Blackwater Fever

Right under our noses the patient had lost the number of red cells contained in almost a quart of blood--and nobody had the faintest clue why.

By Tony Dajer|Friday, May 01, 1992
RELATED TAGS: INFECTIOUS DISEASES
He looks sick to me. Really sick.

The worried tone in the resident’s voice, even amid the hubbub of a busy emergency room, caught my attention like a shout. I quickly finished with the chart I was writing and made myself available.

What’s the story? I asked her.

Twenty-year-old Chinese male came in last night complaining of headaches and fevers. The night team thought it might be meningitis, so they did a spinal tap. But the lab just called, and the fluid’s clear, so there’s no meningitis. And now his temperature is back up to 103.

Before Barbara, the resident, had found me, she had mentioned the case to the staff neurologist, who was in the emergency room to examine someone else. A quick detour into our patient’s room was enough to plant a worried frown on his owlish features.

I can’t find anything abnormal, he said, after giving our patient a quick neurological exam. There was nothing that might indicate a brain tumor, stroke, abscess, or other obvious source of head pain. Unfortunately he doesn’t speak any English, so it’s tough to get the story. But one thing’s for sure: he’s got a heck of a headache. He suggested it might not be a bad idea to get a CT scan.

As we clustered outside the patient’s room, a nurse handed us the results of his second blood count. We all gaped. Six hours earlier the fraction of his blood made up of red cells had been 36 percent--low, but not dangerous. Now it was 30 percent. Right under our noses he had lost the number of red cells contained in almost a quart of blood--and nobody had the faintest clue why.

I turned to Barbara. Where’s this kid from?

Southern China, we think, came the reply. There were no interpreters who spoke Cantonese in the hospital last night. Two of the night team examined him, and as best as they could tell, he’s been in the States for three or four months. Apparently he’s had bad headaches for a while.

As if unleashed from deep within some mnemonic curio box, a swarm of tropical diseases suddenly came to mind, a veritable menagerie of illnesses caused by protozoa, nematodes, fungi, viruses, and bacteria. But no obvious candidates to explain the young man’s symptoms came into focus.

Okay, before we do anything else, let me take a look, I said, more to fulfill my role as Barbara’s supervisor than out of any hope, as the fifth doctor in line, of sniffing out any missing clues.

After a parting good luck from the neurologist, we trooped back into the exam room. I gave the young patient my best friendly wave, but all he could do was hold his head in a way that says agony in any language. I felt his forehead. It was burning. His sheets were soaked. But with the rest of his exam I drew a blank. Everything was normal: neck supple, lungs clear, heart regular, abdomen soft, skin unblemished. When I was done, Barbara and I quickly reviewed where we were and what we knew. The answer was, to quote Dashiell Hammett: Nowhere and nothing.

There was only one thing to do. I tilted my head back and shouted: Anybody here speak Cantonese? Two nurses turned and pointed to Judith.

Judith was one of the best nurses in the emergency room-- indispensable for keeping young residents out of trouble and older attending physicians in line. I trotted over to her and clasped my hands together in a gesture of supplication.

With Barbara and me in tow, Judith approached the young man’s bedside. I told her what little we knew of his medical history, then asked her to take it from the top: How long had he been in the States? When did he get sick? From the stream of rapid-fire Cantonese that followed, I realized she was, unprompted, moving on to the next several questions on my list.
While we waited for Judith’s translation, I glanced at the patient’s clear plastic urinal. It was almost full and the urine was brown, a deep mahogany brown. Suddenly, as if it had been kicked in just the right spot, my brain’s gearbox came unstuck.

Have you ever heard the term blackwater fever? I asked Barbara.

Um, no, she answered, then gave me an expectant look.

I pointed to the urinal.

In the old days they used to call falciparum malaria--the most severe form of the disease--blackwater fever because the intense destruction of red cells it causes turns a patient’s urine black. My hunch seemed farfetched, though. Many other diseases cause dark urine, and malaria is no longer indigenous to this country. Virtually all U.S. cases-- about 1,100 in 1990--are found in travelers or newly arrived immigrants. Most American doctors never even see a case. I could hardly wait to hear where this guy had been.

Judith supplied us with the answers. He’s only been in the States three weeks, not three months. He’s had fevers and headaches since he got off the plane. Went to three doctors in Chinatown who gave him pills, but none helped.

Where did he fly in from? I asked.

Thailand, said Judith

And where did he start out from?

Southern China.

But, I dimly remembered, Thailand and China had no common border. How did he get to Thailand?

He left China by crossing through Burma, came the reply. On foot. All the way. The journey took about two weeks.

Now his symptoms began to make more sense. Eastern Burma is a hotbed of malaria, especially falciparum malaria, which is resistant to chloroquine, the standard drug used to treat the disease. And the incubation period for malaria is two weeks. Had he been bitten by a malaria-carrying mosquito in the jungles of Burma, the fevers and headaches wouldn’t have started until he arrived in the United States.

For a firm diagnosis, however, a smear of blood would have to be put under the microscope and inspected for malaria parasites. Bloodsucking mosquitoes merely transmit malaria from one human host to the next; the actual cause of the disease is one of several tiny parasites that attack the red cells in human blood. The exam would tell us which strain of malaria the young man had--provided, of course, that it was malaria we were dealing with. We sent off a tube of blood to the lab right away, but it would take 30 minutes to prepare the slide. Not that we had time to sit around; there were plenty of other patients in the emergency room with maladies less exotic but no less urgent.

Malaria is now rare in the United States, but it once was a killer. It loosened its grip on the American South only in the late 1940s. Over the centuries it has brought down empires, decimated armies, and depopulated vast tracts of land, especially in equatorial countries. Indeed, the force of its onslaught is inscribed in our very genes. Sickle- cell anemia is a major health problem among African Americans; it arises from a mutation in the gene for hemoglobin, which carries oxygen and colors blood cells red. Before the advent of modern medical care, inheriting a pair of sickle genes, one from each parent, would have doomed a person to a painful early death. But inheriting only one sickle gene offered a critical advantage: greater resistance to malaria. In other words, a potentially deadly gene flourished because, for some, it conferred protection against malaria. Unfortunately, for an individual living in a malaria-free country such as ours, the mutant gene no longer has benefits, only costs.

In the tropical world, however, malaria remains a plague. In 1991 some 150 million people contracted it, and almost 2 million--mostly children--died. Malaria has not only withstood everything that modern medicine has thrown at it but it is even regaining lost ground. In the 1950s global campaigns were launched to stamp out the disease and its pesky mosquito vector. DDT became the new miracle insecticide, and chloroquine the new antimalaria magic bullet. Yet 35 years and billions of dollars later, all that has changed is that from Peru to Nigeria to Vietnam, mosquitoes have become DDT-resistant and falciparum malaria has become impervious to chloroquine. Meanwhile, even the world’s greatest immunology labs have failed to come up with a vaccine that works.

As a final slap in the face to modern technology, the ultimate drug against malaria is still quinine, just as it was 300 years ago. And old prevention methods, such as using mosquito nets and draining stagnant pools where mosquitoes breed, have recaptured center stage. Our ancient foe, it seems, is sending us a very modern warning about nature’s capacity for retaliatory strikes.

Here, though, I wasn’t going to let this grim disease gain the upper hand. But before we could treat our patient, we still needed confirmation of my diagnostic hunch. Finally, we got the call from the lab. Barbara grabbed the phone. It took only seconds to relay the message.
It’s malaria! she cried. And it looks like falciparum.

I collared the other resident on duty.

Come on, you won’t see a slide like this every day.

The three of us charged out of the emergency room and grabbed the elevator to the lab. The technician had the slide ready. She adjusted the microscope.

There, right in the middle of the field, you can see the ‘signet ring.’

My eyes adjusted to the scope, and I focused on several of the pale pink blood cells. Smack in the middle of one of them was the bluish circular band crowned by a tiny ruby: the one-celled protozoan named Plasmodium falciparum. Yet there was no obvious evidence of the destruction wrought by this pretty killer. That, too, I learned, is one of falciparum’s tricks. It doesn’t simply do its dirty work by destroying red cells. It also makes their membranes sticky and causes them to clump in vital organs such as the liver, the kidneys, and the brain, cutting off their blood flow. The result is often permanent organ damage or, in the case of cerebral malaria, death.

The residents took turns looking through the microscope. Exclamations filled the room as an image they had seen only in textbooks came into focus. We had our diagnosis. Now it was just a matter of administering the right dose of quinine, adding a boost of tetracycline, and our young visitor would be cured.

On our way out of the lab, we looked like a team trading high fives in the end zone. As I looked at the happy faces, I knew mine was no different. It occurred to me then what an odd bunch we doctors are-- celebrating tiny smudges on microscope slides and all articulating the same astonished monosyllable in the face of a deadly pathogen: Wow!
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