Scientists Study Slums for Signs of Spreading Superbugs

Scientists Study Slums for Signs of Spreading Superbugs

Scientists Study Slums for Signs of Spreading Superbugs

The next superbug could emerge from the slums of the developing world, researchers warn.

Rapid, unplanned growth in many urban areas has people, livestock and wildlife living in close proximity and with inadequate sanitation. These are ideal conditions for microbes to evolve and spread.

So a major project is underway, designed to shed light on how microbes move through the slums of Nairobi and beyond.

It’s known as the Urban Zoo project. “Zoo” is short for zoonosis, the spread of diseases from animals to humans. From salmonella to swine flu, that’s how we get most of our diseases.

Slum farm

But “zoo” also suggests the menagerie of creatures found in Nairobi’s slums that could carry those diseases.

At the garbage dump in Nairobi’s Viwandani neighborhood, people, goats and Marabou storks pick through the trash side by side. (Credit: S. Baragona/VOA)

At the garbage dump in Nairobi’s Viwandani neighborhood, people, goats and Marabou storks pick through the trash side by side. (Credit: S. Baragona/VOA)

Fenced in by sheets of rusting corrugated metal in Nairobi’s Viwandani neighborhood, Joseph Mwai and his family share a couple thousand square feet with three cows, a handful of chickens, about a dozen goats and a small herd of pigs.

These are far from optimal conditions for raising livestock. But Mwai says he doesn’t have much of a choice.

“It’s important to me because I don’t have any job to do,” he said. “I make a living from them.”

A garbage dump smolders behind Mwai’s tiny homestead, across a stream polluted with raw sewage. People, goats and Marabou storks pick through the trash side by side, looking for anything useful or edible. Plastic bags are pulled from the heaps, rinsed in the contaminated river and resold.

It’s a rich environment for the spread of bacteria and other microbes.

Gene swappers

The Urban Zoo project is watching one microbe in particular: E. coli.

Mostly harmless, E. coli usually leads a quiet life in the digestive tract of warmblooded animals, from humans to birds to mice.

But some strains cause disease. And it’s of special interest to researchers for two other reasons.

Molecular biologist John Kiiru studies drug-resistant bacteria spreading in Nairobi’s slums at the Kenya Medical Research Institute. (Credit: S. Baragona/VOA)

Molecular biologist John Kiiru studies drug-resistant bacteria spreading in Nairobi’s slums at the Kenya Medical Research Institute. (Credit: S. Baragona/VOA)

First, it can spread easily and widely, according to molecular biologist John Kiiru with the Kenya Medical Research Institute. He explained, “E. coli is able to survive in the environment and it can also be shared between humans and animals.”

And E. coli are exceptionally good at swapping genes with other microbes, including genes that transform harmless bacteria into dangerous germs, or that render them immune to antibiotics.

These genes “can actually be transferred to other organisms which could be pathogenic,” Kiiru said.

That’s not a hypothetical. Kiiru says his team has identified E. coli that are resistant to four antibiotics, then found that same resistance pattern spreading to another germ, salmonella.

“And when we sequenced and analyzed these resistances,” he said, “we found that the same block of resistance genes that we had found in E. coli were actually now in salmonella.”

Even more concerning: Cholera germs may have picked up those resistance genes as well. “What you end up creating is a superbug” that’s highly virulent and highly resistant, Kiiru said.

Germ movement

But scientists know very little about how any bacteria move through this complex environment.

So the Urban Zoo project is visiting 99 households across Nairobi, rich and poor, with livestock and without. They’re taking samples from people, their animals, and whatever wildlife they can find nearby (and catch): storks, mice, bats, et cetera. They’re sampling the ground around homes, yards and livestock pens with white paper booties.

The aim, says University of Liverpool veterinarian Judy Bettridge, is “to try and understand on a small scale how those bacteria are shared” among each household’s people, livestock and environment. “And then when we scale it up, are the bacteria here being shared with the household that’s 50 meters over there? Or 100 meters over there? So, how far can they actually spread?”

Once they find out, Kiiru says, the researchers need to be sensitive about how they present their results. Livestock are technically illegal in the city, but they are important sources of food and income.

And they don’t want to make pariahs of people who are already marginalized.

“We are not necessarily investigating who is spreading the resistant or the virulent organisms,” he said. “But actually we are trying to solve a problem.”

Food networks

Another question is the role that food plays in spreading those bacteria. Mwai’s city livestock are one small part of the vast network that delivers meat, milk and eggs throughout Nairobi.

The Urban Zoo project is mapping those routes. In this modernizing East African capital, that includes everything from shiny, modern supermarkets to grimy street-food stalls.

Street food and other informal vendors are especially important in communities like Viwandani, where many people don’t have time — or kitchens — to prepare their own meals.

WATCH: Small Shops in Nairobi Get Food Safety Training

0:00:00

“You can find [residents] depending entirely on the [informal] food vendors,” says Nicholas Ngomi with the African Population and Health Research Center. That makes street-food hawkers and cooks in tiny corner shops key to protecting the health of Viwandani’s residents, he adds.

But food poisoning is rampant here. As Urban Zoo researchers mapped Viwandani’s food networks, they talked with these informal cooks about foodborne disease. One request kept coming up, Ngomi said: “ ‘Teach us about how these diseases come about.’ ”

The project didn’t have much money to spare. But they set up a half-day training session for 25 neighborhood food handlers.

Lessons in food safety

They covered the basics: how to wash hands, produce and cutting surfaces, plus basic microbiology and food spoilage.

James Kuria, owner of the 11th Hour Butchery, learned that the meat that hangs in bright red slabs in his shop window goes bad quickly without refrigeration.

After learning how quickly meat spoils without refrigeration, butcher James Kuria buys less and keeps it for less time. (Credit: S. Baragona/VOA)
After learning how quickly meat spoils without refrigeration, butcher James Kuria buys less and keeps it for less time. (Credit: S. Baragona/VOA)

“If it will last here for long, it will maybe bring some diseases to my customers,” he said. Now he only buys enough to last a couple of days. That also means he throws away less, he added, which cuts his losses.

For Charity Nyambura, who sells rice, beans and vegetables at a nearby street stall, the big discovery was that her cutting boards can harbor bacteria.

“When you cut the kale there are particles that come off the board, and you unknowingly give them to the customers along with the kale,” she said. “So, they eat the particles in the food and in the long run it affects their health.”

Now she washes her cutting boards, knives and vegetables before she starts chopping.

Only a few hawkers got training. But success breeds imitation, Nyambura said.

“In this business there’s a lot of competition,” she said. “They’re always trying to copy what I’m doing so they can also try and get customers.”

Charity Nyambura was one of 25 food vendors in Viwandani who received basic food safety training. (Credit: S. Baragona/VOA)

Charity Nyambura was one of 25 food vendors in Viwandani who received basic food safety training. (Credit: S. Baragona/VOA)

The hope is that other vendors will copy Nyambura, Kuria and the other trainees, so food safety practices will spread through the neighborhood, slowing the spread of illness.

Ultimately, the Urban Zoo project aims to provide evidence that will help policymakers improve conditions in Nairobi’s slums.

They are already making worrying discoveries.

“We have started seeing resistance among organisms that are easily recovered from animals or animal food products,” Kiiru said. “This evidence is going to give us a chance to … confidently tell the government, ‘We think there’s a challenge. Let’s improve the sanitation, the hygiene.’ ”

Originally appeared at the Voice of America website: http://www.voanews.com/content/scientists-study-slums-signs-spreading-superbugs/3116155.html

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Global Disease Detection Stories: Tracking and Taming Zoonotic Diseases in South Africa

Global Disease Detection Stories: Tracking and Taming Zoonotic Diseases in South Africa

Global Disease Detection Stories: Tracking and Taming Zoonotic Diseases in South Africa

A One Health program in South Africa connects physicians and veterinarians to better understand causes of human disease by looking at animals in a new light.

How do you tonsil swab a wild African buffalo? More importantly, why? The answer is that buffaloes are reservoirs for certain “zoonotic” diseases, or diseases that can be passed from animals to humans. Many infectious diseases (such as rabies and Rift Valley Fever) are transmitted through animals, which is why tracking animal diseases that could potentially jump to humans is a crucial aspect of public health. Early detection means spotting these diseases in animals before they make people sick.

Tracking disease in a national park

Dr. Marietjie Venter of the Global Disease Detection program in South Africa, visited Kruger National Park along with Jumari Steyn, a PhD student from the University of Pretoria. As part of a wildlife surveillance program, a skilled group of veterinarians sampled 30 buffalo in three hours. They swabbed tonsils and collected blood, fecal, and stomach content to investigate foot and mouth disease (FMD), which can cause major outbreaks in cattle if they come into contact with infected buffalo.

“Early detection means spotting diseases in animals before they make people sick.”

While buffalo are natural reservoirs for FMD, they are also thought to carry Rift Valley Fever, bovine tuberculosis, and other bacteria and viruses that could potentially spread to humans. The University’s research unit will use the collected samples to investigate for these zoonotic diseases which have been detected in wildlife, farm animals and humans.

An expanded partnership between the Centers for Disease Control and Prevention (CDC) South Africa and the University’s research unit improves surveillance capacity to include priority zoonotic diseases in the region: anthrax, brucellosis, rodent- and bat-borne pathogens, and many others. It also adds additional data collection sites and enhances reporting.

Bridging animal health and human health

Tracking diseases in domestic animals and wildlife has been happening for a long time, but linking that information to humans who are sick or could become sick has not. South Africa has strong surveillance systems; CDC’s role has been to support and expand them through its One Health program.

Buffalo are natural reservoirs for foot and mouth disease.

Buffalo are natural reservoirs for foot and mouth disease.

While it makes sense to get human and animal experts together, this is not an easy task. The One Health initiative has programs all over the world and builds bridges between people who may not otherwise work together. The success of the program lies in the regularity of the exchanges. One Health programs explores connections between human health, animal health, and the environment, bringing together experts in fields as diverse as climate change, farming practices, and wildlife management. According to Dr. Wanda Markotter, the Principal Investigator for CDC’s original agreement with the University of Pretoria, “This new project will significantly enhance the collaboration between the Health and Veterinary faculties to develop joint surveillance and diagnostic programs on zoonotic disease in South Africa and provide feedback to the Ministries of Health and Agriculture in South Africa.”

So back to that buffalo. Are you curious about how those specimens are collected?

       Step 1: Tranquilizer dart.
Step 2: Apply blindfold.
Step 3: Drag with tractor to recovery area.
Step 4: Collect sample.
Step 5: Provide tranquilizer antidote.
Step 6: Run! Doctors treating humans may want to count their blessings.

Originally posted at the CDC website under the Global Health Protection and Security at: http://www.cdc.gov/globalhealth/healthprotection/gdd/stories/south_africa_zoonotic_diseases.html

 

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Cost-effective rabies prevention strategy

Cost-effective rabies prevention strategy

Cost-effective rabies prevention strategy

Mass dog vaccination is the most cost-effective way to control rabies and decrease human deaths. from the figure below it is clear that with a higher vaccination coverage of the dog population there are multiple benefits, in terms of: (1) reduction in number of human mortalities (2) cost savings in terms of expenditure on treatment and control (3) healthier dogs and humans and everyone is happy 🙂

Costeffective Rabies control

Originally posted on twitter by @OIE

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India Virtually Eliminates Tetanus as a Killer

India Virtually Eliminates Tetanus as a Killer

India Virtually Eliminates Tetanus as a Killer

A year after eliminating polio, India has scored another public health victory. Following a 15-year campaign, the country has virtually eliminated tetanus as a killer of newborns and mothers.

Tetanus, caused by a bacterium common in soil and animal dung, usually infects newborns when the umbilical cord is cut with a dirty blade. Mothers often receive the infection by giving birth on dirty surfaces or being aided by midwives with unwashed hands.

The disease — also known as lockjaw, after its muscle spasms — usually sets in about a week after a birth and is invariably fatal if not promptly treated. Fifteen years ago, the World Health Organization estimated that almost 800,000 newborns died of tetanus each year; now fewer than 50,000 do.

But the effort to reduce tetanus has gone slowly. The World Health Assembly — the annual gathering of the world’s health ministers in Geneva — originally set 1995 as the target date for its global elimination as a health threat.

Unlike polio or smallpox, tetanus can never be eradicated because bacterial spores exist in soil everywhere, said Dr. Poonam Khetrapal Singh, the director of the W.H.O.’s Southeast Asia region.

India has reduced cases to less than one per 1,000 live births, which the W.H.O. considers “elimination as a public health problem.” The country succeeded through a combination of efforts.

In immunization drives, millions of mothers received tetanus shots, which also protect babies for weeks.

Mothers who insisted on giving birth at home, per local tradition, were given kits containing antibacterial soap, a clean plastic sheet, and a sterile scalpel and plastic clamp for cutting and clamping the cord.

The country also created a program under which mothers were paid up to $21 to give birth in a clinic or hospital. “Lady health workers” from their neighborhoods were paid up to $9 per mother and up to $4 for bus or taxi fare to make sure women in labor went to clinics. The workers earned the full amount only after visiting each baby at home and giving tuberculosis shots.

The program succeeded despite corruption. The Times of India recently reported that an audit had found clearly fraudulent payments — including some to a 60-year-old woman registered as having been pregnant five times in 10 months.

This article originally appeared at the health section of the New York Times.

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Vaccine for MERS coronavirus ‘looks promising’

Vaccine for MERS coronavirus ‘looks promising’

Vaccine for MERS coronavirus ‘looks promising’

A prototype vaccine against the lung infection MERS coronavirus has shown promising results, scientists say. The study, published in the journal Science Translational Medicine, suggests the vaccine guards against the disease in monkeys and camels. Researchers hope with more work it could be turned into a jab for humans.

Mers has infected 1,400 people and claimed 500 lives since 2012. But no specific treatment or preventative medicines exist. In the majority of cases, individuals are thought to have caught Mers (Middle-East respiratory syndrome) through close contact with infected patients in hospital.

5. MERS

Two-prong approach

But experts suspect camels also play an important role – acting as a host for the disease.

The researchers, led by University of Pennsylvania, say their experimental vaccine could be a “valuable tool” in two different ways – first, to immunise camels to stop it spreading to human populations and, secondly, as a jab to protect individuals at risk of getting Mers.

In the trial, the vaccine was tested on blood samples taken from camels and appeared to kick-start the production of antibody proteins that may help mount a defence against the virus.

And when it was given to macaque monkeys later exposed to Mers, the animals did not become ill.

Prof Andrew Easton, from Warwick University, described the research as a “significant step forward in the generation of a vaccine to prevent Mers disease”.

He added: “The data show that the vaccine is capable of generating protective antibodies in laboratory studies and also in camels.

“This is very promising as a possible way to reduce virus spread in camels and therefore to reduce the risk of infection in humans.”

Other experts caution that since the virus tends to affect macaques less severely than humans, it is not yet clear whether it could definitely be used as a vaccine in human populations.

The research was funded in part by the National Institute of Allergy and Infectious Diseases in the US and Inovio Pharmaceuticals.

This post originally appeared on the News section of the BBC website.

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Oral cysticercosis: A contribution of dentists & clinicians to One Health?

Oral cysticercosis: A contribution of dentists & clinicians to One Health?

Oral cysticercosis: A contribution of dentists & clinicians to One Health?

Historical account

Cysticercosis was first described by Johannes Udalric Rumler in 1555 but the connection between tapeworms and cysticercosis in man was still a mystery. In 1855, Kuchenmaister established that human cysticercosis is indeed caused by the larval stage, Cysticercus cellulosae, of the pork tapeworm, Taenia solium[14].

Epidemiology

Cysticercosis is prevalent in several parts of the world. It is endemic and one of the leading causes of acquired epilepsy[10] in developing countries, mainly in parts of Asia, Africa, Latin America and Eastern Europe. This is especially in those areas with uncontrolled free range pig production, poor sanitation and where humans and animals live in close contact[1]. Its incidence is also increasing in developed countries as a result of migration of infected persons and frequent travel to and from endemic areas[27].

In man, cysticercosis frequently involves many parts of the body including the brain (causing fatal neurocysticercosis), subcutaneous tissues, heart, liver, lungs, peritoneum, skeletal muscles and the eye. Although oral involvement by cysticercosis is common in swine, this location is a very rare occurrence in humans[17, 27, 1] where it presents as a component of disseminated cysticercosis and often a diagnostic challenge to clinicians [14].

A literature review conducted in 2012 by Krishnamoorthy and colleagues  [14], revealed 69 cases of oral cysticercosis characterized by a cystic swelling as the only evidence of the disease. They further found that any region of the oral cavity can be involved but review of literature suggested that the tongue was the preferred site comprising 46.37% of the 69 cases, followed by labial and buccal mucosa, with one case documented involving the gingival tissue from India [17]. However, some authors postulate that the muscular activity and high metabolic rate of the oral region may prevent lodging of the cysticerci in the tongue[5]. Other authors have also noted that intraorally, the favored sites for the development of cysticerci are the tongue, labial mucosa (lips), buccal mucosa (cheeks) and the floor of the mouth, however, correct and precise diagnosis is infrequently established [20, 6, 23, 13, 29, 7, 12]

How does man get infected?

Man is the definitive host for the adult pork tapeworm (Taenia solium) while the pig serves as an intermediate host. Human beings are infected by either:

  1. Eating uncooked, partially cooked or inadequately frozen pork containing viable Cysticercus cellulosae.
  2. Ingesting food or water contaminated by infected human faeces containing Taenia solium eggs which further explains cases of cysticercosis in vegetarians [11]
  3. Autoinfection by regurgitation of eggs into the stomach after reverse peristalsis[20, 3, 24]

In the human body the larval form (Cysticercus cellulosae) penetrates the intestinal mucosa and is then distributed through the blood vessels and lymphatics to the various parts of the body where they develop into cysticerci completing the life cycle.

What are the clinical signs?

In humans cysticercosis can develop in various organs and tissues. The larval form (Cysticercus cellulosae) commonly presents as a cyst in the cerebral tissue (brain), meninges, subcutaneous tissue, muscle and the eye [3, 19, 13, 15]. However, it is not commonly considered in the diagnosis of swellings of the maxillofacial region including the oral cavity and cheek muscles.

Most oral presentations of cysticercosis are in the form of painless, well-circumscribed, soft swellings or cystic nodules[12], that may persist or rupture and heal uneventfully[11]. Therefore, oral cysticercosis is a diagnostic challenge to a clinician due to:

  1. The condition mimics other oral nodular lesions like mucoceles, or a benign tumor of mesenchymal origin, such as a lipoma, fibroma, hemangioma, granular cell tumor, or a minor salivary gland adenoma[22]. However, the high intraluminal pressure in oral cysticercosis helps to differentiate it from lipoma and hemangioma.
  2. Cysticercosis is rarely included in the pre-operative differential diagnosis due to relative rarity of the lesion, inadequate knowledge of oral manifestations of parasitic infections and negligence while taking medical history[26].

Generally, the clinical symptoms of cysticercosis depend on the site and the number of cysticerci in the body. Cysticerci are well tolerated in the tissues when they are alive but evoke an inflammatory reaction in the surrounding tissue on  death. During invasion there may be no symptoms or mild muscular pain and fever. Central nervous system involvement may result to the potentially fatal neuro-cysticercosis[9].

Examples of oral cysticercosis case presentation and presumptive diagnosis: 

1. JoshiExample one, Joshi and colleagues (2014)[12]: An 18 year old male from Central India with an asymptomatic solitary cystic nodule in the right mucobuccal fold of upper arch. The patient reported that the lesion was present since 5-6 years with no associated pain. Intra oral examination revealed that the nodule as spherical in shape, 2 x 2 cm in size, firm, smooth surfaced and mobile. Noted in the alveolar mucosa mainly in mucobuccal fold of maxillary right canine region. There was no much change in the size and other features of the lesion in due course. The patient was otherwise healthy without any systemic signs and symptoms.

Example two, Bhatia and colleagues (2014)[1]: A case of eight year old Hindu female and a resident of a slum in Mumbai. The patient came with a swelling inside the oral cavity on the right buccal mucosa since one year which gradually increased in size. On local examination the swelling was non tender, firm and mobile measuring 1 x 0.5cm.

WanjariExample three, Wanjari and colleages (2013)[28]: Clinical presentation for both (2) cases was of diffuse, nontender, soft to fluctuant swelling. Case 1 showed involvement of the right cheek in the lower third of the face in line with the outer canthus of the right eye; however, intraorally overlying mucosa was intact and normal in colour. While case 2 revealed involvement of right labial mucosa in relation to maxillary right anterior region. No submandibular or cervical lymphadenopathy was detected in both cases.

Example four, Venkatraman and colleagues (2013)[27]: A 23 year old male presented with a swelling on the right lateral border of the tongue. The patient reported that the lesion was present since 4 years with no associated pain. Intra oral examination revealed that the lesion was spherical in shape, 2×2 cm in size, firm, compressible, smooth surfaced and mobile within the soft tissue of the tongue.

ChunturiExample five, Chunduri and colleagues(2013) [2]: A 17 year old Indian male presented with a nodule in the right lower lip. Clinical examination revealed a well circumscribed, mobile nodule approximately 1.5 cm in diameter with intact overlying mucosa. The lesion was painless and had been present for about six months, and was slowly growing.

Nervos SantosExample six, Neves Santos and colleagues (2013)[21]: A 21-year-old woman from Poções County (Bahia, Brazil) reported to a private dental center with the chief complaint of a painless nodule on the right side of her tongue that had been present for the past two years. The nodule had increased in size to approximately 3.5 cm in maximum diameter, and clinical examination showed a firm nodule that was covered with normal mucosa. No cervical or submandibular lymphadenopathy was observed. A complete blood count, liver function tests and renal function tests were all normal. A preliminary diagnosis of lipoma was made.

 

 

Krishnamoorthy

Example seven, Krishnamoorthy and colleagues (2012)[14]: A 12-year-old girl with a nodular swelling on the lower lip. She first noticed it 2 months ago. The swelling was painless, remained unchanged in size, and caused a little difficulty while eating and talking. On examination there was a solitary, spherical, well-defined swelling in the lower labial mucosa present on the left side of the midline which measured approximately 1.5 X 1.5 cm. The mucosa over the swelling was normal. On palpation it was not tender, but was tense and nonfluctuant. Differential diagnoses of mucocele, lipoma, and fibroma were considered.

Diagnosis of oral cysticercosis  

Diagnosis of human oral cysticercosis (including other forms of tissue cysticercosis) is impaired by its polymorphic clinical presentations. Excisional biopsy coupled with sections stained with Haematoxylin & Eosin, is the only confirmatory diagnostic procedure for the condition, which demonstrates the presence of the larva in the tissue or the scolex in the cystic lesion. However, other investigations must be considered to detect the disease in the diverse tissues that may be affected, using: Fine Needle Aspiration (FNA), serology, radiologic imaging techniques such as Computer Tomography (CT) or Magnet Resonance Imaging (MRI) and advanced molecular techniques as tools for conformational diagnosis[5][7].

Criteria for diagnosing oral cysticercosis as proposed by Krishnamoorthy and colleagues is: [14]:

  • A compatible clinical presentation
  • FNA aspirated material showing a speck of pearly white content also by[17, 27]
  • Histopathologic demonstration of the parasite on biopsy
  • Cystic lesions with scolex on imaging (muscular cysticercosis)
  • Positive epidemiological factors like household contact, endemic region or travel to or from an endemic area

Examples of oral cysticercosis definitive diagnoses: 

JoshiExample one, Joshi and colleagues (2014)[12]: Microscopically, the excised tissue showed a thin fibrous connective tissue capsule adjacent to a cystic cavity containing a duct like tubal segments that was lined by a homogeneous membrane typical of cysticercosis cellulosae (larval form of Taenia solium); Cyst wall and outer fibrous tissue was presenting in many papillary projections along with numerous inflammatory cell infiltrations and macrophages.

BhatiaExample two, Bhatia and colleagues (2014)[1]: External fibrous capsule with mononuclear cell infiltrate comprised of lymphocytes, histocytes and plasma cells. A double layered membrane consisting of an outer acellular hyaline eosinophilic layer and an inner sparsely cellular layer with aggregates of eosinophils was seen. The cyst contained larval form of T. Solium. The cephalic extremity of larva (scolex) with suckers could be identified suggesting the diagnosis of cysticercosis of right buccal mucosa.

WanjariExample three, Wanjari and colleagues (2013)[28]: Histopathological examination of excisional biopsy specimen revealed external dense, fibrous capsule derived from host tissue surrounding a cystic cavity which contained larval stage of T solium-cysticercus cellulosae. capsule showed intense inflammatory infiltrate consisting of plasma cells and few eosinophils. The larva consisted of a scolex, where suckers and duct-like invaginated segment could be identified at the caudal end. A digitiform coating of homogenous eosinophillic membrane was evident lining the cystic area. A final diagnosis of oral cysticercosis was made. MRI and CT scan were negative which ruled out neurocysticercosis (NCC).

Example four, Venkatramana and colleagues (2013)[27]: Histopathology of the excised tissue revealed a thin capsule of fibrous connective tissue surrounding a cystic cavity, which contained cysticercosis cellulosae (larval form of Taenia solium). The larva composed of a duct like tubal segments that was lined by a homogeneous membrane. Cyst wall and outer fibrous tissue was infiltrated with numerous inflammatory cells, macrophages and few foreign body type giant cells. Based on these findings, a diagnosis of cysticercosis was made

ChunduriExample five, Chunduri and colleagues (2013[2]: Microscopic examination revealed double glycoprotein membrane tissue surrounding a cystic cavity which contained Cysticercus cellulosae. The capsule showed intense inflammatory infiltrate, consisting mainly of lymphocytes and plasma cells. The larva was composed of a scolex, where a sucker could be identified, and a duct-like invaginated segment at the caudal end. No areas of dystrophic calcification were present in the specimen. Based on these findings, a diagnosis of cysticercosis was made.

Neves SantosExample six, Neves Santos and colleagues (2012)[21]: histological sections revealed the presence of a cystic lesion containing a serrated larva (C. cellulosae) with a cuticle and well-defined areolar and cellular layers as well as a cystic capsule exhibiting predominantly mononuclear inflammation. The final diagnosis was cysticercosis of the tongue.

KrishnamoorthyExample seven, Krishnamoorthy and colleagues (2012)[14]: A fine-needle aspiration (FNA) was performed. The aspirate was a clear fluid but the report was not conclusive. Hence the lesion was excised under local anesthesia which was a smooth well-encapsulated mass. Hematoxylline and eosin (H/E) stained sections showed a cystic mass containing the cysticercus cellulosae surrounded by dense fibrous capsule infiltrated with inflammatory cells, mainly lymphocytes and plasma cells. The inner aspect of the capsule was a double-layered membrane in which larval form of T. solium were seen. Larva showed the presence of suckers and caudal to it duct-like invagination segment lined by homogenous membrane. No areas of dystrophic calcifications were present in the tissue specimen. The final diagnosis of cysticercosis of the lip was made.

Differential diagnoses for oral cysticercosis

Oral cystucercosis is usually misdiagnosed as a mucocele, sialocyst or a benign tumor of mesenchymal origin such as lipoma, fibroma, hemangioma, lymphangioma, granular cell tumor  [16, 27], benign salivary gland neoplasms[8] and parasitic cysts e.g. hydatid cyst. Stool examination is usually carried out to rule out parasitic cysts [28].

Treatment

Oral cysticerci, being usually localized and superficial lesions, are easy to excise and have good prognosis. Simple surgical excision is often all that is required to ensure complete removal of the lesion without any postoperative complications in such cases[5]. Lesions involving the muscles like the masseter may be treated conservatively with antiparasitic therapy[18]. Unlike the neurocysticercosis or orbital cysticercosis which are severe in their clinical presentations, the oral cysticercosis are usually well tolerated. However, it is important to exclude the presence of the parasite in other sites through a detailed case study and systematic investigations [14]. Praziquantel and albendazole are used to treat cysticercosis, especially in patient with disseminated cysticercosis or where surgical excision is risky or not possible, such as in neurocysticercosis[4].

Control and prevention

Transmitted via the orofecal route, cysticercosis is potentially eradicable. To prevent and eradicate human cysticercosis supportive measures such as improvement in the sanitary conditions, pork inspection, consumption of boiled water, well washed vegetables, mass education about personal hygiene should be undertaken along with medical treatment (by a registered and approved medical practitioner) which includes larvicidal drugs, corticosteroids, and surgical procedure for removal of the cyst[25, 28].

The role of the dental clinician?

The illustrations above clearly tell us the critical role that clinicians and especially dentists have in the control  of not only oral cysticercosis but cysticercosis as a Neglected Tropical Disease. The patient diagnosis of oral cysticercosis could act as a “sentinel” and insight to further investigate and control the problem in the family or community at large.

It is clear that oral cysticercosis should be considered in the differential diagnosis of intraoral solitary swellings especially in endemic areas. In endemic countries a lesion can be first referred for a FNA which is cost-effective, quick, and reliable. Expensive investigations, like immunological tests and CT, can be undertaken only in the absence of a definitive pathological diagnosis. As much as the histopathological findings of the excised swelling are diagnostic of the lesion a detailed evaluation should be done to exclude the presence of the parasite at other sites[14, 2].

References

  1. Bhatia, V., O., Natekar, A., A., and Valand, A., G., Paediatric Oral Cysticercosis: A Misdiagnosed and a Rare Entity. International Journal of Oral & Maxillofacial Pathology., 2014. 5(2): p. 26-28.
  2. Chunduri, N., S., Goteki, V., Gelli, V., and Madasu, K., Case Report: Oral Cysticercosis. SOUTHEAST ASIAN J TROP MED PUBLIC HEALTH, 2013. 44(2).
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