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A Reptile Dysfunction: Unlikely Sources of Salmonella

Posted:Mon, 24 Mar 2014 14:35:47 +0000

Salmonella may well be one of the most disreputable microbes in Western society. It’s infamous for its food-poisoning capabilities and has a well known history of wrecking the bonhomous vibe following a good summer barbecue, not to mention its singular ability to cast a sickly shadow over the breathtaking bounty of an all-you-can-eat buffet.

A gram stain of a species of Salmonella. Image: CDC.

While Salmonella infection is commonly associated with food and with poultry and eggs in particular, it is a versatile microbe that counts reptiles, amphibians, and even adorable hedgehogs among its many friendly and accommodating hosts. In fact, an estimated 90% of reptiles harbor the bacteria as an asymptomatic intestinal infection and shed the microbe freely throughout their habitats (1). Contact with these animals, their feces or their contaminated food, water or soil can lead to Salmonella infection, and the CDC estimates that as many as a 100,000 Americans acquire salmonellosis from contact with these pets every year (2)(3).

Perhaps it’s not the chicken breast resting on the kitchen counter we should fear but rather the cute (though, truly, not so cuddly) chameleon languidly ogling us from its tank.
Young children are often the victims of reptile-associated salmonellosis with bottle-fed infants at the greatest risk of contracting an infection; the presence of pet reptiles in the home is the most common factor among such infections (4). When Salmonella infection does occur in young children, the disease can be severe and even fatal if it progresses to the point of septicemia and meningitis (5).

A chameleon of unknown species. Image: Zorandim/Shutterstock.

A few dreadful examples: in 2012, a 23-day-old boy was admitted to the hospital with meningitis and was found to be infected with a rarely seen serotype of Salmonella, S. kingabwa. The infant acquired this unusual strain during his visits to his grandmother’s house, where she kept five snakes and five water dragons that crawled throughout the home (6). In the same year, a 10-day-old girl was brought to the hospital for several visits over a period of ten months, showing symptoms of bloody diarrhea. Over the course of her visits, she showed a failure to thrive with poor weight gain, and her stools were found to harbor a strain of S. enterica spp. diarizonae. The source? Her mother kept snakes, lizards, and iguanas in the house, and upon their removal from the home, the infant recovered (7).

The CDC states the facts of the matter bluntly on a webpage devoted to salmonellosis in these animals: “If there are young children in your home, reptiles and amphibians might not be safe pets for your family” (8).

This is all well and good for those of us who prefer our pets to be a little more warm-blooded, but reptiles outside of the home can still pose a Salmonella risk to one’s humble abode. In 2001, a three-month-old Californian infant was brought to the emergency room after a day of fever and bloody diarrhea. The child’s stool sample yielded a rare strain of Salmonella, S. nima, a serotype associated with snakes and iguanas (9)(10). In this highly unusual case, the family home was free of creepy-crawlies, but the father, a high school biology teacher, had a large boa constrictor in his classroom that he confessed to wrapping around his shoulders during classtime. The same S. nima was grown from the snake’s stool culture. From the CDC report:

When interviewed, the father indicated that he knew reptiles carry Salmonella and was careful to wash his hands after handling them or their containers. However, he did not change clothing when he came home from work before holding his child.

His young child, resting on his father’s chest following a hard day’s work of enriching young minds, had become infected while rubbing his face and hands on the same shirt that a boa constrictor had been slithering upon only hours earlier. This particular case typifies the shortcomings of good awareness and education: even simple hygiene precautions such as hand-washing may not be enough in some situations.

When it comes to animal-borne infections, we have to fully consider our interactions with our pets. Do you cuddle with your puppies and kittens? Do your pet birds rest on your shoulders or head? Do you let your pets sleep in or near your bed? Do they crawl throughout your home, traipsing or wriggling over the furniture and kitchen counters? Do they groom you? These innocent behaviors could all lead to inadvertent infections with the microbes residing inside of our dear reptilian, avian, and mammalian companions.

Beyond causing isolated cases of pet-borne infection, reptile and amphibian-associated salmonellosis is also responsible for substantial outbreaks in the greater population. In 2011, over 240 people in 42 states fell ill with gastroenteritis caused by the Salmonella typhimurium following contact with African dwarf frogs sold by a Californian breeder; exposure to the frogs had occurred in pet and toy stores, fairs, and carnivals. Of those infected, 69% were younger than 10 years of age.

An African dwarf frog, Hymenochirus boettgeri, responsible for a multistate outbreak of Salmonella, serotype typhimurium Image: Matt Reinbold/Furryscaly, click for source.

Furthermore, in the past two years, turtles with shells under four inches in length have been implicated in a series of outbreaks responsible for illnesses among 371 people in 40 states (12). Again, children have borne the brunt of this outbreak, with 70% of victims under the age of 10 and a third of the infected under one year of age. This outbreak was particularly troubling as the distribution and sale of turtles of this length – which can harbor over six different species of Salmonella - have been specifically banned by the FDA since 1975 (13).

The point? These outbreaks are not aberrations, but rather they demonstrate a consistent, nationwide pattern of infection from reptiles and amphibians due to a lack of caution or, perhaps, understanding that places these animal lovers and their families in harm’s way. As a 2012 report from the CDC noted, “the public has a generally low level of awareness that Salmonella [species] can be acquired from reptiles and amphibians.”

Educating the public on the risks posed to young children by these types of animals is imperative to preventing needless and potentially lethal infections. Sadly, the CDC conducted a poll in 2003 that found that only 4 American states – California, Connecticut, Maryland, Michigan, and New York – required pet stores to provide information regarding the prevention of reptile-associated salmonellosis to customers purchasing turtles (13). And that’s only turtles – forget about the exotic salamanders, newts, frogs, snakes, and lizards available for purchase. Public health officials, pediatricians, veterinarians, and pet shop owners must do their part to help educate exotic animal lovers of the bacterial risks that accompany their scaly companions, lurking like a snake in the grass.

Resources
There’s another twist to this public health story: reptiles have also been found harboring antibiotic-resistant Salmonella. From Trinidad to Germany to Taiwan, reptiles have been found carrying Salmonella resistant to various antimicrobials, including some of our most prized heavy hitters like ciprofloxacin. See here, here, and here.
From the CDC, a handy poster on “Reducing Your Risk of a Salmonella Infection from Contact with Reptiles and Amphibians.”
In the 1970s, pet turtles under four inches in length were implicated in so many outbreaks of Salmonella – an estimated 280,00 annual cases! – that the FDA stepped in and banned all interstate shipments of the animal. Read the FDA’s Code of Federal Regulations regarding “Turtles intrastate and interstate requirements” to find out more.
Watch as a chameleon shows off his camouflaging abilities, and taste in faux Ray-Ban sunglasses, in this video here. You’re welcome.

References
1. DL Woodward et al. (1997) Human Salmonellosis Associated with Exotic Pets. American Society for Microbiology, 35(11): 2786-2790
2. Centers for Disease Control (CDC) (April 30, 2013) Diseases from Reptiles [Online]. Retrieved March 23, 2014 from http://www.cdc.gov/healthypets/animals/reptiles.htm
3. Food and Drug Administration [FDA]. (July 2005) Pet Turtles: Cute But Contaminated with Salmonella [online]. FDA. Retrieved March 23, 2014 from http://www.fda.gov/forconsumers/consumerupdates/ucm048151.htm
4. Center for Food Security and Public Health. (August 2007) Reptile-Associated Salmonellosis. Center for Food Security & Public Health. Retrieved March 23, 2014 from http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.304.1114&rep=rep1&type=pdf
5. Centers for Disease Control (CDC) What is Salmonellosis? (April 5, 2012) Retrieved March 23, 2014 from http://www.cdc.gov/salmonella/general/
6. A Olariu et al. (2012) Salmonella kingabwa meningitis in a neonate. BMJ Case Rep. Published online here.
7. A Olariu et al. (2012) Reptile Pets–associated Salmonella enterica Subspecies diarizonae Gastroenteritis in a Neonate. Pediatr Infect Dis J, 31(10): 1102–1103
8. Centers for Disease Control (CDC) Reptiles, Amphibians, and Salmonella [Online]. (November 25, 2013) Retrieved March 23, 2014 from http://www.cdc.gov/features/salmonellafrogturtle/
9. [No authors listed] (1986) Salmonella nima in British Columbia. CMAJ, 135(11): 1286
10. ME Kennedy et al. (1973) Salmonella Isolations from Snakes and Other Reptiles. Can J Comp Med, 37(3): 325–326.
11. Centers for Disease Control (CDC) (July 20, 2011) Outbreak of Human Salmonella Typhimurium Infections Associated with African Dwarf Frogs [Online] Retrieved March 23, 2014 from http://www.cdc.gov/salmonella/water-frogs-0411/072011/index.html
12. Centers for Disease Control (CDC) (October 18, 2013) Eight Multistate Outbreaks of Human Salmonella Infections Linked to Small Turtles (Final Update)[Online]. Retrieved March 23, 2014 from http://www.cdc.gov/salmonella/small-turtles-03-12/index.html
13. 21 C.F.R. § 1240.62 (2013)
The post A Reptile Dysfunction: Unlikely Sources of Salmonella appeared first on Body Horrors.
Paved With Good Intentions: Mao Tse-Tung’s “Four Pests” Disaster

Posted:Wed, 26 Feb 2014 15:33:06 +0000

The public health game is a tough one to play. How do you achieve educating and transforming the public’s behavior for the common good without coming off as a bully or dour spoil-sport? The stakes are impossible: The indifferent audience, the management of the reproachful “tsk-tsk, you should know better” tone, and there’s only so many ways to proselytize a message of “getting one’s act together.” And where’s the cash for such endeavors?

“Eradicate pests and diseases and build happiness for ten thousand generations.” A poster from September 1960 by the Red Cross and the Health Propaganda Office of the Health Department of Fujian Province. Note the industrial skyline, the healthy crop of vegetables in the center of the poster and the four pests at the bottom. Source: US National LIbrary of Medicine. Click for source.

But in the 1940s, the governing officials in the People’s Republic of China bulldozed their way through these issues (and more) and succeeded in accomplishing one of the most difficult public health objectives, the eradication of disease and vermin. But in doing so, they created an environmental catastrophe that epitomizes the tenuous balance between doing what’s best for mankind with the quirks and vagaries of Mother Nature.
As the communists ascended to power in the fall of 1949, China was saturated with disabling infectious diseases. Tuberculosis, plague, cholera, polio, malaria, smallpox, and hookworm were endemic throughout much of the country. Roughly 10.5 million people were infected with the water-borne liver parasite schistosomiasis (1). Cholera epidemics raged through the population freely, some years killing tens of thousands (2). Infant mortality was as high as 300 per 1000 live births (1).

“Exterminate the four pests!” A striking 1958 poster by Ding Hao. Image: International Institute of Social History/Stefan R. Landsberger Collections;. Click for source.

In this period of urgent political and social transition, creating a national public health system and eradicating entrenched diseases was an obvious first step in improving the lives of the nation’s people. The Communist government began initiating massive vaccination campaigns against the plague and smallpox, vaccinating nearly 300 million people (1). Sanitation infrastructures for clean drinking water and waste disposal were implemented throughout the country. Emulating the Soviet Union’s model of healthcare, the government established subsets of medical and public health personnel to serve as health stewards to the population, directing them to venture into the rural areas and treat diseases as best as they could with what limited resources were available.
But physicians, immunizations and sanitation can only go so far. Something had to be done about the pests that transmit pestilence and diseases: the mosquitos responsible for malaria, the rodents that spread plague, and those ubiquitous airborne nuisances, flies. And what of those sparrows that eat the hard-won fruits from fields of grain and rice? These four pests – flies, mosquitos, rats and sparrows – were charged with public health treason and widespread irritation. Something had to be done, on a grand and monumental scale, and the Four Pests campaign was just the thing.

“A young propaganda troupe.” A poster from 1949 emphasizing the role of children in the “Four Pests” campaign. The pests can be seen in the pink and yellow banner near the top of the poster and the tools used for their eradication – swatters, nets, gongs and more – are held in the children’s hands. Source: US National LIbrary of Medicine. Click for source.

So began the initiation of the Great Leap Forward with a patriotic health campaign that would target vermin that spread disease, a carte blanche issued to the people to fulfill their duty to their nation through the massacre of small bothersome animals and insects. In 1958, the Chinese took up the cause with merciless efficiency and embarked upon an incredible slaughter of wildlife.
This public health good would be implemented by everyone – from troupes of children to the elderly – with beautifully illustrated posters released to the masses that encouraged the wielding of fly swatters, guns and gongs against the regime’s diminutive enemies.
Public health posters serve as billboards of knowledge and empowerment, but these particular forms of propaganda are also a historical snapshot, a birth announcement from a new political and public health system.

Source: US National LIbrary of Medicine. Click for source.

These Chinese posters epitomize the Republic’s principals, culture and history, of technological and aesthetic styles. Borrowing heavily from the Soviet Union’s highly refined systems of propaganda dissemination and their artistic styles of socialist realism, they radiate dynamism, good will and optimism. They’re a visual representation of one of the most ambitious public health movements in history but they also speak of gross tampering with delicate ecosystems, of an ignorance of the subtle bonds that hold the world around us together.
The causalities of this ambitious “Four Pests” public health campaign? Yes, many infectious diseases were eradicated and their scope diminished but also “1 billion sparrows, 1.5 billion rats, 100 million kilograms of flies and 11 million kilograms of mosquitos” were outright decimated (1). The public health campaign worked well. Too well. The sparrow’s intrinsic role in the ecological balance was unrealized and resulted in an unmitigated, well-orchestrated environmental disaster. Locusts came in droves and devoured fields of grain, their feeding left unencumbered by watchful, hungry sparrows. Novel agricultural techniques recently implemented through the Great Leap Forward further contributed to the disastrous effects of the campaign.
The mass deaths of sparrows and nationwide loss of crops resulted in untold millions starving and 20 to 30 million people dying from 1958 to 1962. A 1984 article on the mass famine put it simply: “China suffered a demographic crisis of enormous proportions” (3).
The “Four Pests” campaign was inordinately successful in achieving its primary goal of vermin eradication. But one of the most successful public health campaigns in history – in terms of establishing a goal and clearly achieving it – came at an extraordinarily grave cost for the Chinese, ecologically and demographically. A sinister truth had emerged: tamper with the unseen balancing beam of predators and prey at your peril or else nature will create a level playing field at your expense.
Resources
Learn more about the representation of history, culture and politics as represented by propaganda posters at Chinese Posters, run by the International Institute of Social History. They have an outstanding collection of posters, including a nice selection of more “Four Pest” campaign posters.
From the U.S National Library of Medicine, check out their short web exhibition, “Health for the People: Continuity and Change in Asian Medicine.”
This list of campaigns of the Communist Party of China is a fascinating trip down history.
References
1. DM Lampton (1972) Public health and politics in China’s past two decades. Health Serv Rep. 87(10): 895–904
2. JW Salaff (1973) Mortality Decline in the People’s Republic of China and the United States. Population Studies. 27(3): 551-576
3. B Ashton et al. (1984) Famine in China, 1958-61. Population and Development Review. 10(4): 613-645
The post Paved With Good Intentions: Mao Tse-Tung’s “Four Pests” Disaster appeared first on Body Horrors.
Hanuman’s Bite: Temple Monkeys & Pathogen Swapping

Posted:Mon, 17 Feb 2014 18:00:53 +0000

Hanuman is a pivotal and memorable character in the Hindu epic poem, the Ramayana. Known for his faithful devotion to Rama, the monkey-king is famous for rescuing Lord Rama’s bride Sita after she is kidnapped by the demon king Ravana, all the while defeating his demon army as commander of his monkey army. Hanuman is revered throughout south and southeast Asia not only for his devotion to Rama, but also for his steadfast spirit, his indefatigable strength, and his noble humility. He is also something of a rogue – the Coyote, the Loki, the trickster of Hindu mythology, the mischievous troublemaking deity with a heart of gold and a glint in his eye.

A macaque resting at the Swayambhunath Stupa, a monkey temple and one of the oldest holiest sites in Kathmandu, Nepal. It is also an important pilgrimage site. Image: Shutterstock.

As incarnations of Hanuman, macaques, the most widespread genus of primates in the world, are tolerated and respected by Hindus. These monkeys are an integral part of the landscape of south Asia and receive protection and food from surrounding communities. Macaque monkeys have thrived in south and southeast Asia due to the benevolence of humans and the primates’ integration in religious mythology and local culture. Both ends of the primate order, whether of genus Macaca or genus Homo, have been living closely together in this region of the world for over 25,000 years (1). The biological concept of sympatry, referring to the geographic and social situation between two species or populations in coexistence, describes perfectly the relationship between macaques and humans in Southeast Asia.

Nowhere is this alliance more visible than in the monkey temples that are found throughout India, Nepal, Malaysia, and Indonesia. These temples are not only devoted entirely to the worship of Hanuman but also to the “monkey forests,” areas of dense monkey settlement surrounding temples that serve as refuges, areas protected by the religious beliefs of locals. These de facto sanctuaries have become tourist destinations where close interaction with our distant cousins is actively sought (2).

The interspecies contact between us humans and the macaques is intimate, and bites and scratches are highly common – yes, yes, they are indeed biting the hand that feeds. Within local populations, worshippers, temple workers, nuns and monks, and market workers, the contact may be frequent and habitual. As Lisa Jones-Engel and her team of researchers quickly discovered while studying temple monkeys in Kathmandu, Nepal,

At these places of worship and the habitats that surround them, there’s bad behavior from both ends of the simian spectrum. As tourists gaze at the serene faces and posing dancers engraved on stone temples, the primates direct their gaze at visitors’ packaged snacks, drinks and precious, glinting cameras. Tourists court trouble by feeding the monkeys by hand. There are frequent reports of teasing in the form of yanking tails and taunting with food. The monkeys, emboldened by free handouts, go on to raid trash receptacles and the gardens and market stalls of villagers, “receiv[ing] significant components of their nutrimental requirements from humans or human activity” (3). As a direct consequence, the macaques often begin to harass and threaten the local (human) community for both food and territory.

“Macaques climb on the heads and shoulders of visitors, which may bring macaque body fluids into contact with visitors’ eyes and nasal and oral mucosa, potential portals of entry for infectious agents. Visitors may also be bitten or scratched by macaques during aggressive encounters, resulting in transcutaneous exposure to infectious agents present in macaque body fluids”(4).
These types of “mucosal splashes” – if those words don’t send a chill down your spine then you are made of a tougher mettle than I – are a tailor-made recipe for pathogen swapping.

A poignant example: the Padangtegal Wanara Wana temple complex in Bali, Indonesia spans two towns with three temples, scattered shrines and statues in 17 acres of forest. It’s commonly marketed as “the sacred monkey forest” and is a major tourist destination in Bali with tens of thousands of visitors, both domestic and international, getting a glimpse of the star attraction, the crab-eating, bewhiskered Macaca fascicularis.

An effigy of the monkey-god Hanuman at Singapore’s Sri Krishnan Hindu Temple. Image: Shutterstock.

Just a short two-month long study conducted in 2001 at this temple complex recorded 420 “aggressive interactions” between visiting tourists and macaques (5). These aggressive interactions included threatening behavior, lunging and chasing, and intense physical contact including bites, with 78% of all interactions recorded being highly aggressive and involving physical contact. Forty-eight instances of bites were recorded, with some breaking skin. Food played a key role in these aggressive interactions – 308 instances or 73% of cases involved food as a major factor of aggression.

Now the kicker. In a 2002 study, a survey of employees at the Sangeh Monkey Forest in Central Bali found that 50% of those interviewed regarding their interactions with the macaques reported a scratch or bite injury (6). Testing of the blood serum from trapped macaques found over 80% of the monkeys had antibodies to herpes virus B, a virus that causes a benign infection in macaques but a severe meningoencephalitis in humans. Both findings suggest that the risk of transmission of primate pathogens to humans is not only very real but a matter of concern for those practicing public health in susceptible local populations and for those caring, before and after, for tourists venturing to these destinations.

At another Balinese temple in the Sangeh Monkey Forest, a 2005 study reported the first known transmission of simian foamy virus (SFV) from a macaque to a human, a long-time daily worshiper at the temple (7). He reported being scratched on multiple occasions during his visits, including at least one bite. This was a particularly intriguing moment for those studying primate retroviruses as SFV is “not known to occur naturally in humans.”
Many of the big name pathogens so familiar to us – tuberculosis, HIV, and SARS, to name a few – originated in animal species and evolved to infect humans. As such, animals are an important source of emerging infectious diseases that can threaten and have repeatedly threatened human populations. The international travel and tourism that increase the likelihood of intimate animal-human interactions also amplify the risks of novel cross-species pathogen transmission.

Wild macaques lounging at an unknown Hindu temple. Image: Shutterstock

At monkey temples, macaques can infect humans with simian T cell lymphotropic viruses (STLV), simian retrovirus (SRV), simian foamy virus (SFV), and herpes B virus (5). And, of course, there’s always the viruses that we don’t know about, the unknown unknowns. For the millions of tourists to monkey temples throughout Southeast Asia, monkey temples are one of the most important “interfaces” that exist between humans and primates. For public health officials, monkey temples are actually “a potential point source for the global dispersal of infectious agents, as world travelers can return to their homes carrying novel infectious agents transmitted from macaques … creat[ing] the potential for rapid global dispersal of primate-borne infectious agents to human populations around the world” (4).
Monkey temples are sanctified zones of interspecies interaction and worship. They also serve as a stage, an eternal petri dish, so to speak, where viruses are swapped, can genetically evolve and even develop into new primate pathogens. It’s vital to watch these commensal zones between humans and animals – especially among animals that are so closely related to humans, genetically and physiologically. Injuries associated with animals are not rare – they account for 10% of all medical consultations sought by returning tourists with dogs and monkeys ranking first and second among all animal-associated incidents (8). The unwatched, ongoing interactive space between temple monkeys and humans is a slow-moving public health train wreck in the waiting. Without monitoring both the primate and the human population and going-ons of this fascinating human-macaque sympatry, both locals and foreign visitors, we cannot know what sort of free-for-all virological party happening between us and our simian cousins. Primate viruses are getting a free pass to evolve into something much nastier with a preference for humans. As echoed in a 2006 article in The Lancet, these temples could be “opening the door for other non-human primate viruses to follow the same path in regions where human beings and non-human primates coexist” (9). And that’s no monkey business.
Resources
There is a heady mixture at play here – economic incentives from tourism, the vital religious acceptance and worship of macaques, and food sustenance and protection for the monkeys. These anthropogenic, economic and ecological factors can’t be ignored. In many temples, the sole source of nutrition for these monkeys is from tourists and sympathetic locals. Similarly, the monkeys and the temples are a vital economic resource for the surrounding communities. Check out just a few of the monkey temples cataloged at Wikipedia to get an idea of how important they are to south and southeast Asia. “Sita Sings the Blues” is a wonderful animated film on the Ramayna using Indian shadow puppets interspersed with songs by jazz singer Annette Hanshaw. You can watch it here.
References
1) L Jones-Engel L et al. (2005) Primate-to-human retroviral transmission in Asia. Emerg Infect Dis. 11(7) :1028-35
2) GA Engel et al. (2002) Human exposure to herpesvirus B-seropositive macaques, Bali, Indonesia. Emerg Infect Dis. 8(8): 789-95
3) S Radhakrishna (Editor), MA Huffman (Editor), and A Sinha (Editor). (August 27, 2012) The Macaque Connection: Cooperation and Conflict between Humans and Macaques. New York: Springer.
4) L Jones-Engel et al. (2006) Temple monkeys and health implications of commensalism, Kathmandu, Nepal. Emerg Infect Dis. 12(6): 900-6
5) A Fuentes and S Gamerl. (2005) Disproportionate Participation by Age/Sex Classes in Aggressive Interactions Between Long-Tailed Macaques (Macaca fascicularis) and Human Tourists at Padangtegal Monkey Forest, Bali, Indonesia. American Journal of Primatology. 66: 197–204
6) GA Engel et al (2002) Human exposure to herpesvirus B-seropositive macaques, Bali, Indonesia. Emerg Infect Dis. 8(8): 789-95
7) L Jones-Engel et al. (2005) Primate-to-human retroviral transmission in Asia. Emerg Infect Dis. 11(7): 1028-35
8) N Ritz et al. (2009) Monkey Bites in Travelers: Should We Think of Herpes B Virus? Pediatric Emergency Care. 25(8): 529-531
9) D Bonn. (2006) Temple monkeys: a risk to human health? Lancet Infectious Diseases. 6(7): 399
The post Hanuman’s Bite: Temple Monkeys & Pathogen Swapping appeared first on Body Horrors.
Chikungunya Virus Makes Inroads into the Americas

Posted:Wed, 15 Jan 2014 15:20:44 +0000

Well, it’s here. The mosquito-borne chikungunya virus finally trekked its way into the Western Hemisphere, arrived in the Americas, and has begun infecting Caribbean mosquitoes, confirming one of the worst fears of public health officials on this side of the prime meridian. This pathogen, notorious for its explosive outbreaks and debilitating joint pains, arrived on the Caribbean island of Saint Martin and has caused over 200 infections since December 5 of 2013. The outbreak marks the first time that chikungunya has been locally transmitted by native mosquitoes in the Americas.

The multisyllabic chikungunya is the new kid on the arbovirus block, a promising member of a squad of up-and-coming arthropod-transmitted viruses that are gaining ever more attention thanks to climate change and globalization. Discovered in southern Tanzania in the early 1950s, it’s tongue-twisting name derives from the Makonde of Tanzania and Mozambique, meaning “stooped walk,” describing the hunched, protected stance of those suffering from the severely debilitating joint pain (1)(2). In Congo, the disease has earned the name “buka-buka,” meaning “broken-broken” (3).
Infection with chikungunya virus via the bite of an infected mosquito results in an acute fever with throbbing, aching joint pain accompanied by a rash and muscle pains. Joints most commonly afflicted include the fingers, wrists, elbows, knees, ankles and toes (4). Chronic disabling joint pain following a bout of chikungunya is common and can last for months and even years.

Countries with reported cases of active or resolved infections of local transmitted chikungunya virus as of January 6, 2014. The map does not include countries where only imported cases of the virus have been documented.

Its clinical presentation resembles dengue infection, a situation that lends itself to many false diagnoses. There is no treatment, and medical care can only alleviate the excruciating symptoms of the disease. Luckily, the virus is rarely fatal, with 1 death in every 1000 cases; deaths most commonly occur in neonates and immunocompromised adults (4). High morbidity and low mortality are the characteristics of chikungunya virus.
The virus is the itinerant hippie backpacker of the arboviral group, having traipsed its way through nearly 40 countries and causing outbreaks throughout Africa, Asia, and Europe since a massive outbreak (1). For many years, chikungunya was localized to the African continent, but its recent history has been dramatic, characterized by geographic expansion ever eastwards. In early 2005, after years of sporadic outbreaks in Africa, chikungunya shifted to the Indian Ocean basin and south Asia. Over a period of two years, it caused massive outbreaks and infected nearly 2 million people, hitting large urban populations within India, Indonesia, Maldives, Myanmar and Thailand (1)(2). In some regions of India, over 45% of the population was infected with the virus (5).
From there, this viral vagabond ventured to Italy and France via an infected traveler returning from India (6). It infected nearly 200 people, spooking European health officials operating under the assumption that tropical arboviruses would never infect mosquitoes of European ilk. This outbreak was unique in that it was largely accelerated by a single nucleotide mutation that enhanced the virus’s ability to replicate in the mosquito species Aedes albopictus, though it typically infects the species of Aedes aegypti (7). The Italian outbreak is a disturbing case study for public health practitioners eyeing the Saint Martin outbreak, as French researchers noted warily in their 2011 report on chikungunya entry to southeastern France (8):

The efficient [chikungunya] transmission in Italy and southeastern France sheds new light on its dissemination potential in Europe from one index case, regardless of the viral genetic background and mosquito species in the region of origin of the imported [chikungunya].
This is why the Caribbean outbreak is so troubling: one index case, one big outbreak. In the beginning days of the Saint Martin outbreak, the European Centre for Disease Prevention and Control (ECDC) warned that there is a high risk of chikungunya expanding into nearby Caribbean islands; already cases are being reported in the isles of Martinique and Saint Barthélemy. The ECDC notes that “the [immunologically] naïve population, the presence of an effective vector in the region and the movement of people in and between islands are factors that make it likely the outbreak will continue to spread geographically and increase in numbers” (9). The onset of the Christmas tourist season did not help matters.

What could be chikungunya’s next destination? From a 2006 article, an approximation of the global distribution of the mosquito species Aedes albopictus (dotted lines) along with the distribution of variants of chikungunya virus (stars) from western Africa to southeastern Asia. The color of the stars reflects the major evolutionary lineages of the virus. Source: Parola P et al. (2006) Novel Chikungunya Virus Variant in Travelers Returning from Indian Ocean Islands. Emerg. Infect. Dis. 12(10): 1493-9.

Chikungunya’s pattern of relentless outbreaks and adaptive evolution to novel mosquito species only underscores the difficulties of containing and controlling the geographical expansion of the virus. These factors, along with its known propensity for globe-trotting, do not bode well for arresting the spread of chikungunya to other Caribbean islands, let alone to the rest of the Americas. Its appearance in the Caribbean is a nasty “happy new year” to public health officials in the region. The outbreak in Saint Martin has largely glided the radar so far as our major news outlets have been concerned, but the appearance of chikungunya on this side of the globe no doubt warrants close attention and quick action to halt its spread throughout the Americas.
This is a pattern that is occurring over and over again, one that has been repeatedly explored in this blog: novel pathogens are gaining a foothold in new territories assisted by changing climates, globalization, and international travel. As we’ve seen with the entry of both West Nile virus and dengue in the United States, this country is exquisitely vulnerable to arboviruses arriving from tropical locales. All signs point strongly to the possibility of chikungunya establishing an endemic presence in the Western hemisphere; it’s just a matter of when.
Resources
Pathogens are finding new homes in a world changed by globalization and climate. Previously on the Body Horrors blog: Imported Goods: Dengue’s Return to the United States, Valley Fever, The Archaeologist’s Scourge, Coming to America: Neglected Tropical Diseases Are Here (To Stay?).
The CDC’s recent travel watch notice regarding chikungunya in the Caribbean.
Read more here about the ECDC’s report on chikungunya’s appearance in Saint Martin rapid assessment.
References
1) World Health Organization. (January 2014 ) Chikungunya Factsheet #327. Accessed on January 13, 2014 here.
2) Chevillon C et al. (2008) The Chikungunya threat: an ecological and evolutionary perspective. Trends Microbiol. 16(2): 80-8
3) Simon F et al. Chikungunya: a paradigm of emergence and globalization of vector-borne diseases. Med Clin North Am. 92(6): 1323-43
4) Weaver SC et al. (2012) Chikungunya virus and prospects for a vaccine. Expert Rev Vaccines. 11(9): 1087-101
5) Panning M et al. (2008) Chikungunya fever in travelers returning to Europe from the Indian Ocean region, 2006. Emerg Infect Dis. 14(3): 416-22
6) Pfeffer M & Dobler G. (2010) Emergence of zoonotic arboviruses by animal trade and migration. Parasit Vectors. 3(1): 35
7) Rosenberg R & Beard CB. (2011) Vector-borne infections. Emerg Infect Dis. 17(5): 769-70
8) Grandadam M et al. (2011) Chikungunya Virus, Southeastern France. Emerg Infect Dis. 17(5): 910-3
9) European Centre for Disease Prevention and Control (ECDC). (December 11, 2013) Rapid risk assessment: Autochthonous cases of chikungunya fever on the Caribbean island, Saint Martin. Accessed on January 14 2014 here.
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Imported Goods: Dengue’s Return to the United States

Posted:Tue, 26 Nov 2013 22:20:13 +0000

Successful World War II-era campaigns to eradicate dengue has kept the United States free from the mosquito-borne virus for almost forty years but the virus is making a comeback and we have globalization to thank: an increased flow in international travel to and from tropical destinations are causing isolated outbreaks in Hawaii, Texas, and Florida. Just last week, Texan public health officials confirmed 18 cases of dengue in the southernmost tip of Texas and a recently discovered case in Long Island, NY suggesting that the virus, dubbed “breakbone fever” for its excruciating aches and pains, is gaining an unwelcome foothold in the States.

Over 380 cases of imported dengue virus were recorded for the year 2013 as of November 19th. Pink counties indicate positive test findings, whereas yellow counties are indicative of negative test findings. Image: US Geological Survey/Centers for Disease Control & Prevention.

Eradication of dengue from a region relies upon breaking the circle of transmission from human to mosquito and back to human. This requires killing every single mosquito infected with the virus while also ensuring that any individual infected with dengue is safe from mosquito bites. It can be a difficult and an extraordinarily costly process. Sadly, we are at the point of losing the hard-won achievement of a dengue-free America.

The United States is at the sweet spot for the reintroduction of this mosquito-dwelling virus. We have the mosquito vectors. We have the climate. We have the human bodies. All that’s needed is an imported case of dengue – either from an American returning from travel overseas or a visitor from a dengue-endemic country – to reintroduce the virus to the millions of biting mosquitoes that are infamous down here in the south.
Two maps from the U.S. Geological Survey perfectly illustrate the current disparity between local and imported cases of dengue. Local cases of dengue in the continental United States are currently confined to Florida and Texas, though this data may not be accurate for the current outbreak in Texas. Imported cases of dengue are another matter, with cases recorded in 36 different states. Herein lies the crux of the matter: a successful and long-standing program of disease control is being undermined by the facts of the modern age, specifically an increased access to international travel. In a few years time, will the numbers of local cases eclipse those of the imported?

Cases of locally acquired dengue virus in the United States as of November 19th for the year 2013. Cases are localized solely to Florida and Texas. Pink counties indicate positive test findings, whereas yellow counties are indicative of negative test findings. Image: US Geological Survey/Centers for Disease Control & Prevention.

As the CDC notes,

“Cases of dengue in returning U.S. travelers have increased steadily during the past 20 years. Dengue is now the leading cause of acute febrile illness in U.S. travelers returning from the Caribbean, South America, and Asia. Many of these travelers are still viremic upon return to the United States and potentially capable of introducing dengue virus into a community with competent mosquito vectors” (1).

And it is being introduced. This past May, researchers in the Laboratory of Emerging Pathogens embedded within the U.S. Food and Drug Administration issued an excellent review on the current state of dengue in the US. Their study identified common characteristics of the dengue outbreaks in the US over the past two decades and found evidence that dengue is indeed being brought into America from overseas (2).

In examining the molecular epidemiological evidence from the large dengue outbreak in 2001 to 2002 on the big island of Maui, HI, it was discovered that the outbreak stemmed from two strains of dengue, both genotypes belonging to the “Pacific subtype” that are phylogenetically similar to Tahitian strains. The epidemiological evidence suggests that at least one person, in their travels to or from or via French Polynesia, brought the dengue virus to Hawaii.
Florida is a dynamic hotspot for imported dengue with over a 100 documented cases since 2009 stemming from over thirty countries. All of the dengue strains from the 2009-2010 Florida outbreaks that have been sequenced thus far are phylogenetically related to strains from Central America, with strains unique to the celebrated travel destinations of Costa Rica, Mexico, and Nicaragua. Since the introduction and dissemination of these foreign strains to the US, the dengue virus has been undergoing “microevolution,” creating a unique “Key West sublineage” (2). In fact, the authors of the Laboratory of Emerging Pathogens review crucially emphasized that the disparate geographical origins of dengue-imported cases – from as far away as Vietnam to Venezuela – “reflects the importance of the Miami International Airport as a gateway to the USA and a possible route of entry for these and other pathogens.”

A female Aedes aegypti mosquito in the process of taking a blood meal. A. aegypti is the primary vector responsible for the transmission of dengue virus. Image: CDC/ Prof. Frank Hadley Collins.

Other major transportation hubs including Atlanta, Washington, D.C., New York City, Los Angeles and San Francisco are also likely epicenters where tropical pathogens such as Japanese encephalitis and Chikungunya virus could be making an extended layover. “Many large cities in the US are important hubs for air travel and receive a high number of individuals potentially infected with pathogens that cause asymptomatic disease … there is an increasing risk of introduction of these ‘exotic’ pathogens to urban conglomerates where mosquito vectors are present or have the potential to become established” (2).

Hunting through the imported dengue maps at the U.S. Geological Survey confirms those fears: most imported dengue cases are clustered in counties with high-density metropolitan areas. Washington’s King County. California’s Alameda and San Diego. Connecticut’s New Haven. New York County. Florida’s Miami-Dade. Dengue is back and it’s coming to a city near you.

Eradication of dengue is contingent on keeping the disease out of the United States and out of our American mosquitoes. We already have the conditions for dengue in many parts of this country – the wide distribution of the mosquito vector Aedes aegypti and a warm, temperate climate across the south - and its reintroduction from tropical areas has allowed for the possibility of (1) the disease returning to its old stomping grounds; (2) evolving into something worse; or (3) increasing its “natural” geographical distribution due to the larger population, greater turnover of people, and enhanced transport and labor connections across this country than that which existed during dengue’s earlier heyday in the 1940s.

Right now, physicians and public health officials encounter dengue as an imported medical problem, an unwelcome souvenir from a vacation abroad. Soon, however, dengue’s exotic status may be replaced with a more mundane label, one that reads, “Made in the USA.”

References

1) Centers for Disease Control and Prevention. (2010) Locally Acquired Dengue — Key West, Florida, 2009–2010. MMWR Morb Mortal Wkly Rep. 59(19): 577-81

2) G Añez & M Rios (2013) Dengue in the United States of America: A Worsening Scenario? Biomed Res Int. Epub 2013 Jun 20. Link.
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Caution to the Wind: Dirty Horns are the Clarion Call for Microbes

Posted:Fri, 15 Nov 2013 00:20:18 +0000

The professional musician who follows her dream of performing on the stage is greeted by an array of unusual occupational hazards. These are not limited to those late night hours spent in bars exposed to cigarette smoke and aggressive groupies but the risks of carpal tunnel, hoarseness, hearing loss, and the longterm effects of strange sleeping schedules as well. For those that provide their marching bands, funk joints, and jazz ensembles with that crucial brass sound, however, they may be at additional risk from a tiny threat hiding within their very own instrument.

What could be hiding in this tenor saxophone? Image: Holbox.

With every breath we take, we inhale dust, microbes, fungi, pollen and even dust mites. These particles and flecks of organic matter are often swiftly dealt with by macrophages in our lungs and cause little trouble in the healthy. But for those repeatedly exposed to airborne particles for long periods of time, the immune system can sometimes mount an attack that results in an inflammatory pneumonia, known as hypersensitivity pneumonitis or extrinsic allergic alveolitis, characterized by coughing and shortness of breath.

This lung condition is often associated with those working in occupations with frequent exposure to organic airborne particles – think farmers, machinists, and woodworkers. Cases recorded in the literature include such exotic causes including cork, chicory, blue cheese, soy sauce, metal, and esparto grass used for making paper and baskets (1-5).
But hypersensitivity pneumonitis doesn’t just strike your ordinary blue-collar blue-cheese worker; it can be a common, if underreported, condition in wind musicians who are, let’s say, a bit lax in maintaining a squeaky clean brass instrument.

In 2010, a 35-year old professional trombonist finally sought medical treatment for a cough that had lasted for 15 years (6). The musician noted that “his symptoms improved significantly when he did not play his trombone for two weeks and that the periods of more severe symptoms had been when he was playing more than usual.” This helpful tip lead to an inspection of his instrument where “innumerable” white plaques were sprinkled throughout, communities of pathologic organisms including the bacterial organisms Escherichia coli, Mycobacterium chelonae abscessus, Stenotrophomonas maltophilia, and a soil fungus of the Fusarium genus. An examination of his blood found serum antibodies to the exact same strains of these organisms, indicating a direct association between his moldy trombone and his cough (7).

Similarly, in 2009, a 48-year old man and life-long saxophonist had found himself experiencing difficulty breathing upon exertion for the past five months (8). A CAT scan showed his lungs filled with a mosaic of microscopic nodules. A sampling from his saxophone’s mouthpiece and the case grew two soil dwelling molds, Ulocladium botrytis and a species of the Phoma genus. After three months of medical treatment “in conjunction with regular drying of the saxophone after playing and cleaning with a disinfectant,” our hobbyist saxophonist beat his moldy lung infection.

And in 1988 a 65-year-old Los Angeleno who played saxophone for a local band was admitted to a hospital with a two-week history of shortness of breath and a cough that was occasionally bloody (9). A culture of his mouthpiece revealed heavy growth of three common household organisms, the fungi Candida albicans, Candida famata and a species of Cryptococcus. The authors noted that after 18 months of treatment, the musician remained healthy and now played his saxophone “with a mouthpiece which is washed with soap and water regularly.”

Two small studies of brass players and their horns have found a solid evidence pointing to frequent fungal colonization of instruments, suggesting that hypersensitivity pneumonitis and other related inflammatory-related lung conditions such as chronic cough and asthma may be related to dirty horns. A study of seven brass musicians, largely trombonists and trumpeters, found that every single player had at least one instrument growing a fungal species or a mycobacterial organism (6). Five of those seven reported lower respiratory symptoms including asthma, chronic cough and occasional shortness of breath.

Another small study looking at both the lungs and instruments of 15 saxophonists found that all but two players had frequent fungal colonization of their saxes (8). Though a wild diversity of fungal organisms were found, including Fusarium oxysporum, C. albicans, Cladosporium sphaerospermum, and additional species of Penicillum, no musicians were found with evidence ofhypersensitivity pneumonitis.

What explains this intimate relationship between saprophytes and saxophones? One key feature is that some musicians may have lax cleaning standards or an interest in preserving that special sound of spit-lined brass. One physician noted in an article on “wind-instruments lung” that “most [saxophonists] brush clean their instruments and in some cases only once or twice a year. Washing with a chlorine solution or isopropyl alcohol was never mentioned” (7). The enclosed, occasionally humid and warm, space of a saxophone, trumpet or clarinet can also create a welcoming, if slightly blustery, petri dish for growing fungi and microbes.
And there’s the fact that there’s a greater expansion of the lungs when playing a wind instrument compared to ordinary breathing and that many “brass players inhale with the instrument at their mouth between measures” (6). For some brass players, every deep inhalation from their instrument can give microbes a straight shot delivery to the alveoli of their lungs, that quick intake of air before a trill or vibrato a breath of not-so-fresh air.

Resources

So how do you clean that filthy thing? From the article, “Trombone Player’s Lung,” the authors noted that, “Because HP from exposure to aerosols containing mycobacteria or fungi is not an unusual, idiosyncratic reaction,our findings suggest that many brass musicians are at risk for HP from contaminated instruments, and standard cleaning methods may not be adequate to prevent this complication. Regular cleaning with 91% isopropyl alcohol appears to be effective.”

For more thorough information on cleaning specific instruments, you can visit this webpage from the Department of Music at the University of Nevada.

This Wiki article has a nice list of musicians – largely saxophonists! – that use circular breathing during their performances.

I would be remiss if I didn’t mention some of the best brass bands that exist and, conveniently, just so happen to live in my city – Rebirth, Dirty Dozen, and Soul Rebels. You can hear some of their music at this NPR article from 2010, “Five New Orleans Brass-Band Jams.”

References

1) A Moreno-Ancillo et al. (1997) Hypersensitivity pneumonitis due to inhalation of fungi-contaminated esparto dust in a plaster worker. Allergy Asthma Proc. 18(6):355-7

2) JA Campbell et al. (1983) Cheese worker’s hypersensitivity pneumonitis. Am Rev Respir Dis.127(4): 495-6

3) MJ Hodgson et al. (2001) Hypersensitivity pneumonitis in a metal-working environment. Am J Ind Med. 39(6): 616-28

4) Y Tsuchiya et al. (1993) Hypersensitivity pneumonitis in a soy sauce brewer caused by Aspergillus oryzae. J Allergy Clin Immunol 91: 688–9

5) G Colin et al. (2007) [Hypersensitivity pneumonitis in a chicory worker]. Rev Mal Respir. 24(9): 1139-42

6) ML Metersky et al (2010) Trombone player’s lung: a probable new cause of hypersensitivity pneumonitis. Chest. 138(3): 754-6

7) Y Cormier. (2010) Wind-Instruments Lung: A Foul Note. Chest. 138(3): 467-8

F Metzger et al. (2010) Hypersensitivity Pneumonitis Due to Molds in a Saxophone Player. Chest. 138(3): 724–726

9) S Lodha & OP Sharma. (1988) Hypersensitivity pneumonitis in a saxophone player. Chest. 93(6): 1322

F Metzger et al. (2010). Hypersensitivity Pneumonitis Due to Molds in a Saxophone Player. Chest DOI: 10.3410/f.5396957.5351055
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Halloween’s Debt to a Demonic Virus

Posted:Thu, 31 Oct 2013 19:50:51 +0000

Our demons have their origins in our dread of death and the unknown. Today is Halloween, a time for costuming ourselves and confronting those fears (and, most importantly, for outsized consumption of sweets). For those of us celebrating Halloween disguised as vampires, werewolves and zombies, we owe a great debt to one of the world’s deadliest and most feared zoonotic viruses, rabies. This past summer I wrote about the fascinating microbial origins of some of our most enduring humanoid monsters in “The Bestial Virus: The Infectious Origins of Werewolves, Zombies & Vampires.”

A woodcut from 1512 of an attacking werewolf by the German painter and printmaker Lucas Cranach the Elder. Image: Gotha, Herzogliches Museum (Landesmuseum).

An unrecognizable family member demonically possessed by some unfathomable but instantly recognizable animal instinct. The frothing at the mouth, the lucid madness, the lost humanity: it’s all here and stems from our ancient, tragic history with rabies and canines. To be human is a sacred and inviolable thing; rabies infection breaches that principal. The animal bite and the transmission of disease represent a moment of transgressive contact between animal mouth and human flesh, the possibility of losing one’s humanity and regressing to an animal state. Our horror stories capitalize on this lurid fear.
Rabies, that bestial virus, that grand transmogrifier, has terrified generations with its guarantee of “a slow warping of the mind and a pained, gruesome demise.” Its inescapable death sentence and dreadful, transformative effects in the infected have seared itself in our public imaginations while infiltrating our literature and cinemas. In celebrating this day of the dead and of temporary transformation, give a thought to one of the oldest and most untamable microbes, the rabies virus.
Read more about the history and mythology of the rabies virus at “The Bestial Virus: The Infectious Origins of Werewolves, Zombies & Vampires.“
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Plague It Again, Sam: Plague in the Twenty-First Century

Posted:Tue, 29 Oct 2013 13:30:31 +0000

The plague is an old microbial foe that has haunted our cities and our ports for millennia, killing millions of people in waves of pandemics since antiquity. But Yersinia pestis no longer has the same presence, or stranglehold, in our society and seems negligible when we consider the current state of microbial affairs – increasing levels of antibiotic resistance and novel and emerging viral pathogens, just to name a couple of today’s most pressing issues. Even its moniker, “the plague,” has been appropriated for more contemporary microorganisms that appear to come from nowhere and quickly, fatally sweep through a population – SARS and HIV are prime examples of two new “plagues.”

A female Xenopsylla cheopis flea, known as the “oriental rat flea,” one of the major vectors for transmission of the bacterium Yersinia pestis, the causative agent of plague. Image: CDC/ World Health Organization.

But the golden oldie is still alive and well in our world and, according to a recent review from the American Journal of Tropical Medicine and Hygiene, still up to its old tricks. Author Thomas Butler looks at the current shape of Yersinia pestis and asks what this old adversary of ours is doing now. What’s the scoop on plague in the 21st century? Is “ring-around-the-rosie” still relevant in this modern era of twerking? What Butler finds in his review on the modern plague is that this ancient disease “continues to surprise us with first-ever events.”
Over the past century, Y. pestis’ presence in society has been largely defanged thanks to widespread improvements in sanitation and urban hygiene. The bacteria is a zoonotic disease, reliant on fleas feasting on various rodent species spreading the infection to humans through bites. Plague is largely absent in developed societies thanks to housing and infrastructures that hinder rodent infestations and delimit exposure to fleas as they jump from their rodent host to a human one.
But in places where those luxuries are less prevalent, plague thrives within various rodent species including shrews, gerbils, prairie dogs, squirrels and voles. The bacteria has established an endemic presence in Africa, where cases of the infection comprise over 97% of the world’s 21,725 cases in the first decade of the 21st century. The Congo takes the lead in highest numbers of cases, largely owing to its widespread social destabilization from years of civil war and a concomitant breakdown in public infrastructures.
The shock value of plague lies in its infamous role in large scale outbreaks that slashed populations – the Plague of Justinian in 541 AD and the Black Death are perhaps the two most well-known historical events – but the norm for this ancient bacteria now seems to be less about massive outbreaks sweeping through populations and increasingly characterized by small, relatively isolated incidents of transmission among sub-communities within larger populations and individuals encountering the disease under less-than-mundane circumstances.
A few illustrative examples of the sub-community phenomenon: Over the course of three months from December 2004 to March 2005, 136 men working in an open-pit diamond mine in the heavily forested region in the eastern region of Oriental Province Democratic Republic of Congo were infected with the most virulent form of the infection, pneumonic plague, and 57 miners succombed to the infection (2). In the Qinghai Province of China in 2009, 12 people were infected after a herdsman was exposed to plague from a sick dog. One high profile case in the United States occurred after a wildlife biologist conducted an autopsy sans gloves and face mask on a mountain lion at Arizona’s Grand Canyon National Park.
The takeaway is not just that the susceptible population has narrowed in recent centuries – after all, virtually the whole of the human population was susceptible for much of history – but also that methods of transmission have grown more eclectic since the glory days of rats and fleas and rings around the rosie and what-have-you. Indeed, sometimes fleas, the classic culprit behind outbreaks of the plague, can be excluded from the equation altogether: outbreaks in Jordan and Afghanistan showed that exposure to meat from camels infected by rodent flea bites prior to butchering can transmit plague. In the Afghan outbreak, 83 people became ill and 17 died following contact with the meat of an infected camel.
Isolated cases and small outbreaks are driven by our interactions with animals, even with our most beloved domesticated pets. Butler writes of the discovery that pet dogs in the United States are capable of plague transmission when they trot into our homes and sleep in our beds, all the while carrying rodent fleas. We now know that “sleeping in a bed with a pet dog [is] a risk factor for human plague.”
It is this sort of series of cases and small outbreaks, from China to Afghanistan to Arizona, that serves as a reminder that this ancient pathogen can still haunt us, hiding in our backyards. Plague has adapted to our new modern world and the constraints imposed by durable housing and public health infrastructures; it now causes smaller outbreaks and isolated cases instead of sweeping pandemics, with unconventional vectors and via unexpected means. No longer a plague but as much a pest as ever.
Reference
T Butler (2013) Plague Gives Surprises in the First Decade of the 21st Century in the United States and Worldwide. Am J Trop Med Hyg. 89(4): 788-93
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The Endless Public Health Challenges of the Hajj

Posted:Wed, 09 Oct 2013 22:45:03 +0000

Next week, the hot and happening place to be is in the Kingdom of Saudi Arabia as millions of Muslims gather to complete their pilgrimage to the sacred city of Mecca, a journey known as the Hajj. For public health practitioners within Saudi Arabia and beyond its borders, the Hajj poses serious challenges in the prevention and control of infectious diseases among the millions of faithful worshipers who seek to complete one of the five pillars of Islam.

Pilgrims circumambulate around the Kaaba, a sacred Islamic building in Mecca during the Hajj. Image: Zurijeta.

It’s not only that the Saudi Ministry of Health must be on the look out for the typical pathogenic fare that thrive on large masses of humans – such as meningitis, various exotic gastrointestinal bugs, or tuberculosis – but also for more troublesome pathogens. This year in particular seems hardwired for trouble as the beginning of flu season is coinciding with continuing instances of polio trickling throughout Northern Africa and the Middle East.
As of this week, cases of polio have been reported in Afghanistan, Ethiopia, Kenya, Nigeria, Pakistan, Somalia, and South Sudan for this calendar year (1). Also of great concern is the latest pathogen to emerge from seemingly nowhere, Middle East Respiratory Syndrome Coronavirus (MERS-CoV). Since 2012, this novel virus has been smoldering in hospitals throughout the Arabian Peninsula and Europe despite the best efforts of many physicians and health officials to extinguish its insidious spread.

And, of course, there’s the possibility of the spread of bloodborne diseases. (You weren’t expecting that one, were you?)

Last year in my article “Buzz Kill: Blood-Borne Disease Transmission at the Hajj,” I wrote of the spread of pathogens such as HIV, hepatitis B, C or D among male pilgrims due to the communal usage of razor blades. A short excerpt:

Following the Stoning of the Devil and the completion of their religious rites, Hajjees migrate to Mina where hundreds of barbers await with razor blades to shave the scalps of male pilgrims and where women will trim a finger-length lock of hair. This last ritual seals the deal, so to speak, allowing pilgrims to compete their observance of the Hajj. Saudi officials require all barbers to be licensed though makeshift barbers still abound, waiting on roads for eager pilgrims with razors in hand. Pilgrims may also buddy up to shave each other’s scalps. These unlicensed barbers and pilgrims can often be found reusing unsterilized blades to communally head-shave Hajjees, a fabulous technique for transmitting blood-borne diseases (BBDs).
Indeed, physicians associated with the Saudi Arabian Field Epidemiology Training Program describe the practice of communal head-shaving at the Hajj as an ‘optimum focal setting for the spread of serious BBDs. There’s a considerable amount of hair-raising unhygienic behaviors going on – not only are unsterilized razors reused on multiple individuals, barbers often do not wear gloves, incur many abrasions on their hands and dispose of the razors improperly.
The Hajj is a powerfully holy and social event for Muslims. But it’s also unique from an epidemiological and public health standpoint: two to three million people from 70 countries meeting in one tiny place is the siren call for respiratory, water-borne and blood-borne microbial diseases. This year Saudi Arabian officials will have their hands full as they monitor and protect their pilgrims from a smorgasbord of pathogens that know no geographic borders, class or religion.
To read more about the Hajj and the unique public health challenges facing its pilgrims, check out “Buzz Kill: Blood-Borne Disease Transmission at the Hajj.”
Resources
Arab News has a wonderful write up on the precautions Saudi health officials are taking with the 2013 Hajj. Read it here.
From the Ministry of Health of the Kingdom of Saudi Arabia, the health requirements for pilgrims visiting Mecca.

Does the Middle East Respiratory Syndrome Coronavirus have a gendered dynamic of transmission in the Arabian Peninsula? I wrote about the possible influence of purdah on the transmission of MERS a few months back in the article “Purdah? I Hardly Know Ya!: Social Influences On Middle East Respiratory Syndrome.” And, yes, we do love puns on this blog.
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The Public Health Legacy of the 1976 Swine Flu Outbreak

Posted:Mon, 30 Sep 2013 13:30:55 +0000

Vaccines were once thought of as an axiomatic good, a longed-for salvation in the form of a syringe, banishing crippling and deadly infections like polio, smallpox and tetanus. But within the past few decades we have seen the emergence of anti-vaccination movements and a rise in cases of childhood diseases that are entirely preventable with a quick jab to the arm.

President Gerald Ford receiving the swine flu vaccine from his White House physician, Dr. William Lukash on October 14, 1976. Image: David Hume Kennerly. Source: Gerald R. Ford Presidential Library and Museum.

Over the past five years, outbreaks of mumps, measles and whooping cough have cropped up throughout the country. And then, of course, there is widespread skepticism among the general public on influenza and the merits of a seasonal flu shot. Even as outbreaks of avian and swine flu have periodically emerged in this country, there are still people who resist vaccination against the flu. This seemingly pervasive opposition to flu vaccination is not without its historical and sociological roots.
Some of the American public’s hesitance to embrace vaccines - the flu vaccine in particular – can be attributed to the long-lasting effects of a failed 1976 political campaign to mass-vaccinate the public against a strain of the swine flu virus. This government-led campaign was widely viewed as a debacle and put an irreparable dent in future public health initiatives, as well as negatively influenced the public’s perception of both the flu and the flu shot in this country.

A long line of people in New Jersey waiting for the opportunity be vaccinated against the 1976 swine flu. Image: CDC

In the late winter of 1976, a completely novel strain of influenza was causing hundreds of respiratory infections at Fort Dix, an army post located in central New Jersey. Initially, this virus appeared to be closely genetically related to the 1918 flu pandemic that killed over a 100 million people globally, a pandemic that shared the very same Fort Dix as one its points of origin. These striking coincidences, along with the virus’s “sustained person-to-person spread,” prompted global public health officials to start planning for what could conceivably burgeon into a series of large and deadly outbreaks, if not an actual pandemic, in the upcoming winter (1).
But while the World Health Organization adopted a cautious “wait and see” policy to monitor the virus’s pattern of disease and to track the number of emerging infections, President Gerald Ford’s administration embarked on a zealous campaign to vaccinate every American with brisk efficiency. In late March, President Ford announced in a press conference the government’s plan to vaccinate “every man, woman, and child in the United States.” (1) Emergency legislation for the “National Swine Flu Immunization Program” was signed shortly thereafter on April 15th, 1976 and six months later high profile photos of celebrities and political figures receiving the flu jab appeared in the media. Even President Ford himself was photographed in his office receiving his shot from the White House doctor.

“Get a shot of protection. The swine flu shot.” The video above shows the Ford Administration’s advertisements for vaccinating agianst the swine flu.
Within 10 months, nearly 25% of the US population, or 45 million citizens, was vaccinated, but serious problems persisted throughout the process (2). Due to the urgency of creating new immunizations for a novel virus, the government used an attenuated “live virus” for the vaccine instead of a inactivated or “killed” form, increasing the probability of adverse side effects among susceptible groups of people receiving the vaccination. Furthermore, prominent American scientists and health professionals began questioning the campaign’s large expense and its drain on scarce public health resources (2).
With President Ford’s reelection campaign looming on the horizon, the campaign increasingly appeared politically motivated. The rationale for mass vaccination seemed to stem from only the barest of biological reasoning – it turned out that the flu wasn’t even related to the virus that caused the grisly 1918 epidemic and, indeed, those who were infected with the flu only suffered from a mild illness while the vaccine, for the reasons stated above, resulted in over four-hundred and fifty people developing the paralyzing Guillain-Barré syndrome. Meanwhile, outside the United States’ borders, the flu never mushroomed into the anticipated public health disaster. It was the pandemic that never was. The New York Times went so far as to dub the whole affair a “fiasco,” damning one of the largest and probably one of the most well-intentioned public health initiatives by the US government (1).

A woman receiving a vaccination with a jet injector during the swine flu nationwide vaccination campaign, which began October 1, 1976. Image: CDC.

As the historian George Dehner wrote in his 2010 review on the lessons learned from the 1976 flu response,

The Swine Flu Program was marred by a series of logistical problems ranging from the production of the wrong vaccine strain to a confrontation over liability protection to a temporal connection of the vaccine and a cluster of deaths among an elderly population in Pittsburgh. The most damning charge against the vaccination program was that the shots were correlated with an increase in the number of patients diagnosed with an obscure neurological disease known as Guillain–Barré syndrome (1).
The American public can be notably skeptical of forceful government enterprises in public health, whether involving vaccine advocacy or limitations on the size of soft drinks sold in fast food chains or even information campaigns against emerging outbreaks. The events of 1976 “triggered an enduring public backlash against flu vaccination, embarrassed the federal government and cost the director of the U.S. Center for Disease Control his job.” It may have even compromised Gerald Ford’s presidential re-election as well as the government’s response to a new sexually transmitted virus that emerged only a few years later in the early ‘80s, killing young gay men and intravenous drug users. What happened in 1976 is a cautionary public health tale, the story of a vaccination quagmire that still resonates in the public psyche and in our discussions about vaccines today.
N.B.
Of the 45 million people vaccinated against the 1976 swine flu, four hundred and fifty people developed the rare syndrome Guillain-Barré. From the CDC,

In 1976 there was a small increased risk of GBS following vaccination with an influenza vaccine made to protect against a swine flu virus. The increased risk was approximately 1 additional case of GBS per 100,000 people who got the swine flu vaccine. The Institute of Medicine (IOM) conducted a thorough scientific review of this issue in 2003 and concluded that people who received the 1976 swine influenza vaccine had an increased risk for developing GBS. Scientists have multiple theories on why this increased risk may have occurred, but the exact reason for this association remains unknown.
It is important to keep in mind that severe illness and death are associated with influenza, and vaccination is the best way to prevent influenza infection and its complications.
Resources
“No one can predict with absolute certainty what future directions pandemic influenza might take, but we would be ill-served if we did not consider past experience.” Check out this 2009 paper from the UPMC Center for Health Security examining the “Public Health and Medical Responses to the 1957-58 Influenza Pandemic.”
An incredible factoid about President Gerald Ford from the NYT’s blog The Sixth Floor: Ford ate the same, gag-inducing lunch everyday: “Day in and day out, Mr. Ford eats exactly the same lunch — a ball of cottage cheese, over which he pours a small pitcherful of A-1 Sauce, a sliced onion or a quartered tomato, and a small helping of butter-pecan ice cream. “Eating and sleeping,” he says to me, “are a waste of time.”
How are flu vaccines made? Well, some are made using 1,200,000,000 chicken eggs.
Getting the flu shot may provide protection against heart disease, heart attacks and strokes.
September is National Preparedness Month and October marks the beginning of flu season. So why not kill two birds with one stone and get your flu shot? Use Healthmap’s Vaccine Finder to locate a pharmacy near you to be prepared for this year’s flu season.
References
1) G Dehner (2010) WHO Knows Best?: National and International Responses to Pandemic Threats and the “Lessons” of 1976. J Hist Med Allied Sci. 65(4): 478-513
3) R Krause (2006) The Swine Flu Episode and the Fog of Epidemics. Emerg Infect Dis. 12(1): 40-3
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