Archive for the 'Differential diagnosis of Ebola' Category


October 8, 2014


Dr. Lawrence Broxmeyer, M.D.


The CDC recently declared:

“Diagnosing Ebola in a person who has been infected for only a few days is difficult, because the early symptoms, such as fever, are nonspecific to Ebola infection and are seen often in patients with more commonly occurring diseases, such as malaria and typhoid fever.”

Only a sin of omission. then, would explain why anyone or any group would not want to specifically mention the most commonly occurring cause of infectious death in Africa ― tuberculosis ― whose sky-high rates in West Africa make Ebola look like a dropper-full of water squeezed into the Mississippi.

If by October, 2014, Ebola had laid claim to what some say is 3,000-plus deaths since its February outbreak, certainly this ought to be weighed in the light of the approximately 600,000 Africans killed by TB in the same time-frame. Furthermore, although TB incidence is decreasing globally, incidence rates are increasing in most of West Africa (1) ― ground zero for the current Ebola outburst. Just as curiously, almost half of all TB cases in the West African Ebola zone are caused by an unusual, yet just as deadly member of tubercular family, Mycobacterium africanum ― a strain of tuberculosis exclusive to West Africa, which is fast becoming a microbe of great public ― and now possibly global concern.

Surely the CDC is aware that there is not a sign or symptom of Ebola, including its hemorrhagic tendencies that cannot be found in acute disseminated miliary (blood-bourne) tuberculosis, once called “galloping consumption” ― the single most feared form of the disease ever. And most likely it is also aware that such tuberculosis has its own viral-like forms, some of which can simulate the Ebola. Such viral TB is generally acknowledged to be TB’s preferred form ― as a survival strategy to storm any inclement conditions the microbe might find itself in. (2)

Then why did the CDC not mention TB, by name, in their short-list of possibilities that could cause Ebola-like symptoms? If such oversight stopped there it would be unremarkable, but it seems to have been carried over in the very design of the most recent diagnostic tests issued to detect Ebola.


In September of 1978, about 40 years ago, a team ― including a 27-year-old medical graduate, training as a clinical microbiologist at the Institute of Tropical Medicine in Antwerp, Belgium, received a blue thermos from Zaire. It was filled with the two 5ml. clotted blood specimens of an African-based Flemish nun. The Belgium doctor who sent it, Jacques Courteille, practicing in Kinshasa, included a note saying that he was at a complete loss for the nun’s mysterious, yet deadly illness. Also, could the samples be tested for Yellow Fever? This thermos had traveled from Zaire’s capital city of Kinshasa, on a Sabena commercial flight to Belgium ― inside its deliverer’s hand luggage. When the samples were received, Peter Piot, the 27-year-old medical graduate and his colleagues, among other things, placed the blood samples under an electron microscope. Piot: “We saw a gigantic worm like structure ― gigantic by viral standards. It’s a very unusual shape for a virus, only one other virus looked like that and that was the Marburg virus.”

But the new “virus” needed a name. Piot relates the interesting tale of how Ebola came to be named as Ebola:

“On that day our team sat together late into the night – we had also had a couple of drinks – discussing the question. We definitely didn’t want to name the new pathogen “Yambuku virus”, because that would have stigmatized the place forever. There was a map hanging on the wall and our American team leader suggested looking for the nearest river and giving the virus its name. It was the Ebola River. So by around three or four in the morning we had found a name. But the map was small and inexact. We only learned later that the nearest river was actually a different one. But Ebola is a nice name, isn’t it?” (3)

Depends upon how you look at it.

Piot’s specimens proved negative for Yellow Fever and he mentions that the tests for Lassa fever and typhoid were also negative. What, then, could it be? Piot: “To isolate any virus material” small amounts of the blood samples were injected into VERO cells and into mice. Several of these mice subsequently and abruptly died ― “a sign that a pathogenic virus was probably present in the blood samples that we had used to inoculate them.”

The fact that the mice died did not mean that it was at the hands of a “pathogenic virus”. Piot’s boss, Stefaan Pattyn, who Piot admitted “could be a bit of a bully”, supposedly specialized in the study of mycobacteria ― tuberculosis and leprosy, yet seemed unaware of the hemorrhagic consequences of acute TB, nor had he taken the time to use special stains and cultures to detect its viral cell-wall-deficient forms. Instead Pattyn followed his current passion. He had recently worked in Zaire for six or seven years and exotic viral illnesses were now “right up his alley”. So Pattyn’s team likewise never really considered a strain of acute miliary TB or its viral cell-wall-deficient forms in his rule-outs for an acute hemorrhagic or epidemic fever ― among them Mycobacterium tuberculosis and Mycobacterium africanum.

The Ebola of its day on steroids, “galloping” acute consumptive tuberculosis could kill in days ― the mere memory of which, just a few generations ago, brought terror to the faces of those who had witnessed and were describing it. Dubos made clear that “galloping consumption” was not an isolated, but a frequent diagnosis in the 19th and early 20th centuries. (4) And despite persistent myths to the contrary, in the early phase of any new TB epidemic from a new and virulent strain, tuberculosis manifests itself as an acute disease and only much later as the chronic pulmonary tuberculosis that we know in today’s western world. An example of this can be found in the high mortality during the 1918 influenza pandemic, when African-Americans were brought to fight in France during World War I ― large numbers of them dying from a fast-tracked tubercular “galloping consumption.”

Many often underestimate the speed, contagiousness and ferocity of a TB epidemic. Khomenko’s 1993 study (5) should have cemented the notion that the explosive contagiousness of just such Ebola and influenza-like viral forms of tuberculosis are exactly the stuff that previous epidemics and pandemics could have been made of. But it didn’t.

In the US, the CDC and NIH seemed to feel differently, ignoring the historic possibility. There was much the same viral passion, at that time over “Influenza”, when in 1990, a new multi-drug-resistant (MDR) tuberculosis outbreak took place in a large Miami municipal hospital. Soon thereafter, similar outbreaks in three New York City hospitals left many sufferers dying within weeks. By 1992, approximately two years later, drug-resistant tuberculosis had spread to deadly mini-epidemics in seventeen US states, and was reported, not by the American, but the international media, as out of control. Viral forms of swine, avian and human TB can be transmitted from one species to another. So can exotic strains of tuberculosis and Mycobacterium africanum, imported into the United States through countries such as Liberia. By 1993 the World Health Organization (WHO) had proclaimed tuberculosis a global health emergency (6). That emergency has never been lifted.
Anderson pointed out that such acute, untreated disseminated, “galloping”, blood-dispersed TB could kill in hours or days (7) ― its mortality, according to Saleem and Azher even today approaching 100%. (8) Ebola itself can take up to a month to kill its victims, said Ben Neuman, an expert in viruses at Britain’s Reading University ― although there are many cases that also kill in hours or days. Not only were tubercular hemorrhaging and fever both mentioned by Fox (9), but hemorrhaging of the serous cavities, the gums, and the nose, into the joints, the skin, and the bowels. Appleman (10), in the American Journal of Ophthalmology, considering massive spontaneous hemorrhages into the vitreous, mentions that Axenfeld considered acute tuberculosis an important possibility in the rule-out for bleeding into the eye. Coughing-up blood has always been a well-known scenario for TB. Hemorrhages of significance fro Read the rest of this entry »