It can be hard to comprehend the damage that pathogenic viruses and microbes can inflict on the human body, especially if you have scientists prattling on about cells, using multi-syllabic acronyms and tossing around – god forbid! – actual numbers. It’s helpful to have easily understood images to help put diseases into perspective, to understand that viruses like HIV have tangible and real effects. That’s why I’m so happy to have stumbled upon an incredible image from a 2004 paper that is a pictorial testament to the immunological blitzkrieg that is HIV infection.
This is the story of a sailor and a pirate, and the two different types of oceans that they traversed. There are seven on Earth but only one courses through man. This ocean contains no mysterious and pale sea creatures, bottomless depths or brightly-flashing predators, but it does brim with industrious cells, with dissolved carbon dioxide and occasionally with unwanted parasites.
In August of 1961, a Norwegian teenager sailed from a fjord in Oslo through the North Sea and the Atlantic Ocean to Douala, Cameroon, a port tucked under the outward slab that makes up West Africa. He was a freshly turned fifteen year old and was working as a kitchen hand on a Norwegian merchant vessel. From Cameroon, he and his crew on the Hoegh Aronde sailed northwesterly from port to port, docking at Nigeria, Ghana, Cote D’Ivoire, Liberia, Guinea and Senegal over a period of 10 months before returning to his homeland (1).
It was an exotic start to what would be a short but wide-ranging career as a sailor – over a period of four years, he would call at ports in Asia, Europe, Canada and throughout the Caribbean. Though he would never find himself in West Africa again, he would always carry a souvenir of his visit to this incredibly diverse and ecologically rich niche of the world.
His journeys were lonesome, solitary. In Cameroon the sailor unburdened himself of his loneliness and slept with at least one woman, catching gonorrhea – this much is known. Perhaps it was the same woman or another that infected him with an unfamiliar virus simmering away in West Africa just waiting to travel foreign oceans and lands. A viral hitchhiker with a proclivity for the horizon, a pirate if you will. This virus, a certain strain of HIV included in the rare outlier group O that is genetically and immunologically distinct from the main group M that is plaguing the world today, a HIV group that native to West Africa and to Cameroon in particular but found itself in a Norwegian man who would travel the world.
When he returned to his homeland in 1965, he married and became a father to two children in a short two-year span. In spite of his exciting new role as husband and father, he often felt unwell and his family was plagued with strange illnesses. His muscles ached, a red rash covered his body and he found himself often besieged by respiratory ailments (2). In 1967, his wife became ill with fevers, an omnipresent yeast infection as well as the same respiratory infections that lurked in her husband. The next year, the sailor would see his youngest daughter developing unusual diseases not often seen in toddlers – arthritis, blood and bone infections, along with the same yeast and respiratory infections afflicting her family.
Despite his poor health, the sailor found himself crossing the sea again to Europe. From 1969 to 1973, he worked as a long-distance truck driver delivering cargo as he traversed Belgium, the Netherlands, France, Germany, Austria, Switzerland and Italy (1).
With his ailing family far away across the North Sea, the sailor would seek refuge again in Europe. His coworkers would later say that he slept with many women and prostitutes along his long and lonely lorry routes. Often beginning his route in Wesseling, Germany, he would deliver to Liége and Lyons in France, occasionally stopping in Reims between the two cities (1). Investigators in this part of France would later find cases of HIV group O in individuals that had died in the late 1970s and early 1980s but had never visited verdant Cameroon.
In 1974, the sailor fell deeply ill. He died two years later, at the age of 29, his body riddled by bizarre diseases and was followed quickly in death by his wife and his youngest daughter. Autopsies would find puzzling results – overwhelming systemic infections not often seen except in the severely immunocompromised. The pathologist conducting the autopsy would save the sailor’s lymph node, liver, kidney and lung, the mother’s leg muscle and the daughter’s lymph node, spleen and liver and, years later, the family’s serum samples would test positive for HIV antibodies. This unfortunate family, to this day unidentified, represent the first recorded cluster of confirmed HIV/AIDS infections in the pre-AIDS era, before the AIDS pandemic sparked in the late 1970s and early 1980s. The sailor’s daughter is the earliest known case of pediatric AIDS (3).
“The sea has neither sense nor pity,” wrote Anton Chekov in his short story “Gusev”. Blood churns, dark liquids pumped through the valves by the stalwart heart, all the while feeding our bodies oxygen. A corrosive virus pirates the sea, hijacking cells and visiting the ports of our body, our brain, muscles, spleen and liver. Why infect that one person, at that moment in time? There is no meaning or sense to it. The tides rise, the tides fall. The earth spins, blood spills. A ship makes its port on schedule, becomes lost or is brought to the bottom of the sea. A man dies from an infection caught 15 years earlier in a distant port, a salty partner that he introduced to his family. There is no meaning, little salvation and only grief.
This article was awarded the Best Life-In-Science post at the inaugural ScienceSeeker awards for 2012-2013.
If you’d like to read the “Gusev” story by Chekhov, you can do so here.
Shortly after the researchers’ work into the Norwegian AIDS cluster, researchers from Tulane discovered evidence that a St. Louis teenager, Robert Rayford, was infected and died of AIDS in 1969. His case is troubling – a 15 year old succumbing to an infection that typically takes year before progression to AIDS and death. Some sources claim he was a gay prostitute while others say that he was sexually abused as a child. Whichever tragic alternative it may be, the fact remains that this boy had never traveled outside of St. Louis, someone infected him and that AIDS was most certainly circulating in a limited fashion in the United States before the 1970s. Read more about him in this 1988 New York Times article.
A few months back, I created a playlist of hip hop and R&B artists singing about the HIV/AIDS crisis and admonishing safe sex to their listeners. Check out the playlist and accompanying article “Let’s Talk About Sex: Hip Hop on HIV” here.
1) Hooper E. (1997) Sailors and star-bursts, and the arrival of HIV. BMJ. 315(7123): 1689-91
2) Lindboe CF et al. (1986) Autopsy findings in three family members with a presumably acquired immunodeficiency syndrome of unknown etiology. Acta Pathol Microbiol Immunol Scand A. 94(2):117-23
3) Frøland, SS et al. (1988) HIV-1 infection in Norwegian Family before 1970. Lancet. 1(8598): 1344-5
Frøland SS, Jenum P, Lindboe CF, Wefring KW, Linnestad PJ, & Böhmer T (1988). HIV-1 infection in Norwegian family before 1970. Lancet, 1 (8598), 1344-5 PMID: 2897596
I know that the study of infectious diseases seems grim. Bacteria are increasingly becoming antibiotic resistant, baby parasites nest in your brain and tuberculosis spreads to your toes. I get it – all this devotion to the study of what gruesome-thing-du-jour is in your blood and saliva isn’t sunshine, puppies and rainbows. So in the interests of maintaining public optimism, I offer you GBV-C, a virus that has been found to offer a protective, antiviral effect against HIV infection. Yes, that HIV.
With Hanukkah and Christmas just recently past and Chinese New Year fast approaching, it seems a suitable time to consider the topic of religious celebrations and infectious diseases, no? ‘Tis the spirit and all! I’ll be looking at one of most intriguing religious events in the world, the Islamic pilgrimage to Mecca known as the Hajj, and the special epidemiological event that accompanies it.
Every profession seems to have its own tailor-made occupational hazard. Veterinarians suffer bites and scratches, office workers struggle with carpal tunnel syndrome, anxiety torments professional graduate students and so on. A few years ago, I was stunned to hear that butchers, fish-mongers and those intimately involved in the meat-handling trade (please don’t read into that any more than is necessary) are more likely to be infected with a certain strain of Human Papillomavirus (HPV). Odd, huh? And kind of gross.
So I haven’t shown my face around here for a few months. What can I say? It’s a disgracefully long absence.
My excuse is that I enforced a blog black-out due to a big time-consuming “life project” I’m cultivating. Since May, I’ve had a jaw-dropping number of applications and essays and transcripts and requests and what-not to worry about; dedicating a few hours to researching and writing about fun diseases was not in the works. I sincerely apologize if you had been planning on reading riveting Body Horrors blog material on your beach vacation. But not to worry! I plan on publishing articles with some regularity now that I have some time on my hands. Expect fun stuff about botulism, Ebola, onchocerciasis and other frightful microbiological demons.
As a peace offering to tide you over until the next article, I provide you visual stimulation from the Youtube domain. Behold!
These two delights come from the French NGO Aides, an organization focusing on awareness of HIV/AIDS and viral hepatitis. They produce some genuinely saucy animated PSAs addressing condom usage and HIV/AIDs transmission. These are supremely R-rated, NSFW videos that strike me as distinctly French. It stretches the limits of my imagination to think of these showing in the United States. My favorite is the xenophilic Smutley, a cat frolicking to the tune of Joan Jett’s “Bad Reputation” in the first PSA. The second video emphasizes the effortlessness of rapid finger-stick testing for HIV/AIDs infection along demonstrating a few other (sexually explicit) uses for your fingertips.
I’m begging you: please don’t watch these at work or with children in the room.
Also! Have you seen the Contagion trailer? “Someone doesn’t have to weaponize bird flu. The birds are doing that.” LOL! Weapons of avian destruction, I presume? Holy bird flu, Batman, put watching this movie on your to-do list!
See you soon. I promise.
A recent article detailing the sad situation of a transplant patient contracting AIDS from the kidney of a living donor, despite negative tests 11 weeks prior to the surgery, had me thinking about transfusions, the blood supply and the spread of infectious disease (a). Unsavory musings, yes, but there’s one particularly exotic disease and a rather sensitive public health situation that I was thinking about that I wanted to explore in this post.
Chagas disease (Trypanosoma cruzi), otherwise known as American trypanosomiasis, is a protozoan parasite endemic to Central and South America. The CDC estimates that a staggering 16-18 million people are infected with T. cruzi in Latin America, mostly in rural locales, with another 25,000 to 100,000 infected immigrants in the United States (b). Typically, the disease is transmitted by triatomine insects that blood-feed on a humans. Their infective feces often enter the bite wound, oral or nasal mucosa, or conjunctivas and transmit the flagellate parasite.
The disease has two specific phases. The acute phase is usually a mild febrile infection lasting anywhere from weeks to months. Following this acute phase, researchers believe there is life-long infection with the parasites hiding in the blood and organs of the infected person. Years or decades later, 10 to 30% of those cases can progress to chronic Chagas disease.
The clinical manifestations of chronic Chagas disease are ugly business, characterized by enlargement of the heart and digestive tract, “megaesophagus” and “megacolon” being two common presentations of digestive tract pathologies. Electrocardiographic abnormalities, myocardial lesions, constipation and dysphagia (difficult or painful swallowing) are just a few of the symptoms resulting from infection (c)(d). There is no vaccine for primary infection and no effective drug therapy available for the chronic stages.
The disease may also be spread by congenital infection, oral infection through contaminated fruit, and, as you can guess, by blood transfusion and organ transplantation. Platelet transfusions and renal transplants in particular seem to be problematic, suggesting an as yet unknown immunological component of T. cruzi infection; the liver, pancreas and heart have also been implicated in so-called “allographic transmission” resulting from organ transplantation (b)(h)(i).
Prior to the successful Southern Cone Initiative that tackled both the eradication of the triatomine bug as well as initiating large-scale blood-screening efforts in Latin America in 1991, blood transfusion-transmitted Chagas was a critical public health problem with infectivity rates ranging from 13 to 49% (f). As the issue started drawing attention in public health sectors in the United States, the American Red Cross (ARC) conducted a study and observed evidence of increasing prevalence of the disease in blood donors in Southern California throughout the early 1990s (g). This increase was attributed not only to changes in donor and population demographics but also as a result of recruitment efforts directed towards minority donors in Los Angeles at the time (h).
As late as the year 2007, no policies were in place for compulsory blood-bank screening for Chagas in the United States (b). Upon the release of the first F.D.A. licensed serological test using a parasite lysate ELISA for T. cruzi blood screening in January of 2007, the ARC and Blood Systems Laboratories conducted a study using the test on 14 million blood donors over 16 months. They detected over 500 confirmed Chagas-infected donations (28% of the sample), with the majority of those cases from California and Florida (g).
In terms of actual transmission events in North America, the only reliable numbers I was able to hunt down in the literature were five blood transfusion-transmission and five organ transplant-transmission cases since 1993, an extraordinarily low number (g). Indeed, researchers believe that number to be too low to serve as any true indication of this phenomenon in the US (g)(d).
Of course, this Chagas story has traces of the HIV-infected blood transfusion panic in the late 1980s. Regrettably, there’s even a minority group entangled in the plot-line; evidence strongly suggests that Chagas-infected blood and organs originate from seropositive immigrants from T. cruzi endemic Latin American countries. Luckily, research has consistently indicated that blood donor recipients from seropositive donors are rarely infected with Chagas disease (f)(g)(h). Compared to the 93% of recipients that contract HIV after an infected blood donation, only 13% of recipients become infected after blood transfusion owing to factors such as parasite strain and levels of donor parasitemia (g). Recipients of platelets appear to be most at risk, most likely due to their immunocompromised state (f). The risk for allographic transmission seems to be much greater, determined to be as high as 35% for recipients of infected kidneys (i).
The past several decades have seen the proliferation of blood-bank screening for blood-borne diseases such as HIV-1 and HIV-2, hepatitis B and C, HTLV-I and -II and the etiological agent of syphilis, Treponema pallidum. The HIV epidemic really dragged this issue kicking and screaming to the forefront and since then there have been fantastic strides in implementing screening efforts as well as increasing public awareness of these issues. Chagas disease is the latest infectious disease agent to enter the equation and public health officials have put several tests in place to screen both blood and organ donors for antibodies to previous or ongoing Chagas infection. Of course, blood transfusions and organ transplants are never risk-free but knowing what blood-borne pathogens are lurking out there is the biggest part of the battle.
(a) “Transplant patient got AIDS from new kidney; living donor was infected” Arizona Daily Star. 17 Mar. 2011. Web: 20 Mar. 2011
(b) Centers for Disease Control and Prevention (CDC) (2002) Chagas disease after organ transplantation – United States, 2001. MMWR Morb Mortal Wkly Rep. 15:51(10):210-2
(c) Despommier, D, Gwadz RW, Hotez PJ & Knirsch CA. Parasitic Diseases. 5th ed. New York: Apple Trees Production, LLC. 2006
(d) Dias E, Laranja FS, Miranda A & Nobrega G. (1956) Chagas’ Disease: A Clinical, Epidemiologic, and Pathologic Study. Circulation. 14(6):1035-60
(e) Busch MP, Kleinman SH & Nemo GJ. (2003) Current and Emerging Infectious Risks of Blood Transfusions JAMA. 289(8):959-62.
(f) Leiby DA, Read EJ, Lenes BA, Yund AJ, Stumpf RJ, Kirchhoff LV & Dodd RY. (1997) Seroepidemiology of Trypanosoma cruzi, Etiologic Agent of Chagas’ Disease, in US Blood Donors. J Infect Dis. 176(4):1047-52.
(g) Bern C, Montgomery SP, Katz L, Caglioti S & Stramer SL. (2008) Chagas disease and the US blood supply. Curr Opin Infect Dis. 21(5):476-82.
(h) Leiby DA, Herron RM Jr, Read EJ, Lenes BA & Stumpf RJ. (2002) Trypanosoma cruzi in Los Angeles and Miami blood donors: impact of evolving donor demographics on seroprevalence and implications for transfusion transmission. Transfusion. 42(5):549-55.
(i )Kun H, Moore A, Mascola L, Steurer F, Lawrence G, Kubak B, Radhakrishna S, Leiby D, Herron R, Mone T, Hunter R, Kuehnert M; Chagas Disease in Transplant Recipients Investigation Team (2009) Transmission of Trypanosoma cruzi by heart transplantation. Clin Infect Dis. 48(11):1534-40
Centers for Disease Control and Prevention (CDC) (2002). Chagas disease after organ transplantation–United States, 2001. MMWR. Morbidity and mortality weekly report, 51 (10), 210-2 PMID: 11922190