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Teenage emigrant presents with fever, headache, myalgia
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A 16-year-old boy presents to his primary care office in the month of January with 5 days of fever, chills, headache and myalgia, with no nausea, vomiting, diarrhea, cough, congestion, rash or other complaints — only fever. Further history revealed that the patient emigrated from Nigeria, Western Africa 2 1/2 weeks earlier, which was about 2 weeks before the onset of his illness.
The patient is visiting the U.S. for his college education, and staying with relatives. All other members of the household are well, with no other known sick contacts. His immunizations are up to date and documented. When growing up in Nigeria, he had a few episodes of malaria, including at least one hospitalization, but his past medical history is otherwise that of a healthy adolescent boy. According to the patient, his last episode of malaria was apparently about 5 months earlier, but there are no medical records with the patient.
Examination in the office revealed a very bright adolescent male with a fever (temperature, 103°F) and a normal exam. A rapid flu test in the office was negative, and he was sent to the local children’s hospital ED, where he had a full sepsis work-up, including a lumbar puncture because of the headache. All lab tests were normal except the WBC count on the CBC, which was only 4.1, with some unusual-appearing RBCs (Figures 1-2).
Case Discussion
Even though he emigrated from Africa, clearly, this was not a Zika virus infection. This is a case of malaria (A), with the smear showing the ring form of Plasmodium falciparum within the RBC (erythrocytic stage). Depending on the stage of the infection, there are other forms, such as the extra-erythrocytic gametocyte (Figure 3), that may be seen on the same smear, which the Anopheles mosquito (Figure 4) picks up as she takes a blood meal. The organism is a protozoan, which parasitizes the red blood cells through a fairly complex life cycle, the details of which are beyond the scope of this brief column. One should be aware that once infected through the bite of the mosquito, there is a liver phase and a blood phase, which includes the erythrocytic phase.
There are five species of Plasmodium: falciparum, vivax, ovale, malariae and knowlesi. P. falciparum is most common in Africa. Symptoms typically begin within 2 weeks of being bitten, with fever being the most common symptom, often with vomiting and fatigue. Sometimes, headache is present, which may raise concerns for central nervous system involvement, which may result in seizures and death. Because malaria is not endemic in the United States, all you really need to know is that malaria is high on the differential diagnosis of a patient with unexplained fever who has recently traveled to, or lived in, an endemic area, especially if he or she did not take malaria prophylaxis.
The next step is to obtain a thick and thin smear of blood for the lab to review for the presence of the characteristic intraerythrocytic parasites. If positive, the next step is to call the Malaria Division of the CDC (1-770-488-7788), or you can call an infectious diseases consultant, who will call when you hang up (at least, that’s what I do the few times I have seen malaria). The CDC consultant will know all about the resistance pattern in the area where the patient had visited and will give very specific advice on treatment.
In the above case, the recommendation was to treat with atovaquone/proguanil hydrochloride (Malarone, GlaxoSmithKline) for 3 days, with an uneventful recovery. In fact, the patient knew what he had, and thought we were “nuts” for putting him through a full sepsis work-up when all he needed was a few doses of atovaquone/proguanil hydrochloride.
One might ask why was he not immune? After all, he supposedly had malaria on at least a couple of other occasions in Nigeria. The answer is that you can never be permanently immune. Repeated infections provide some partial immunity. However, after a few months, immunity wanes and certainly after a few years without reinfection, the patient may be just as susceptible as if never infected before. This fact was unfortunately demonstrated when Ali Maow Maalin died of severe malaria July 22, 2013, at 58 years of age.
Mr. Maalin became famous as being the last person to have endemic smallpox in October 1977 in Somalia. He dedicated his life to helping with the polio eradication project, working as a certified vaccinator. As a lifelong resident of Somalia, he certainly had been infected with malaria in his past, but that did not help when he became infected with a severe, fatal case of malaria later in life. This can be a difficult concept to get across to the adults who have not visited their home country in recent years, and want to take their children to see their grandparents. They frequently think that because they grew up in a country with malaria, that they are immune, and therefore, do not need prophylaxis. I often use Mr. Maalin’s story to convince them otherwise.
There are genetic factors that help protect some members of the population from malaria. Hemoglobinopathies, such as sickle cell trait, hemoglobin C, thalassemia and glucose-6-phosphate dehydrogenase deficiency provide some natural protection, as apparently, these protozoa do not find the erythrocytes of these patients suitable.
Please refer to my column in May 2003 for another case of malaria with more discussion. There is a live, attenuated vaccine in development that apparently shows promise. Stay tuned.
Babesiosis is caused by another intraerythrocytic parasite, Babesia microti (Figure 5), which is transmitted by the bite of a tick, causing a flu-like illness, similar to malaria in most symptomatic cases. Most infections are asymptomatic, but in some individuals, it can be life threatening. Babesiosis is seen in the United States in the Northeastern and Midwestern parts of the country. If the “Maltese Cross” form is seen, as seen in Figure 5, it is virtually diagnostic. Antibody testing can be used in cases where no parasites are seen microscopically. Treatment is usually with clindamycin plus quinine or atovaquone plus azithromycin for 7 to 10 days.
Leishmaniasis should not be in the differential diagnosis. It has been featured in my column on three occasions; August 1991, March 1996 and January 2014, which you may find useful.
- Reference:
- Snider R, et al. Pediatr Infect Dis J. 1993;12(2):145-148.
- For more information:
- James H. Brien, DO, is with the department of infectious diseases at McLane Children’s Hospital, Baylor Scott & White Health, Texas A&M College of Medicine in Temple, Texas. He also is a member of the Infectious Diseases in Children Editorial Board. Brien can be reached at: jhbrien@aol.com.
Disclosure: Brien reports no relevant financial disclosures.