Microbial Misadventures is a recurring series on Body Horrors looking at instances and incidents where human meets microbe in novel and unusual circumstances that challenge our assumptions about how infections are spread.
Shout “fire” in a crowded room and watch the occupants fly for the exits. Speak the word “malaria” and watch as all within earshot reach for the nearest can of DEET. The incontrovertible fact of malaria’s relationship with mosquitos is one that has been known since Sir Ronald Ross discovered the parasite nesting within the belly of a mosquito in 1897. Such is the natural order, an incontestable necessity of the protozoan parasite’s life cycle. Humans, however, are rather adept at bucking that system – see cronuts, labradoodles, and the college bowl ranking system for examples. Also due to the interference of mankind, as a 1995 Taiwanese medical mystery proved, malaria can indeed be spread without the assistance of their obnoxious arthropod cronies.
The Democratic Republic of Congo is home to one of the largest and most biologically diverse rain forests in the world, featuring an incredible variety of animals including bonobos, forest elephants, and mountain gorillas. The country is also the stomping ground of a staggering array of microbial organisms and the region is well known as a wellspring of novel human pathogens, some with big household names and others little known. Some of these diseases, such as HIV/AIDS, have emerged as recognizably major pandemics; others, such as Ebola virus, have been limited to small, localized outbreaks; others still, such as the mosquito-borne Chikungunya virus, pose the risk of becoming new threats to global health.
Parasites and viruses once thought to make their homes exclusively in exotic locales beyond America’s borders are now gaining a foothold in the country and they are exacting significant economic tolls and placing heavy burdens on health care systems. Neglected tropical diseases such as cysticercosis, echinococcus, toxocariasis, dengue, West Nile virus and Chagas have found their way into the country due to a synergistic combination of factors, including globalization, migration, trade and climate change.
If you ever find yourself working in an infectious disease laboratory, whether it’s of the diagnostic or research variety, the overarching goal is not to put any microbes in your eye, an open wound or your mouth. Easy enough, right? Wear gloves, maybe goggles, work in fume hoods and don’t mouth pipette. When working with pathogenic bacteria and viruses, priority number one is Do Not Self-Inoculate.
Nobel Prizes! We all want one, don’t we? While fantasizing about heavy gold medallions and the Swedish Nobel Assembly, I wondered how many of the Nobel Laureate prizes in Physiology and/or Medicine have gone towards scientists studying infectious diseases, immunology and the tropical medicine field. Snooze button alert, am I right? This is the product of a one-track mind so you have my apologies. But! If it’s any consolation, there’s a story hidden in this article of a Nobel Laureate Nazi sympathizer that infected mental patients with malaria to cure them of their psychoses.
The Soviet invasion of Afghanistan from 1979 to 1988, by all accounts, did not go as well as they had anticipated. The locals were unsupportive of their efforts against the Mujahideen, the notoriously craggy terrain regularly chewed through soldiers’ boots, the Soviet army was frequently unable to provide suitable equipment, food and water to its own troops, and so on.
A parasite that infects the human brain, subtly changing its personality and social behavior, and capable of passing from mother to infect an infant in utero? That is the essence of a body horror, but this little rascal isn’t fiction. And it gets better: this parasite is considered to be one of the most successful parasites in the world due to its widespread, global distribution as well as its capacity to infect nearly every type of body tissue in all warm-blooded vertebrates (a). Schedule a phone conference with Spielberg and Cruise ASAP, guys, we’ve got the next sci-fi-action blockbuster on our hands (brains?). We’re looking at the ubiquitous protozoa Toxoplasma gondii and research on its capacity to modulate human personality and behavior.
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