Iron Deficiency Anemia Linked to Severe Pediculosis Capitis in a 12-Year-Old Boy

Introduction

Pediculus humanus capitis, colloquially known as the head louse, causes the most prevalent form of human pediculosis, affecting millions of individuals worldwide across all socioeconomic strata each year [1]. An estimated 6 to 12 million individuals in the United States are treated for head lice annually, with children aged 3 to 12 years representing the largest group affected [1]. Head lice are transmitted exclusively among humans, primarily through direct head-to-head contact or indirectly via sharing infested personal items [2]. Diagnosis is confirmed through the direct visualization of lice, which can be achieved using the naked eye, magnification devices, or fine-toothed combs [2]. Treatment aims for the complete eradication of lice, which, depending on the severity of the infestation, may require a multi-step, multifactorial approach. Physical lice removal methods include shaving the affected hair, wet combing, or manually removing each louse and nit [1]. However, even a single surviving louse or viable nit is sufficient to sustain the infestation. Consequently, topical pediculicides are considered the first-line treatment for lice infestations [1]. These pediculicides function as neurotoxins, inducing paralysis of the lice, and by physically suffocating the lice, ensuring effective eradication [1]. While much of the literature highlights the social implications of head lice, this paper shifts focus to a potentially serious medical complication arising from prolonged, severe infestations: iron deficiency anemia (IDA).

Iron deficiency is the leading cause of anemia in the United States, representing 50% of all anemias [3]. However, the prevalence of IDA among males under 50 years of age is less than 1% [3]. Iron deficiency can arise from one or a combination of the following factors: inadequate intake, impaired absorption, blood loss, or increased systemic demand [3]. Growth spurts are associated with a substantial rise in hemoglobin concentration, necessitating increased levels of iron [4]. This heightened iron demand during the adolescent growth spurt makes this age group especially susceptible to the adverse effects of iron deficiency.

Although a direct causative relationship between head lice and IDA has not been established, several case reports and case series have suggested a potential association, particularly in the absence of other identifiable causes. Two separate case series, presented by Al Ghadeer et al [5] and Guss et al [6], describe patients of varying ages, genders, and demographics who developed IDA in the context of severe lice infestations. Al Ghadeer et al reported cases involving young female siblings [5], while Guss et al focused on adult patients [6]. In both series, the authors attributed the anemia to chronic blood loss from lice feeding, referencing a study by Speare et al that estimated a daily blood loss of 0.7 mL in individuals with heavy infestations [7]. Additional case reports have drawn similar conclusions, including those of a 13-year-old girl reported by Ogbuji et al [8] and an 11-year-old boy described by Hau and Muhi-Iddin [9].

The present report presents the case of a 12-year-old boy from Missouri, USA, presenting with IDA and a chronic infestation of head lice. This case report is published with written parental permission.

Case Report

We present the case of a 12-year-old boy with a medical history significant for asthma and eczema who was admitted to the pediatric intensive care unit (PICU) for severe IDA and concurrent head lice infestation after presenting to his pediatrician complaining of vomiting.

Prior to his initial presentation, the patient had experienced several months of fatigue, postural lightheadedness, headaches, nausea, vomiting, and a non-productive cough. There were no symptoms suggesting an obvious source of blood loss, such as hematochezia, melena, epistaxis, or easy bleeding or bruising. Over the preceding 3 months, he had been sent home from school on 5 separate occasions due to illness and required frequent daytime naps. His mother reported living in an overcrowded, unhygienic trailer. Nutritionally, the patient had an imbalanced diet, potentially lacking sufficient iron-rich foods, and he consumed between 24 and 30 ounces of cow’s milk daily.

His pediatrician ordered basic laboratory tests, including a complete blood count (CBC), which revealed a hemoglobin level of 3.4 g/dL, prompting immediate transportation to the emergency department (ED). Examination in the ED was notable for slight tachycardia with a heart rate exceeding 100 beats per minute, diffuse pallor, and an incidental discovery of extensive pediculosis capitus (Figure 1), with scalp erosions and excoriations extending across his neck, upper chest, and bilateral upper extremities. The lice infestation was promptly addressed by shaving the affected hair and applying topical permethrin 1%. Further laboratory workup in the ED confirmed marked IDA. CBC showed microcytic hypochromic anemia: hemoglobin 3.3 g/dL, hematocrit 14.8%, mean corpuscular volume (MCV) 50.3 fL, and mean corpuscular hemoglobin concentration (MCHC) 22.3 g/dL. Iron panel revealed profound iron deficiency: iron level 8 μg/dL, ferritin 1.7 ng/dL, iron saturation 1.9%. A packed red blood cell (pRBC) transfusion was initiated in the ED to address the boy’s anemia, and he was admitted to the PICU for continued workup and treatment.

During the patient’s 4-day hospital admission, he underwent extensive testing to investigate any other potential sources of anemia, all of which returned unremarkable. Peripheral blood smear demonstrated markedly microcytic, hypochromatic erythrocytes without sickle cells or findings suggestive of thalassemia. A negative fecal occult blood test (FOBT) and computed tomography (CT) scan of the chest, abdomen, and pelvis ruled out a gastrointestinal bleed as a cause of his anemia. A thorough infectious disease workup, including tests for HIV, acute hepatitis, syphilis, inflammatory markers, blood cultures, and stool ova/parasites, was non-contributory. Hemolysis markers, including bilirubin, haptoglobin, lactate dehydrogenase (LDH), and Coombs, were all within normal limits. A comprehensive metabolic panel (CMP) showed a creatinine level of 0.43 mg/dL, indicating adequate renal function and erythropoiesis.

Further treatment while hospitalized included a second application of topical permethrin 1% to his shaved scalp and 2 additional aliquots of pRBC transfused at 5 mL/kg over 3–4 hours. On the day of discharge, his hemoglobin had improved to 8.2 g/dL with an MCV of 64.7 fL. He and his mother received inpatient nutritional counseling and instructions to substantially reduce or eliminate cow’s milk consumption. Case management provided the mother with education on treating other household members and ensuring proper eradication of lice at home to prevent reinfection. The patient was discharged on continued oral iron supplementation with ferrous sulfate 325 mg twice daily.

Following discharge, the patient continued outpatient follow-up with Pediatric Hematology and Oncology for 5 months, with resolution of his microcytic hypochromic anemia, iron deficiency, and associated symptoms. By the time of his official discharge from the clinic, his laboratory results had stabilized, showing a hemoglobin level of 12.8 g/dL, hematocrit 39.8%, MCV 84.7 fL, MCHC 32.2 g/dL, and ferritin 37.0 ng/mL.

Discussion

This case highlights the importance of considering multiple contributing factors when evaluating severe IDA in pediatric patients, and underscores the need for a thorough workup to identify the underlying etiology of anemia. Furthermore, it emphasizes the role of comprehensive management that addresses not only the primary condition but also any co-existing issues, such as the nutritional deficiencies and lice infestation seen in this patient.

The 12-year-old boy discussed in this case reported milk consumption of up to 30 ounces per day. Cow’s milk is rich in calcium and a milk protein known as casein, both of which strongly inhibit the gastrointestinal absorption of iron [10]. Casein prevents absorption of non-heme iron, the primary form of dietary iron, while calcium competes with both heme and non-heme iron for absorption [10]. Additionally, cow’s milk contains minimal ascorbic acid (Vitamin C), which enhances the absorption and utilization of iron [11]. However, nutritional factors alone do not fully explain his initial hemoglobin of 3.3 g/dL. Poor iron absorption related to excess cow’s milk consumption in conjunction with possibly insufficient dietary iron intake likely predisposed this patient to low physiologic iron stores, which steadily fell to dangerously low levels in the setting of prolonged blood loss due to head lice infestation.

A similar presentation was described by Hau and Muhi-Iddin, who reported an 11-year-old boy with a hemoglobin level of 4.2 g/dL in the setting of prolonged pediculosis capitus [9]. This patient shared a similar background of insufficient nutritional intake and poor living conditions, and like our patient, he developed severe IDA requiring a pRBC transfusion after suffering from a head lice infestation lasting over 3 months [9]. Closely resembling the pattern of disease resolution observed in our patient, his hemoglobin normalized without recurrence of anemia following treatment of the lice infestation [9]. A common factor among cases reported in the literature linking IDA to an underlying lice infestation is limited access to personal hygiene products. In addition to our patient and the case described by Hau and Muhi-Iddin [9], Ogbuji et al reported a 13-year-old girl from a home without running water presenting with a hemoglobin of 5.3 g/dL [8]; Al Ghadeer et al described 5 female siblings from a disadvantaged socioeconomic status [5]; and Guss et al presented a case series involving unhoused patients [6].

It is important to note that our patient’s stool ova/parasite microscopy did return positive for Blastocystis hominis and Dientamoeba fragilis, but these organisms are not thought to have played a role in his symptomology or acute anemia presentation. Infectious disease specialists reviewed his case and suspected his stool findings to be a reflection of poor hygiene given the fecal/oral transmission of those organisms, which is supported by his mother’s description of their living quarters.

In light of these findings, this case emphasizes the need for a thorough and multifaceted approach to evaluating and managing pediatric IDA. However, limitations, such as its retrospective nature and reliance on clinical history, prevent drawing definitive conclusions about causal pathways. Future research should investigate the direct mechanisms through which lice infestations contribute to anemia, considering both adequate and inadequate hygiene practices and nutritional intake. Additionally, exploring targeted interventions for at-risk children, including improved hygiene and nutrition, could help prevent similar cases of severe IDA in vulnerable populations.

Conclusions

In conclusion, this case highlights the potential link between chronic head lice infestations (pediculosis capitis) and severe IDA in pediatric patients. The treatment approach should include a thorough assessment of other potential contributors to the underlying anemia, as well as comprehensive management that addresses medical, nutritional, and environmental factors.