Category Archives: Africa

Reactivation of Ancient Plague Foci in Libya, 2009

Landscape around Oran, Algeria,  and Tobruk, Lybia in 2009 that produced plague cases. (Cabanel et al, 2013)
Landscape around Oran, Algeria (2003), and Tobruk, Lybia (2009) that produced plague cases. (Cabanel et al, 2013)

Plague has been called a re-emerging disease primarily because cases have begun to appear in areas where plague has been absent for decades. Two recent surprising outbreaks occurred in Algeria, where plague had been absent for over 50 years, and in Libya after a 25 year absence. A team led by the Institut Pasteur explored possible relationships between the recent Libyan outbreak and the Algerian outbreaks. All of the information in this post comes from their report to be published in the February issue of Emerging Infectious Diseases (citation and link below).

The outbreaks under consideration were just south of Oran, Algeria in 2003, at Lanhouat, Algeria in 2008 and near Tobruk near the Libyan-Egyptian border in 2009. Another possible outbreak of plague occurred at Tobruk during the Libyan revolution in 2011.  Political unrest prevented a complete disease investigation of the 2011 Libyan epidemic. Past Libyan plague outbreaks have occurred from 1913-1920, 1972, 1976, 1977, and 1984. The largest outbreak in 1917 is credited with 1,449 deaths.

The 2009 Libyan index cases consisted of three children from one nomad family; one child died after two days of intensive care and the other two eventually recovered. Only one child had a tender cervical node. The other two, including the child who died, had signs of a severe infection but no visible buboes. The father reported having axillary lymphadenitis and a couple of sudden deaths in the region in the previous two months. A week after admission Libyan authorities reported 13 possible cases to the World Health Organization and requested assistance. The WHO-Libyan team identified two more women with painful inguinal nodes and “infectious syndrome”, but also concluded the initial estimate overstated the number of cases. There are five confirmed cases. The cases were spread 30-60 km from the index family’s home in Eltarsha, 30 km south of Toburk. Regional response included antibiotic treatment of contact persons, and insect and rodent control measures. No further cases were reported.

Diagnosis was confirmed by standard bacteriological assays and molecular characterization. All five confirmed cases were positive with the F1 antigen dipstick.  Yersinia pestis cultures were isolated from three patients,  all phenotyped to the Medievalis biovar by metabolic assays. Molecular characterization confirmed that all are the same Medievalis strain. Hybridization analysis indicates that it is most closely related to, but distinct from, strains isolated from Iranian Kurdistan in 1947 – 1951.

Using the same methods, the 2003 Algerian isolates were phenotyped to the Orientalis biovar. Molecular characterization confirmed that they are all related but not identical Orientalis strains. Activation of multiple related strains from an ancient foci in the same year suggests an environmental trigger. Comparing the 2003 strains to those isolated in 1944 and 1945 illustrate the complexities of plague foci. The 1944 isolate is a Orientalis strain that belongs to the same cluster of strains as the 2003 isolates and other strains from Morocco and Senegal.  The 1945 strain matched a molecular characterization of  Orientalis isolates from Saigon, Vietnam and is believed to have been transmitted by military transports during World War II.  Cabanel et al conclude that the 2003 Algerian outbreaks were caused by local Yersinia pestis strains. It should be noted that the third pandemic from the turn of the 20th century was a Orientalis biovar (1.Ori1).

Cabanel et al. note this is the only instance they could find of a Medievalis strain in Africa. The spread of cases over a 30-60 km region and isolation of related but different strains support the reactivation of an ancient plague focus. Unfortunately they did not have access to isolates from previous 20th century Libyan outbreaks (if they exist) that could have provided more certainty.

Reactivation of plague foci around the Mediterranean has been associated with climate change. They note that an unusually humid winter and good crops in Libya in 2009 favored rodent and flea abundance. Long dormancies may be part of Yersinia pestis’ natural history particularly in resource limited environments. This possibility will be one of the topics of my next post.

Cabanel et al. note that camel meat and livers have been associated with human plague cases in Libya (1976), Saudi Arabia (1994), Jordan (1997), and Afghanistan (2007). Additional local evidence suggested that the highly susceptible camels contracted the plague from local foci in these instances. Although camels do not survive plague long enough to transmit it very far, camel caravan routes may still have played a role in transmission if only by the other organisms also along the camel caravan route. Camels would have provided an abundant host to amplify the organism along the route. Camel fleas could have been carried among the cargo not unlike rat fleas in ship cargoes. Camel caravans would provide an ancient route for a Medievalis strain to reach Libya from the central Asia.

Reference

Cabanel, N., Leclercq, A., Chenal-Francisque, V., Annajar, B., Rajerison, M., Bekkhoucha, S., Bertherat, E., & Carniel, E. (2013). Plague Outbreak in Libya, 2009, Unrelated to Plague in Algeria Emerging Infectious Diseases, 19 (2), 230-236 DOI: 10.3201/eid1902.121031

ResearchBlogging.orgplague series

When Yellow Fever Came to the Americas

“Yellow Jack”, Cornhill Mag., 1892

In the early Americas, nothing scared people more than when Yellow Jack came knocking at the door of their city. Yellow Jack, or as we know it better today Yellow Fever, has rightly been called the plague of the Americas.

It has long been assumed that yellow fever came to the Americas with its vector, Aedes aegypti, in the hold of slave ships. These ships would have been an irresistible feast to the mosquito. Yet, little was known about the origin, locations, and dates of transmission to South America. Juliet Bryant, Edwarld Holmes and Alan Barrett (2007) looked to DNA analysis of yellow fever virus (YFV) strains from 22 countries ( 14 African and 8 South American) to resolve and date the phylogentic tree for YFV. They analyzed 133 isolates from humans and animal hosts collected over a 75 year period.

Bryant, Holmes and Barrett (2007: e75) made four clear observations.

  1. The American strains represent a single clade (monophyletic).
  2. There are two distinct sub-clades in east and west South America respectively.
  3. The South American clade is most similar to the West African isolates.
  4. The East African clade is the most distinctive.

These observations support an east or central African origin for the Yellow Fever Virus dominated by enzootic transmission. Its development parallels the transmission of its vector Aedes aegypti.

The split between the east and west African clades has been calculated to an average distance of 723 years (roughly 1284 AD). The West African isolates are the most diverse in Senegal, suggesting this was an early focus for West African YSF. From West Africa Yellow Fever was transmitted to Brazil a calculated average of 470 years ago (roughly 1537 AD). Early Portuguese seamen frequented this part of Africa and Brazil was their largest colony, founded in 1500. This suggests that Yellow Fever was transmitted to Brazil virtually from the beginning of the Portuguese colony. It is possible that Yellow Fever was one of the imported diseases brought by the Portuguese that decimated native Brazilians before large-scale importation of Africa slaves. The South American clade split into eastern and western populations when it was transmitted to Peru a calculated average of 306 years ago (roughly 1700). There is no evidence of transmission back to Africa or other areas where Aedes aegypti have spread in Asia. Byrant, Holmes and Barrett (2007) argue that sylvatic transmission is the primary means of maintaining YSF in South America. They note that there hasn’t been an urban epidemic of YSF in South America since 1928, unlike the annual urban outbreaks in West Africa.

Auguste et al (2010) confirmed the overall structure of the YSF phylogenetic tree in the Americas, including its Brazilian origin in the Americas. Their analysis of strains collected over the last decade also confirm that Brazil is the reservoir and origin for most strains in the Americas today with the Peruvian strains remaining primarily localized in Peru and neighboring Bolivia. The analysis of Auguste et al (2010) also supports enzootic maintenance and local evolution in areas of spread from Brazil such as Trinidad and Columbia.

What I find most surprising about the YSF tree is its relative youth. This all suggests that Yellow Fever originated in the Middle Ages and probably did not circulate outside of local areas of central Africa until the late medieval period. We still have a lot of learn about the landscape epidemiology of yellow fever including possible vertical transmission among mosquitoes and the importance of difference primate species as reservoirs. Although we have had an effective vaccine for decades, yellow fever is still a very clear and present danger in both the Americas and Africa.

References:

J E Bryant, E C Holmes, & A D T Barrett (2007). Out of Africa: A Molecular Perspective on the Introduction of Yellow Fever Virus into the Americas PLOS Pathogens, 3 (5) : doi:10.1371/journal.ppat.0030075

Auguste, A.J., Lemey, P., Pybus, O.G., Suchard, M.A., Salas, R.A., Adesiyun, A.A., Barrett, A.D., Tesh, R.B., Weaver, S.C. & Carrington, C.V.F. (2010). Yellow Fever Virus Maintenance in Trinidad and Its Dispersal throughout the Americas, Journal of Virology, 84 (19) 9977. DOI: 10.1128/JVI.00588-10

Uganda’s 2006 Plague Outbreak

People are sometimes surprised to learn that the plague still exists today. They ask me why they  have never heard about it in the news. Well, it is occasionally in the news for a day and then we go on to the next crisis. Today plague outbreaks occur in parts of the world that don’t get  good or sustained news coverage.

About 90% of plague cases reported to the World Health Organization today  come from Africa.  Uganda experiences about 200-400 cases per year with an case fatality rate of 30%. This cluster of 127 cases occurred between July and December of 2006 in the Arua and Nebbi districts of northwestern Uganda. Some of the initial patients did not seek medical care because they believed the illness and deaths were due to a local feud. Only when people not associated with the feud died did they begin to seek medical treatment at a local clinic. Diagnosis of plague by symptoms can be difficult enough without patients attributing illness to supernatural causes.  Cases were spread over the region with four villages producing ten or more cases and nine villages producing at least two cases.

Due to a lack of clinical laboratories in the region, most patients had to be diagnosed by clinical symptoms: a sudden fever, chills, headache, fatigue, and a painful, swollen lymph node(s) in bubonic plague or a bloody cough in pneumonic plague. Development of the plague rapid diagnostic test was done for areas like this region of Uganda where lab facilities are sparse. These newer tests appear not to have been available for this outbreak. Of the 127 recognized patients, 88% had bubonic plague and 12% had pneumonic plague. Once villagers began seeking treatment they were given antibiotics and most recovered. The overall fatality rate for this outbreak was 22%, although 11 of 12 cases of pneumonic plague died.

Pneumonic cases clustered in families. In one documented cluster, a 10 year old boy initially developed bubonic plague with a bubo on his neck. He developed a bloody cough and soon died, to be followed by the deaths of mother, grandmother and aunt. Two others from this village also died of pneumonic plague. In another cluster related to this outbreak (but excluded from study data) a 15 year old girl contracted pneumonic plague while visiting relatives in the Nebbi region and returned to her home district of Masindi, starting an outbreak the killed seven.

Interviews were conducted with 39 recovered patients from two villages. Dead rats reported in or around the homes of 59% of the interviewed patients, including some who buried the dead rats near their homes. Four of eight dead rats collected by the investigative team from these two villages tested positive for Yersinia pestis. Trapped live rats were found to have an average of two fleas per rat; more than one flea per rat is associated with increased risk of plague transmission.

While this outbreak may seem small compared to medieval plagues, this is the spark from which a great epidemic can grow. Antibiotics and knowledge of the importance of rodents in transmission prevent these epidemics from growing. The people in these villages didn’t associate rat deaths with their illness and neither did medieval people. Plague is still very much on the radar screen of ministries of health throughout Africa and around the world.

Reference:
ResearchBlogging.org
Centers for Disease Control and Prevention (CDC) (2009). Bubonic and pneumonic plague – Uganda, 2006. MMWR. Morbidity and mortality weekly report, 58 (28), 778-81 PMID: 19629028