A Woman Had 14 Worms in Her Eye And Doctors Didn’t Even Know It Was Possible


This species doesn’t usually attack humans.

A parasitic eye worm called Thelazia gulosa is pretty common in the northern US and southern Canada – at least in cows.

Now, for the first time, it’s been observed jumping over to humans, infecting the eye of an Oregon woman.

The 26-year old patient reported feeling an irritation in her left eye, before removing the first worm eight days later.

Over a 20-day period, 14 worms less than 13 millimetres (half an inch) in length had to be removed from her conjunctiva and the surface of her eyeball.

Typically, the eye worms are spread between cattle by flies that feed on the fluid that lubricates the eyeball.

“Cases of eye worm parasitic infections are rare in the USA, and this case turned out to be a species of the Thelazia that had never been reported in humans,” said case report lead author Richard Bradbury of the CDC’s Division of Parasitic Diseases and Malaria.

“Previously, it was thought that there were only two different species of these (Thelazia) eye worms that infected humans worldwide. Now, we have to add Thelazia gulosa, a third one to the list.”

The other two types of eye worms that infect humans are Thelazia callipaeda, found in Asia, and Thelazia californiensis, found across Asia and Europe.

Previously, only 10 cases of thelaziasis, the infection caused by Thelazia, had been reported in the US, and all had ended up being the result of Thelazia californiensis worms.

More commonly, thelaziasis occurs in animals such as cats, dogs and foxes, spread by different types of flies. If humans do end up infected, they tend to be the very young and the very old – possibly, the doctors noted, because they can’t as easily brush flies away from their faces.

Typically, patients infected with these parasitic eye worms report feeling similarly to the 26-year-old patient – eye irritation, and the sensation of a foreign body in the eye.

The doctors believe she may have contracted the worms while practising horseback riding in a region of Oregon where cattle farming is common.

“We immediately thought it could be Thelazia californiensis because that is the only species that was known to infect humans in the US,” Bradbury said.

“It was only after we looked more carefully that we realized some differences in anatomy that meant it could not be T. californiensis. We had to go back to papers published in German back in 1928 to help identify this worm as Thelazia gulosa.”

Thankfully, it’s pretty easy to get rid of these eye worms, since they stay on the surface of the eye and the conjunctiva, but that doesn’t mean the worms aren’t dangerous.

If the worms move across the surface of the eye, they can scar the cornea and even cause blindness, the doctors noted in the case report.

The worms were all removed manually – 6 by doctors, and the remaining 8 by the patient herself, over the space of several days.

Since the 14th worm left the patient’s eye, she has experienced no further symptoms.

The case report has been published in The American Journal of Tropical Medicine and Hygiene.

A parasitic eye worm called Thelazia gulosa is pretty common in the northern US and southern Canada – at least in cows.

Now, for the first time, it’s been observed jumping over to humans, infecting the eye of an Oregon woman.

The 26-year old patient reported feeling an irritation in her left eye, before removing the first worm eight days later.

Over a 20-day period, 14 worms less than 13 millimetres (half an inch) in length had to be removed from her conjunctiva and the surface of her eyeball.

Typically, the eye worms are spread between cattle by flies that feed on the fluid that lubricates the eyeball.

“Cases of eye worm parasitic infections are rare in the USA, and this case turned out to be a species of the Thelazia that had never been reported in humans,” said case report lead author Richard Bradbury of the CDC’s Division of Parasitic Diseases and Malaria.

“Previously, it was thought that there were only two different species of these (Thelazia) eye worms that infected humans worldwide. Now, we have to add Thelazia gulosa, a third one to the list.”

The other two types of eye worms that infect humans are Thelazia callipaeda, found in Asia, and Thelazia californiensis, found across Asia and Europe.

Previously, only 10 cases of thelaziasis, the infection caused by Thelazia, had been reported in the US, and all had ended up being the result of Thelazia californiensis worms.

More commonly, thelaziasis occurs in animals such as cats, dogs and foxes, spread by different types of flies. If humans do end up infected, they tend to be the very young and the very old – possibly, the doctors noted, because they can’t as easily brush flies away from their faces.

Typically, patients infected with these parasitic eye worms report feeling similarly to the 26-year-old patient – eye irritation, and the sensation of a foreign body in the eye.

The doctors believe she may have contracted the worms while practising horseback riding in a region of Oregon where cattle farming is common.

“We immediately thought it could be Thelazia californiensis because that is the only species that was known to infect humans in the US,” Bradbury said.

“It was only after we looked more carefully that we realized some differences in anatomy that meant it could not be T. californiensis. We had to go back to papers published in German back in 1928 to help identify this worm as Thelazia gulosa.”

Thankfully, it’s pretty easy to get rid of these eye worms, since they stay on the surface of the eye and the conjunctiva, but that doesn’t mean the worms aren’t dangerous.

If the worms move across the surface of the eye, they can scar the cornea and even cause blindness, the doctors noted in the case report.

The worms were all removed manually – 6 by doctors, and the remaining 8 by the patient herself, over the space of several days.

Since the 14th worm left the patient’s eye, she has experienced no further symptoms.

The case report has been published in The American Journal of Tropical Medicine and Hygiene.

A parasitic eye worm called Thelazia gulosa is pretty common in the northern US and southern Canada – at least in cows.

Now, for the first time, it’s been observed jumping over to humans, infecting the eye of an Oregon woman.

The 26-year old patient reported feeling an irritation in her left eye, before removing the first worm eight days later.

Over a 20-day period, 14 worms less than 13 millimetres (half an inch) in length had to be removed from her conjunctiva and the surface of her eyeball.

Typically, the eye worms are spread between cattle by flies that feed on the fluid that lubricates the eyeball.

“Cases of eye worm parasitic infections are rare in the USA, and this case turned out to be a species of the Thelazia that had never been reported in humans,” said case report lead author Richard Bradbury of the CDC’s Division of Parasitic Diseases and Malaria.

“Previously, it was thought that there were only two different species of these (Thelazia) eye worms that infected humans worldwide. Now, we have to add Thelazia gulosa, a third one to the list.”

The other two types of eye worms that infect humans are Thelazia callipaeda, found in Asia, and Thelazia californiensis, found across Asia and Europe.

Previously, only 10 cases of thelaziasis, the infection caused by Thelazia, had been reported in the US, and all had ended up being the result of Thelazia californiensis worms.

More commonly, thelaziasis occurs in animals such as cats, dogs and foxes, spread by different types of flies. If humans do end up infected, they tend to be the very young and the very old – possibly, the doctors noted, because they can’t as easily brush flies away from their faces.

Typically, patients infected with these parasitic eye worms report feeling similarly to the 26-year-old patient – eye irritation, and the sensation of a foreign body in the eye.

The doctors believe she may have contracted the worms while practising horseback riding in a region of Oregon where cattle farming is common.

“We immediately thought it could be Thelazia californiensis because that is the only species that was known to infect humans in the US,” Bradbury said.

“It was only after we looked more carefully that we realized some differences in anatomy that meant it could not be T. californiensis. We had to go back to papers published in German back in 1928 to help identify this worm as Thelazia gulosa.”

Thankfully, it’s pretty easy to get rid of these eye worms, since they stay on the surface of the eye and the conjunctiva, but that doesn’t mean the worms aren’t dangerous.

If the worms move across the surface of the eye, they can scar the cornea and even cause blindness, the doctors noted in the case report.

The worms were all removed manually – 6 by doctors, and the remaining 8 by the patient herself, over the space of several days.

Since the 14th worm left the patient’s eye, she has experienced no further symptoms.

The case report has been published in The American Journal of Tropical Medicine and Hygiene.

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Herpetic Whitlow


nejmicm1711479_f1

A previously healthy 1-year-old girl was admitted to the hospital with a 4-day history of fever, along with erythema and swelling of the left third finger. Bacterial cellulitis was suspected, and intravenous cefazolin was initiated. However, over the next 36 hours, the fever persisted (with a maximum temperature of 39°C), the finger was noted to have visible vesicles, and the fingertip became pale (Panels A and B). Further history revealed that the child often sucked her fingers, and examination of the oral cavity was notable for gingival inflammation and tongue lesions (Panel C, arrow). Polymerase-chain-reaction assay of a specimen from an oral lesion was positive for herpes simplex virus type 1 (HSV-1). Primary HSV-1 infection in young children commonly causes gingivostomatitis and fever. Thumb and finger sucking can lead to digital HSV infection, known as herpetic whitlow. In this patient, cefazolin was discontinued and intravenous acyclovir was initiated. Within 2 days, the symptoms began to resolve, and treatment was switched to oral valacyclovir. The patient was discharged home and completed a 10-day course of antiviral therapy. Resolution of the skin lesion was confirmed at the outpatient clinic 9 days after discharge.

A Newborn with Thrombocytopenia, Cataracts, and Hepatosplenomegaly


http://www.nejm.org/doi/full/10.1056/NEJMcpc1706110?utm_medium=referral&utm_source=r360

A Newborn with Thrombocytopenia, Cataracts, and Hepatosplenomegaly


How common is the use of the rubella vaccine worldwide?

The acronym TORCH (toxoplasmosis, other [syphilis, varicella, parvovirus B19 infection, HIV infection], rubella, cytomegalovirus infection, and herpes simplex virus infection) is often used to identify possible congenital infections.

Clinical Pearls

Q: What are some of the clinical manifestations of the congenital rubella syndrome?

A: Cataracts, thrombocytopenia, bony abnormalities, and deafness are consistent with the congenital rubella syndrome.

Table 2. (10.1056/NEJMcpc1706110/T2) Manifestations of the Congenital Rubella Syndrome.

Q: How is the congenital rubella syndrome diagnosed?

A: Newborns with the congenital rubella syndrome shed rubella virus in the throat, nasopharynx, and urine. Because growth of the virus in cultured mammalian cell lines is relatively slow and cultivation and identification of the virus are labor-intensive, nucleic acid amplification tests have been developed to directly detect rubella virus RNA in clinical samples.

Morning Report Questions

Q: Can serologic testing also establish the diagnosis of the congenital rubella syndrome?

A: In addition to direct viral detection, evidence of the production of antibodies to rubella virus in an infant can be used to establish a diagnosis of the congenital rubella syndrome. Affected newborns produce IgM antibodies to rubella virus. These antibodies can usually be detected at birth with the use of a capture enzyme-linked immunosorbent assay; the level increases during the first 3 months of life and then declines over time. At birth, tests for IgG antibodies to rubella virus cannot be used to distinguish between transplacentally acquired maternal antibodies and antibodies produced by the neonate. However, another means of establishing a diagnosis of the congenital rubella syndrome is showing that the level of IgG antibodies to rubella virus does not substantially decrease during the first few months of life, as the maternal antibodies decay. Finally, IgG antibodies to rubella virus that are produced by infants with congenital infection are typically of low avidity; therefore, a diagnosis of the congenital rubella syndrome can be established by detecting low-avidity antibodies in the blood after the maternal antibodies have waned.

Q: How common is use of the rubella vaccine worldwide?

A: The estimated number of cases of the congenital rubella syndrome worldwide is still approximately 100,000 per year. Rubella and the congenital rubella syndrome have been eradicated from the Western hemisphere because of good vaccine coverage. Unfortunately, although rubella has been controlled in many countries in Europe, opposition to vaccination in some countries has prevented the elimination of rubella, and there is much work to be done. In contrast, routine vaccination against rubella has just begun in some Asian countries, including India, Thailand, China, Japan, and Indonesia. Coverage in Africa is spotty, but a few countries have introduced the vaccine. In Nigeria, vaccination is limited to private providers, and coverage is less than 10%. There is a campaign to introduce the combined measles–rubella vaccine throughout the world, and all regions have goals to eradicate both diseases.

A step further towards developing Gonorrhea vaccine


https://speciality.medicaldialogues.in/a-step-further-towards-developing-gonorrhea-vaccine/

Urothelial Carcinoma


Video

Digital Object ThumbnailUrothelial Carcinoma (00:08)

A 69-year-old woman presented to the emergency department with new-onset gross hematuria. Her medical history was notable for 20 pack-years of smoking. Results of a physical examination, complete blood count, and metabolic panel were normal. Urinalysis showed more than 100 red cells per high-power field and 5 to 10 white cells per high-power field. A urine culture was negative, and results of urine cytologic testing showed no malignant cells. A computed tomographic urogram showed a filling defect in the right ureter. Examination of the bladder with a rigid cystoscope revealed a papillary mass that protruded through the right ureteral orifice during ureteral peristalsis (see video). In a ureteroscopic examination, it was determined that the mass was 4 cm in length and had a cylindrical stalk that was 5 mm in diameter; numerous smaller distal ureteral masses were also revealed. Biopsy was performed, and pathological examination confirmed the diagnosis of papillary urothelial carcinoma. Smoking and other chemical exposures are risk factors for urothelial carcinoma. After discussion of the treatment options, the patient elected to undergo robot-assisted laparoscopic nephroureterectomy with excision of a bladder cuff. The final pathological evaluation showed high-grade, multifocal urothelial cancer along the ureter, with negative surgical margins. Three months after the procedure, the patient was well and had no further hematuria, and surveillance cystoscopy showed no evidence of disease recurrence.

What is Stone Man Syndrome? (Fibrodysplasia ossificans progressiva)


Stone man syndrome is a rare disorder that affects the connective tissues of the muscles. Stone man syndrome or Fibrodysplasia ossificans progressiva is a mutation caused in the repair mechanism of the body that affects the fibrous tissue including muscles, ligament and tendon. When the fibrous tissue is damaged, it gets ossified i.e. muscles undergo changes to form bones. To be more specific, muscles are replaced by bones. Bones are formed as if there is an extra skeletal structure is formed other than the original skeleton. Formation of bones by replacing muscles restricts the movement of the person who is affected with this disorder. This disorder is only found in 1 in 2 million people in the world.

Symptoms of stone man syndrome

Fibrodysplasia ossificans progressiva is generally found during early childhood. The progression of the disorders starts from the neck to shoulders, and gradually proceeds to lower parts of the body and finally to the legs. Body movements will be restricted progressively because the joints get affected with the disorder. The patient finds it difficult to open mouth, which in turn causes trouble while eating and speaking. Gradually, the people affected with this disorder will experience lack of nutrition due to the difficulty in eating. Stone man syndrome also causes breathing difficulties because of the additional bone formation surrounding the rib cage, which obstructs the lungs capacity to expand.

Muscle injuries or trauma caused in an individual suffering from this syndrome may trigger inflammation and swelling in the muscles, which is followed by the ossification in the area of injury. Injury caused by surgical procedures and fall triggers the formation of bones. Individuals suffering from stone man syndrome generally have abnormal toes, which helps to differentiate stone man syndrome from other muscle and bone problems. These individuals also suffer from other abnormalities in skeleton and have small thumbs. Most patients experience sudden appearance of lumps in their body.

As this disorder is affected very rarely, the symptoms of this disorder can be diagnosed as fibrosis or cancer. Misdiagnosis will lead to biopsies and other related tests of cancer.

How mutation is caused

In patients with fibrodysplasia ossificans progressiva, the gene ACVR1 will get mutated. This genes provide instructions for the production of a certain protein known as BMP or bone morphogenetic protein type 1 receptors. This protein can be found in several body tissues such as cartilage and skeletal muscles. It controls the development of muscles and bones, which includes the replacement of cartilages into bones. Replacement of cartilages into bones is known as ossification and it occurs as a normal process from birth to teenage.

According to researchers, the gene that is mutated will change the shape and functions of the receptor at certain circumstances. This results in the constant activation of the receptor causing the overgrowth of cartilage and bone, and fusing of joints. This results in the symptoms of stone man syndrome. In most cases, people without any history of this disorder in the family are affected with this disorder. Rarely, individuals will inherit the mutated gene from the parent.

Sickle cell anaemia on chest radiograph


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Lungs and pleural spaces are clear. Cardiomediastinal contours are normal. The bones are diffusely sclerotic and there are H-shaped vertebral bodies in keeping with sickle cell anaemia.

The Vaccine Did It: Mutated MMR Mumps Virus in the Brain of a Child Caused His Death, British Researchers Confirm


The Vaccine Did It: Mutated MMR Mumps Virus in the Brain of a Child Caused His Death, British Researchers Confirm

The Vaccine Did It

A toddler who developed severe neurological symptoms including blindness associated with chronic encephalitis and died following MMR vaccination was found to have vaccine-derived mumps virus in his brain, a new study reports.

Published in the current issue of the journal, Acta Neuropathologica, the study is the first of its kind to conclusively demonstrate chronic brain damage in the form of “panencephalitis” due to a vaccine-derived strain of the mumps virus. In light of a recent epidemic of mumps in highly vaccinated populations, the research raises questions about the dangers of live vaccine virus mutations and about public health claims that the MMR is a completely safe and effective vaccine without serious side effects.

MMR, BRAIN INFECTION AND DEATH

The study describes an 18-month old infant who was diagnosed with Severe Combined Immunodeficiency Disease (SCID) — a serious immune system defect that may follow infection — four months after he received the triple Measles Mumps Rubella vaccine that contains live viruses.

The baby was treated for the illness but six months later became ill again with fever, rash, diarrhoea, lethargy and seizures. MRI scans of his brain showed evidence of encephalitis — brain inflammation due to infection.

The toddler was treated with antimicrobials, antivirals and steroids and sent home on anticonvulsant drugs.  Over the next few months, behavioural problems became obvious, his hearing was impaired and his speech and language were delayed. A year later, by then four years old, he was still suffering from seizures and he became increasingly lethargic, disoriented and agitated. His walking was increasingly uncoordinated and he began to lose his eyesight.

A repeat MRI scan of the boy’s brain revealed abnormalities and a brain biopsy was taken at Great Ormond Street Hospital for Children in London. It revealed neuronal death and evidence of central nervous system damage and chronic inflammation. Despite aggressive treatment, his seizures increased, he became weak on his left side, went blind and the five-year-old died seven weeks later.

VACCINE VIRUS CONFIRMED

Spinal fluid and urine samples collected during the boy’s last hospitalisation, as well as RNA re-extracted from his brain biopsy, were sent to the Public Health England Virus Reference Laboratory for sequencing.

Researchers, led by Sofia Morfopoulou of the Division of Infection and Immunity, University College London, and at the National Institute for Biological Standards and Control, used deep sequencing technology to identify the MuV –JL5 vaccine virus strain in the boy’s brain biopsy which was negative for all other viruses.

Genetic Drift and Outbreaks

Mutations in the mumps vaccine virus from that in the batch of the vaccine the boy had received were also detected. The study refers to a 2015 study confirming “genetic instability” of mumps vaccine virus that leads to “genetic drift” between different vaccine batches and may explain why some mumps vaccines induce more serious adverse reactions than others, especially when they are grown on different media.

This science may also explain why the mumps vaccine is failing. A recent outbreak among more than 1,600 mostly vaccinated people in Arkansas has public health officers there admitting that the vaccine isn’t protecting against emerging new strains of the virus.

It’s part of a growing phenomenon that scientists are reporting in many vaccines called “sero-conversion” – when vaccines diminish the strain of a virus they are targeting, but another strain of the same virus blooms — just as antibiotics wipe out bacterial infections but leave antibiotic-resistant superbugs to thrive.

One study in chickens found that vaccination against one disease virus “enhances the fitness of more virulent strains”, making it possible for superbug strains to develop and be transmitted to other chickens, creating “conditions that promote the emergence of pathogen strains that cause more severe disease in unvaccinated hosts”.

A 2015 study of humans in the journal Microbiome, found that the nasal flu vaccine did the same thing. The researchers concluded that the vaccine activates the immune system in a way “may foster the disproportionate emergence of potentially pathogenic species such as S. aureus”– a bug associated with ear infections and serious neuropsychiatric disorders like PANDAS.

Sero-replacement is a recognized snag for numerous vaccines. A 2017 study  tries to quantify the problem with a pneumococcal vaccine. It’s a documented difficulty with a rotavirus vaccine.  And it’s a long-documented problem with the polio vaccine. This 2016  study , for example, acknowledges that live attenuated oral poliomyelitis vaccine strains are “genetically unstable”, and their circulation (unavoidable when people defecate the vaccine virus which can hang around for decades), “can lead to the emergence of pathogenic circulating vaccine-derived polioviruses”. It turns out, the vaccine virus mutates and recombines with other circulating strains and produces something even more “neurovirulent”.

That is why the World Health Organisation is losing its battle with polio in India. More children are paralyzed and die there now than would ever be harmed by wild polio because they are afflicted with a new “acute flaccid paralysis” — a polio they won’t call polio because it’s made in their laboratories. It’s also strikingly similar to the polio-like “mystery illness” paralysing children in America.

JUST LIKE MEASLES ENCEPHALITIS

The British researchers in the current study compare this mumps encephalitis case to documented measles encephalitis and suggest a “common pathogenic process” is at work.  They cite a 2015 study in the journal Science and Translational Medicine that describes a 13-month-old baby who died from encephalitis after the MMR where vaccine virus was found in his brain and throughout his body. These results make a “strong case for deep sequencing of brain tissue where other methods have failed” to identify a pathogen, the study said.

In their conclusion, the researchers give heed to the “highly effective and safe vaccine” mantra required to keep publishing.  As usual, there is no hint of apology for physician-induced death. No consideration of how often this same pathology might play a role in SIDS or autism, of course, although public health has been scratching their heads about those for a very long time. But they do say “this case highlights the importance of developing strategies such as newborn screening to exclude the very small proportion of infants at extremely high risk of complications from live-attenuated vaccines.”

That presumes there is a way to screen children at risk of live virus vaccines which include the MMR, the chickenpox and flu vaccines. There is no evidence that the little boy in the study was ill before he got his MMR.  Yet they have begun the quest for his deficiency or genetic weakness. And they may find some because we all have them. But they are ignoring the research they just cited, that there is problem inherent in the vaccine manufacturing process and with genetic drift of the viruses. It’s more evidence that the old medical paradigm, which sees something wrong with the person who cannot tolerate the drug rather than with the drug itself, is getting older by the minute.

The answer from public health, of course, is always the same: time for another vaccine. Another dose, another strain, another booster for this group or that.  And an endless, circuitous virus chase. But in public health, the question if there might be a better way to fight disease in unthinkable. They would never seek to understand why most kids get through measles without a hitch and are left with lifelong protection against the disease and more protection too against diseases like cancer, or to find out what is lacking in the immune systems of the few children who don’t. But can we really continue this aim of vaccinating everyone against everything? What if it came down to something as simple as making sure kids got vitamins instead of vaccines? Too dangerous? At least vitamins couldn’t mutate and infect their brains.

BRING ON RFK JR., PLEASE

Even if screening high-risk newborns from vaccines were possible, (and it’s a great idea), there’s no chance of it happening in the current public health paradigm. Because for public health to start screening newborns for susceptibility to vaccine dangers, they would first have to admit what this science shows clearly, that vaccines have dangers. That they can and do cause serious brain damage and even death. And if they admit that, then they have to concede the possibility that vaccines may have a role in other neurodevelopmental disorders that are epidemic in children today.

How likely is that to happen at the Centers for Disease Control where people like Colleen Boyle and Frank DeStefano still oversee immunisation safety? People who, everyone knows, including their colleague who blew the whistle on them, knowingly manipulated, buried and shredded evidence to hide a link between the MMR and autism. People who would deceive the American public, and people across the globe, to protect their vaccines rather than the children who get them. And who would watch as millions of children suffer as a result, and do nothing?

What this science shows more than anything else, is how desperately we need President-elect Trump to move forward in 2017 with his commission on vaccine safety and scientific integrity.

Ascaris in the urinary tract: A case report and review of the literature


Abbreviations

  • CTcomputerized tomography;
  • U/Sultrasound;
  • EDemergency department;
  • CVAcostovertebral angle;
  • GIgastrointestinal

1. Introduction

The sites of physical migration of adult Ascaris include a biliary duct, liver parenchyma, pancreas, peritoneum, thoracic cavity, lacrimal duct, Eustachian tube, fallopian tube, brain, and even a pulmonary artery.1 Areas that are not organically part of the Ascaris migration pattern are accessed through fistulization from sites that are normally infested with Ascaris.

Only a limited number of reports are available describing the location of adult Ascaris forms in the urinary system. This report is the first description of urinary ascariasis that has caused upper tract obstruction and the first case to describe ureteroscopic manipulation of Ascaris lumbricoides.

2. Case presentation

A 30 year old female was admitted from the emergency department (ED) with complaints of severe sharp pain in the left lumbar region. She reported dull pain for two weeks prior to admission to the hospital. She had an acute worsening of symptoms which evolved to sharp and severe pain necessitating her to come to the ED. She had no previous history of urinary stone disease or urinary tract infections. On the time of admission to the ED she had normal vital signs and normal physical findings except tenderness in the left groin and positive left costovertebral angle tenderness.

Abdominal and retroperitoneal U/S, complete blood count, and urinalysis were performed in the ED. U/S revealed left proximal hydroureter and moderate left hydronephrosis. Laboratory analysis showed mild leukocytosis of 12000/mm3, normal creatinine, and urinalysis demonstrated calcium oxylate crystals but no evidence of microscopic hematuria.

She was hospitalized in the urology department for presumptive left upper tract obstruction from unknown source. Conservative treatment was initially pursued and a non-contrast CT scan was done one day after admission; however, it did not show a source of obstruction (Fig. 1 ;  Fig. 2). Exploratory ureteroscopy was then performed on hospital day six due to continuing renal colic.

Fig. 1
Fig. 1.

CT of pelvis shows no obstructing source in the pelvis that was identifiable.

Fig. 2
Fig. 2.

Coronal images of the CT of the abdomen show no obstructing source.

During ureteroscopy, a six to seven mm wax-like structure was found in the distal third of the left ureter. This presumed foreign body was relocated with a Dormia N.Stone basket (Coloplast Minneapolis, MN) into the bladder, where it was then extracted cystoscopically with rigid forceps. The removed object was 11cm in length, 6–7mm wide, dark-brown, and of tight elastic consistency. The specimen underwent pathologic review and was determined to be Ascaris lumbracoides (Fig. 3).

Fig. 3
Fig. 3.

Adult form of Ascaris lumbricoides after ureteroscopic extraction.

The patient had an uneventful recovery. Stool for ova and parasites was negative for Ascaris eggs, larvae, or worms. The patient had no other source of Ascaris that was identified during her hospital stay, and she was discharged home in satisfactory condition.

3. Discussion

Prior studies have shown that maturation of the Ascaris larva into the adult worm form is only possible in the GI system. Currently there are only two theories on how Ascaris lumbricoides can be introduced into the urinary system. This includes fistula formation between the GI and urinary system or by retrograde migration of the adult worm through the urethra. Urethral migration is generally precipitated by stressful conditions such as fever, illness, anesthesia, or prior anthelmintic medications. 1,2

The most commonly reported site of urinary ascariasis is the bladder. There are only two other case reports which describe Ascaris localizing to other parts of the urinary system. Quick et al. reported a case of 39 year old male who expelled the worm form through urination and had no symptoms other than tingling sensation in the penis and painless gross hematuria.3 Further investigation showed no connection between the gastrointestinal tract and the urinary system, but revealed a right renal stone. Examinations for ova and parasites were negative for Ascaris.

Gupta et al. described a case of a 55 year old male with generalized edema and anuria. After catheterization two worms were entrapped into urine collection bag.4 Singh at al. reported a case of a 35 year old female with acute urinary retention that started two days after mebendazole treatment.5Ascaris lumbricoides was excreted through the urinary catheter in this case. She also had Ascaris noted in a stool analysis and passed two Ascaris forms through the anus in next 24 hours.

Bustamante-Sarabia described a case of a 25 year old female with a history of three adult Ascaris worms released from a subcutaneous abscess.2 On postmortem examination, a fistula that connected the transverse colon, proximal third of left ureter, and subcutaneous tissue was found. There were also six live adult Ascaris forms occupying the renal pelvis and major calyces. The middle third of the ipsilateral ureter was blocked with a one cm stone, and was presumptively the reason why only retrograde migration and fistulization possible.

Taylor gave us an example of a 6 year old boy who was hospitalized a few days after anti-helminthic treatment was started. He was originally admitted with abdominal pain, cough, loss of appetite, fever, and passage of two adult Ascaris worms from the urethra.1 Isotope renal scan showed that the right kidney was non-functional and it was then surgically removed. On pathologic analysis, Ascaris lumbricoides ova in the kidney specimen were discovered.

Given the current data, we believe that our patient experienced retrograde invasion of Ascaris through urethra. No signs of fistulization were present either radiographically or by direct visual inspection. The patient also did not have any illness recently or receive prior anthelmintic treatment that could precipitate urinary migration of Ascaris forms.

4. Conclusion

This case was different and unique from the prior cases reported in the literature. This is the first case of urinary ascariasis presenting with upper tract obstruction and renal colic. This was also the first ureteroscopic extraction of Ascaris lumbracoides that was presented in the literature. This case reinforces the concept that diagnostic ureteroscopy has a role in patients with signs of obstruction but no true identifiable source.

References

    • 1
    • K.L. Taylor
    • Ascariasis of the kidney
    • Pediatr Pathol Lab Med, 15 (1995), pp. 609–615
    • 2
    • J. Bustemente-Sarabia, A. Martuscelli, J. Tay
    • Ectopic ascariasis
    • Am J Trop Med, 26 (1977), pp. 568–569
    • 3
    • G. Quick, S.H. Sheikho, J.S. Walker
    • Urinary ascariasis in a man with hematuria
    • South Med J, 94 (2001), pp. 454–455
    • 4
    • P. Gupta, V. Sundaram, G. Abraham, G.P. Shantha, M. Mathew
    • Obstructive uropathy from Ascaris lumbricoides
    • Kidney Int, 75 (2009), p. 1242
    • 5
    • D. Singh, P. Vasudeve, D. Dalela, S.N. Sankhwar
    • Ascaris lumbrisoides: a stranger in the urinary bladder causing urinary retention
    • J Postgrad Med, 56 (2010), pp. 222–223