Fever FAQ & Backstory


  • How do bacteria make people sick?

    Some bacteria, such as those that cause diphtheria and tetanus (lockjaw), possess toxic proteins that poison various chemical pathways of people. Similarly, the red rash of scarlet fever is caused by a toxin from strep bacteria. Other bacteria interact with our immune system in very complicated ways, and the products of these interactions may damage human tissues. The symptoms of bacterial meningitis is an example of that.

  • How did the bacteria that caused Brazilian Purpuric Fever, the infection highlighted in Fever, make children so deathly ill?

    Don’t know. It may have something to do with the way the BPF bacteria, once they get into the blood of the patients, interact with the insides of blood vessels. Possible mechanisms include binding of the human protein called complement factor H to bacterial proteins called factor H binding proteins, with subsequent abnormalities in the patient’s complement system. Other possibilities may involve BPF bacterial proteins that act as toxins for the cells lining blood vessels.  The reason that the usually benign BPF bacteria caused such deadly infections in healthy children in Brazil remains a mystery. 

  • What happened to the ordinary bacteria that turned them into the deadly BPF strain?

    Again, don’t know. Somehow, while the bacteria were living peacefully in the throats of children (where they normally live without causing any trouble), they picked up a new characteristic: the ability to live in the blood of people and then to cause the lethal symptoms of BPF.  Bacteria, like all living things, commonly change, ie genetically evolve into new variants. Every time they reproduce, a mistake may occur in their DNA that changes the function of the proteins made by that stretch of DNA. Most of the time the new characteristics of the variants damage the bacteria and they don’t survive. Rarely, new characteristics of the bacteria may cause previously unrecognized, and possibly serious, illnesses in people.  This likely happened with BPF, although the exact new characteristic acquired by mutation isn’t known.

  • Why did the outbreaks of BPF infections disappear?

    Likely, while the BPF strain was deadly for a few otherwise healthy children, it was a weakling that was unable to successfully compete for nutrients with the non-BPF bacteria that normally live in people’s throats. The non-BPF bacteria won the war, and the BPF bacteria disappeared. 


In late 1984, ten healthy young children from Promissāo, a farming village in Sāo Paulo State, Brazil, developed pink eye, followed several days later by high fever, expanding purple patches on their skin, cardiovascular collapse, and death. Brazilian health officials contacted an American expert in infectious diseases, who then contacted the Centers for Disease Control and Prevention in Atlanta, Georgia. Numerous clinical tests on the sick children from Promissāo, including blood cultures, antibody measurements, and autopsies, failed to reveal the cause of the illness, which was called Brazilian Purpuric Fever (BPF) to reflect the country of origin and two major symptoms, purple skin patches and fever.

A year and a half later, eleven children from Serrana, another farming village in Sāo Paulo State, developed BPF. Most were hospitalized at a nearby teaching hospital in Ribeirāo Preto. There, microbial cultures of blood and other bodily fluids from the children grew the bacteria that the author studied her entire professional career. The form of the bacteria from the children with BPF almost never causes serious infections. Years of study by many scientists has yet to identify how these usually benign bacterial variants became so deadly. The mystery remains.  Fortunately, the outbreaks stopped on their own and have yet to reappear.

The novel Fever is a fictional representation of what could have transpired during the search for the cause of BPF and for measures to prevent and treat it.

A scientific review of the BPF story appears in Clinical Microbiology Reviews, Oct. 2008, p. 594–605 Vol. 21, No. 4; doi:10.1128/CMR.00020-08.