are graphic images of infection following! There are pictures of open wounds and lesions. I will repost this without images if anyone wants to see that.
Cutaneous Leishmaniasis (CL) is caused by four species of Leishmania, but we’re only going to cover three of the most common ones.
- L. major
- L. tropica
- L. mexicana
Several million people suffer from CL every year, and is difficult to eradicate due to having two reservoir hosts: wild dogs and rodents. It is however the easiest to treat when caught early on. In the Middle East doctors discovered inoculation with scrapings from an open lesion could result in permanent immunity to further infections, if you have carried these parasites once they will not infect you twice.
We’ve already gone over the basic lifecycle in the previous post, so I won’t repeat myself. The special result in CL is the development of an open lesion at the site of infection after amastigotes invade macrophages.
Above are examples of a recent infection, a healing/scarred one, and a healing ulcerated case known as “Jericho Buttons”. Lesions can develop into ulcers if not treated. The infection is first noticed by a red papule at the bite site 2-8 weeks after the bite, and progresses to a painless 1cm nodule, before finally ulcerating and depressing the skin as seen above. After the wound heals over and scars, permanent immunity against other CL infections is achieved, this is after treatment! Should not progress this far, and should be treated if lesion develops! Live sspecimens of amastigotes will only be found at the edges of wounds. CL can cause a wide spectrum of lesion producing diseases, and open wounds should be covered and monitored for secondary infections.
CL should always be expected in soldiers after returning home and travelers to endemic areas, endemic areas include: Saudi Arabia, Kenya, Ethiopia.
Diagnosis depends on PCR exclusively as it can otherwise be confused with other lesion producing diseases. For quicker diagnosis, examination of scrapings from lesions can also be useful, as PCR is slow.
A picture of histological stain of amastigotes invading macrophages is above.
Treatment can be kind of rough as the drug of choice is sodium stibogluconate which has serious side effects including: rashes, headaches, pancreatitis, joint pain, muscle pain, and liver damage. Cure rates average out at 85%-95%, 100% cure rate results from retreatment. Ketoconazole is an anti-fungal medication and is effective but not as good as sodium stibogluconate. A drug called fluconazole is showing promising results right now as well!
As transmission from person to person cannot occur, prevention is possible. Dogs can be fitted with pyrethoid-covered collars, and sleeping under insecticide covered bed netting are good measures. Limiting outside activity early in the day and late at night, when sand flies are most active, is another good preventative measure. A vaccine may also soon be available!
Pictures from: [x] [x] [x] [x]
Info from here: [x]
The next group I want to look at has several specific and unique species, so I will separate it into a few posts. The genus Leishmania comprises a wide variety of species of vector-borne haemoflagelated (flagellated parasites in the blood) parasites. They’re transmitted by their vector, the sand fly, and are found all throughout the western hemisphere.
They’re primarily, though not always, zoonotic, and able to infect a diverse group of vertebrates. All species live as obligate intracellular parasites inside of macrophages!
As your immune system attempts to defend itself by recruiting macrophages to the site of the bite, the parasites work their way inside the cells on purpose, and use them as taxis to travel about inside you. (A gross oversimplification, but you get my drift.) They also all share a structure called a kinetoplast (a network of circular, like in bacterial plasmids, inside a large mitochondrion [the powerhouse of the cell :P] that contain many copies of the mitochondrial genome.)
Beyond that the species vary widely in mode of transmission, biochemistry, immunobiology, etc.
The clinical conditions vary greatly as well, though they’re classified in three forms: cutaneous (easily contained, not so scary), much-cutaneous (oh goodness gracious only google pictures if you are not faint of heart and stomach), and visceral (the most terrifying.)
There are no available vaccines yet, but infection with one species will result in permanent immunity to that species should the host survive. The human genome project is helping make progress in discovering a vaccine!
Back life cycle!
It all starts with a bite from a sand fly, the fly carries the promastigotes (sort of a larval baby parasite form) in its salivary glands, and when it bites it releases this fluid, as well as the parasites within, to slow blood clotting so it can feast. Macrophages are recruited by the body as an immediate (innate) immune response, they gobble up intruders usually and tell the body what it’s up against and if it’s ever faced it before. The promastigotes, however, know what’s up, and worm their way inside on purpose! The process by which this is done took me a week of immunology research to understand, so if you’re interested, message me and I am perfectly willing to try and explain! From there they divide into hundreds of amastigotes, they pop the cell they’re inside and move throughout the bloodstream. Where eventually they get picked up by a sandfly again, and transform back into promastigotes in the flies gut. And the cycle begins anew.
Most of what we know about this terrifying protozoa is derived from mouse models and the after effects of infected people, so we still have a ways to go.
From here the species diverge!
Lifecycle image from the CDC.
Will add my pictures later.
Info from here: [x]
Schistosoma, or blood flukes, are probably one of my favorite parasitic worms. I read about them first in a book called Parasite Rex by science writer Carl Zimmer.
Blood flukes are so many shades of adorable that it's ridiculous they are also remarkably long living. A blood fluke begins it’s life as a free-swimming larvae in a pond or stream. These flukes then seek out an intermediate host, a snail, and in this snail they feed and produce thousands of tiny flukes. These little flukes head back to the water in search of human skin. When they find their prize they drill inside making their way to the circulatory system and traveling to wither the small intestine or behind the bladder. Unlike most trematodes they grow up to be male or female and have to reproduce sexually. The female flukes are thin and long, the males are canoe shaped with a sucker on their head to assist in movement. When two flukes meet, the female will curl up into the grove of the male and they’ll stay like that indefinitely, the male feeding the female blood, and the female producing eggs which are evacuated from the host in feces or urine.
Blood fluke couples were known to be monogamous staying together for up to 40 years in some cases. They were also unique in that if 2 males blood flukes happened to find one another, they would also mate up, with one male curling up inside the other. Obviously no eggs are produced in this situation, which is good for the host as egg production is what can make a host sick. (If the eggs wind up in you liver it can cause schistisomiasis.) Blood fluke couple, whether 2 males or a male and female would very quickly regroup and rejoin if forcibly separated.
Adorable right? Unfortunately this fluke-ridden fairy tale has been spoiled by reports from researchers at Cambridge and the University of Perpignan. They found that if presented with a large variety of males, females will leave their partners in search of a more genetically dissimilar partner.
Even microscopic flatworms experience troubles of the heart apparently. Luckily for the fairytale joining of these lovesick flukes, a host is not usually infected with enough males suitors for infidelity to become an issue, and these happy couples can spoon and bleed their host together, until proper diagnosis and care do they part.
