Malaria was a major risk for American troops during World War II. The US Army enlisted the help of Theodor Geisil, Dr Seuss, to produce educational booklets and pamphlets (discussed here). They also turned to moving pictures to educate the troops. Private Snafu was featured in a catalog of 26 SNAFU training films based on characters originally developed by Theodore Geisil and Phil Eastman and produced by Warner Bros. If these World War II cartoons has a familiar look, they were produced by Chuck Jones who produced most of the Looney Tunes and Merrie Melodies cartoons we all grew up with. These are the only two on malaria that I have found. Enjoy!
Last week photos of Roman toilets were splashed across the web breaking the news that the Romans were not a healthy as most people seem to have assumed. As with many public health interventions, the real value of a sanitation system is out of view (and out of mind) to most people. Its not the toilet that keeps us healthy; its the water treatment plant. Plumbing just moves waste with its microbes and parasites from one place to another.
Paleoparasitology specialist Piers Mitchell put the Roman public health system to the test by evaluating the evidence for human parasites in archaeological remains from before, during and after the Roman Empire. Comparisons before and after the empire are more difficult in North Africa and the Middle East because these areas had long standing sophisticated civilizations before the Roman empire. There is more clarity between civilizations in Europe since Celtic and Germanic societies did not have anything like Roman infrastructure. Contrary to his expectations, there were just as many parasites and ectoparasites in the Roman era as before or after. In some cases the empire helped spread parasites across Europe. Relative amounts of parasites across times is difficult to ascertain for a huge variety of reasons. So while the same parasites were present, the degree of infestation would have varied by place and time period, and archaeology can’t reliably predict this.
The Roman achilles’ heel was their use of human waste for fertilizer and fecal contamination of rivers. Human waste was added to the other manure and redistributed to farm fields and the watershed. What they could not have understood is that human waste is a greater risk for the transmission of human parasites and bacterial diseases. Mitchell also suggests that Roman bath water, that was rarely changed, could have transmitted worm eggs and other parasites. Aquaducts did bring in cleaner water to some of the larger cities but the system could be contaminated and not all Roman sites had access to water from aquaducts. Walter Scheidel (2015:8) has claimed that the city of Rome itself was an example of the”urban graveyard” effect with a very unhealthy population despite having a “heavily subsidized food and water supply”. Scheidel emphasizes the impact of malaria and gastrointestinal disease. We should also keep in mind that a large proportion of gastrointestinal disease would have been bacterial or viral.
As the mosaic to the left shows, the Romans did change agriculture throughout the empire. They spread Mediterranean preferences for cereals and more fish and other aquatic food sources. Mitchell suggests that the Roman love for fish products, especially the fermented fish sauce garum, probably help spread fish tapeworms found throughout the empire. Many parasites and bacterial spores have evolved to withstand preserving methods like smoking, pickling, and osmotic preservation (like salting or sugaring). Whipworm was the most common parasite found, but round worms and tape worms were also common. Lancet liver flukes were widespread and indicate the (presumably accidental) consumption of ants. Antibody based detection (ELISA) has been able to identify Entamoeba histolytica that causes the usually endemic amoebic dysentery (as opposed to the epidemic bacterial dysentery caused by Shigella species). Although not strictly speaking parasites, Mitchell notes an abundance of evidence for flies around cesspits suggesting that they contributed to the spread of diseases associated with fecal contamination. He also notes that schistosomiasis has not been identified in Roman Europe, even though it has been found in medieval European remains.
Turning to ectoparasites, Mitchell found ample evidence of head lice, body lice, public lice, human fleas and bed bugs across the Romanized world. Human fleas (pulex irritans) have been particularly well preserved in Roman, Anglo-Scandinavian and medieval York in Britain. Mitchell notes that human fleas and body lice were present in over 50 archaeological layers at York. He concludes that “the Roman habit of washing in public baths does not seem to have decreased their risk of contracting ectoparasites, compared with Viking and Medieval people who did not use public baths in the same way” (Mitchell 2016: 6). Mitchell suggests that there were enough ectoparasites to support particularly lice transmitted diseases. He notes that Plague of Justinian was transmitted by fleas but is non-committal on the likely specific vector.
In examining the impact of the Roman empire, Mitchell notes that the transition from a wide variety of zoonotic parasites to those primarily associated with human fecal contamination had already occurred before the Roman expansion out of Italy. This shift is paralleled elsewhere and is tied to shift from hunter-gathers to settled agriculture. Whipworm, roundworm and amoebic dysentery were the primary parasites of Roman Europe, while the Romans seem to have made a lesser impact on North Africa and the Middle East where endemic zones of parasites were well established.
Malaria is the one parasitic disease I would have liked to see Mitchell discuss more. Mitchell notes that malarial aDNA has been found in Egypt and anemia possibly caused by malaria in Italy. He overlooks all the malaria work by Robert Sallares including malarial aDNA from Late Roman Italy and better anemia studies correlating with malaria have been done in Italy and Britain by Rebecca Gowland’s group. Yet, malaria is such a big topic that it would be hard to cover along with all the other parasites.
Hall, A., & Kenward, H. (2015). Sewers, Cesspits, and middens: a survey of the evidence of 2000 years of waste disposal in York, UK. In P. D. Mitchell (Ed.), Sanitation, latrines and intestinal parasites in past populations (pp. 99–120).
There are over a hundred different species of the malaria-causing Plasmodium parasites in reptiles, birds and mammals. Being so widespread among terrestrial vertebrates, zoonotic transfer of Plasmodium has come at humans from multiple different sources. Plasmodium knowlesi had been known for some time as a parasite of long-tailed macaques but was not considered a significant human parasite until 2004 when a large number of human infections were identified in Borneo. Molecular analysis implies that Plasmodium knowlesi is as old as Plasmodium vivax and Plasmodium falciparum.
Diagnosis is complicated by the histological similarity between Plasmodium knowlesi and Plasmodium malariae. They can’t be distinguished in blood smears like those shown here, so infections were most often misdiagnosed as P. malariae even though they cause a quotidian (daily) fever. The WHO recommends that microscopic detection in areas where P. knowlesi is found report positive results as “P. malariae/P. knowlesi”. It can only be securely diagnosed by molecular methods that can distinguish all five human malarial species. PCR based detection methods have shown promise but no one method has been clinically tested with a large enough number of cases to become the standard of care. Antibody-based Rapid Diagnostic Tests (RDT dipstick tests) for malaria do not reliably detect knowlesi malaria which was discovered in humans after the RDT tests were developed. For now in resource poor areas, microscopic analysis followed by molecular testing where available is the only way to detect knowlesi malaria. Clinical research continues for a RDT test that can be employed areas with poor laboratory resources.
Infections have now been confirmed in all of the countries of southeast Asia. Between 2000 and 2011, 881 cases of local P. knowlesi local transmission have been identified in Borneo, with only 8 cases of P. malariae. It is now suspected that past diagnoses of P. malariae in the region were actually P. knowlesi. Unlike other forms of malaria, P. knowlesi infects more adults than children, although actual infection rates are still not known.
Long-tailed and pig-tailed macaques are the reservoirs for P. knowlesi. In some areas of Malaysia the macaques are around 90% seropositive for malaria, in one study 87% were P. knowlesi. The malaria vector for P. knowlesi and other malarial parasites is Anopheles leucosphyrus group which is also concentrated in southeastern Asia. Anopheles balabacensis is the most efficient vector, capable of transmitting P. knowlesi from monkey-to-human, human-to-human and human-to-monkey. A. latens, on the other hand, has been most commonly indicated as the vector to humans in Borneo, where it feeds in the high elevation canopy. As the map below shows, the macacque reservoir and the mosquito vectors are limited to the islands and peninsulas south-east Asia. It has been hypothesized, based on genetic diversity, that P. knowlesi has caused human malaria as long as humans, macaques and the Anopheles vectors have all been on the islands of south-east Asia.
Difficulty in diagnosis has made it made it challenging to study the full spectrum of knowlesi malaria across the population. What studies have been done show that it produces a full spectrum of malarial disease from mild to fatal. Most cases reported to-date are in adult males, making an occupational exposure a significant possibility.
Symptoms are representative of other malarial infections: fever, chills and rigor, headache, along with a cough, abdominal pain and diarrhea. Gastrointestinal symptoms correlate with high levels of the parasite in the blood. Thrombocytopenia (low platelet counts) is the most common clinical finding and more severe than in either vivax or falciparum malaria, while anemia appears to be mild in knowlesi malaria. In the few pediatric cases that have been observed, they all responded to anti-malarial therapy. In the few cases of severe disease reported, abdominal symptoms have been so severe in some that malaria was not initially suspected. Acute Respiratory Distress Syndrome (ARDS) has been reported in about 50% of severe cases and acute renal failure in approximately 40%. There have not yet been enough confirmed cases of knowlesi malaria to accurately determine the case fatality rate. Although it appears to respond to a wide range of anti-malarial drugs, an optimized treatment based on a sufficient number of cases was not yet available in 2013.
The discovery of Plasmodium knowlesi in humans comes in the context of increasingly successful control of vivax and falciparum malaria in southeastern Asia. Some of the latest epidemiology from Malaysia suggest that 50-60% of the cases of malaria are now knowlesi. There are fears that knowlesi will jeopardize regional malaria elimination efforts. Is the rate really increasing or is it only apparent as levels of falciparum and vivax decrease? Does a real increase represent an opening niche for knowlesi as vivax and falciparum decrease? Only time and more data will answer our questions.
Singh, B., & Daneshvar, C. (2013). Human Infections and Detection of Plasmodium knowlesi. Clinical Microbiology Reviews, 26(2), 165–184. doi:10.1128/CMR.00079-12
For additional epidemiology from Malaysia:
Yusof, R., Lau, Y. L., Mahmud, R., Fong, M. Y., Jelip, J., Ngian, H. U., et al. (2014). High proportion of knowlesi malaria in recent malaria cases in Malaysia, Malaria Journal13(1), 1–9. doi:10.1186/1475-2875-13-168
William, T., Jelip, J., Menon, J., Anderios, F., Mohammad, R., Mohammad, T. A. A., et al. (2014). Changing epidemiology of malaria in Sabah, Malaysia: increasing incidence of Plasmodium knowlesi, Malaria Journal13(1), 1–11. doi:10.1186/1475-2875-13-390