Danielle Yee, MD

To the Editor:

Cutaneous myiasis is a skin infestation with dipterous larvae that feed on the host’s tissue and cause a wide range of manifestations depending on the location of infestation. Cutaneous myiasis, which includes furuncular, wound, and migratory types, is the most common clinical form of this condition.¹ It is endemic to tropical and subtropical areas and is not common in the United States, thus it can pose a diagnostic challenge when presenting in nonendemic areas. We present the case of a woman from Michigan who acquired furuncular myiasis without travel history to a tropical or subtropical locale.

A 72-year-old woman presented to our clinic with a chief concern of a burning, pruritic, migratory skin lesion on the left arm of approximately 1 week’s duration. She had a medical history of squamous cell carcinoma, keratoacanthoma, and multiple tick bites. She reported that the lesion started on the distal aspect of the left arm as an eraser-sized, perfectly round, raised bruise with a dark pepperlike bump in the center. The lesion then spread proximally over the course of 1 week, creating 3 more identical lesions. As one lesion resolved, a new lesion appeared approximately 2 to 4 cm proximal to the preceding lesion. The patient had traveled to England, Scotland, and Ireland 2 months prior but otherwise denied leaving the state of Michigan. She reported frequent exposure to gardens, meadows, and wetlands in search of milkweed and monarch butterfly larvae that she raises in northeast Michigan. She denied any recent illness or associated systemic symptoms. Initial evaluation by a primary care physician resulted in a diagnosis of a furuncle or tick bite; she completed a 10-day course of amoxicillin and a methylprednisolone dose pack without improvement.

Physical examination revealed a 1-cm, firm, violaceous nodule with a small distinct central punctum and surrounding erythema on the proximal aspect of the left arm. Dermoscopy revealed a pulsating motion and expulsion of serosanguineous fluid from the central punctum (Figure 1). Further inspection of the patient’s left arm exposed several noninflammatory puncta distal to the primary lesion spaced at 2- to 4-cm intervals.

Gross examination of a 6-mm punch biopsy from the primary inflammatory nodule uncovered a small, motile, gray-white larval organism in the inferior portion of the specimen (Figure 2). Histopathology revealed superficial and deep eosinophil-rich inflammation, fibrosis, and hemorrhage. There was a complex wedge-shaped organism with extensive internal muscle bounded by a thin cuticle bearing rows of chitinous hooklets located at one side within the deep dermis (Figure 3). The findings were consistent with a diagnosis of cutaneous myiasis. No further treatment was required, as the organism was completely excised with the biopsy.

The most common causative agents of furuncular myiasis obtained from travelers returning from Mexico and Central and South America are Dermatobia hominis and Cordylobia anthropophaga. Cases of furuncular myiasis acquired in the United States without recent foreign travel are rare. Most of these cases are caused by larvae of the Cuterebra species (also known as the rabbit botfly or rodent botfly).² In a 2003 literature review by Safdar et al³ on 56 cases of furuncular myiasis in the United States, the median age of patients was 14 years, 87% of cases occurred in August and September, and most involved exposure in rural or suburban settings; 53% of cases presented in the northeastern United States.

Furuncular myiasis occurs when the organism’s ova are deposited on the skin of a human host by the parent organism or a mosquito vector. The heat of the skin causes the eggs to hatch and the dipteran larvae must penetrate the skin within 20 days.¹ Signs of infection typically are seen 6 to 10 days after infestation.³ The larvae then feed on human tissue and burrow deep in the dermis, forming an erythematous furunculoid nodule containing one or multiple maggots. After 5 to 10 weeks, the adult larvae drop to the ground, where they mature into adult organisms in the soil.¹

The most reported symptoms of furuncular myiasis include pruritus, pain, and movement sensation, typically occurring suddenly at night.⁴ The most common presentation is a furunclelike lesion that exudes serosanguineous or purulent fluid,¹ but there have been reports of vesicular, bullous, pustular, erosive, ecchymotic, and ulcerative lesions.⁵Dermatobia hominis usually presents on an exposed site, such as the scalp, face, and extremities. It may present with paroxysmal episodes of lancinating pain. Over time, the lesion usually heals without a scar, though hyperpigmentation and scarring can occur. The most reported complication is secondary bacterial infection.⁴ Local lymphadenopathy or systemic symptoms should raise concern for infection. Staphylococcus aureus and group B Streptococcus have been cultured from lesions.^6,7

The differential diagnosis for myiasis should include furuncle, insect bite, insect prurigo, pyoderma, inflamed cyst, and tungiasis. Myiasis also can present similarly to severe soft tissue infections or cellulitis. If located on the breasts, it can be mistaken for periductal mastitis, a benign mass with microcalcification, or inflammatory carcinoma. Lastly, due to pain, erythema, pruritus, small vesicles, and crusting, it may be confused for herpes simplex virus.¹

Furuncular myiasis typically is diagnosed based on clinical presentation, especially in endemic regions. In nonendemic areas, the patient’s history may reveal recent travel or predisposition to myiasis. In cases where there is uncertainty, dermoscopy may be used to identify the maggot in the lesion, or ultrasonography can be used to confirm myiasis through the detection of larval movement.⁸ Dermoscopy will reveal a furuncular lesion with a central opening surrounded by dilated blood vessels and a yellowish structure with black barblike spines.⁹ Within the dermis is a fibrous cystic sinus tract containing the dipteran larva. Laboratory studies typically are unremarkable. In chronic cases, a complete blood cell count and other laboratory tests may show systemic inflammation, peripheral eosinophilia, and elevated IgE.¹⁰ Biopsies of furuncular myiasis are not necessary for diagnosis. Histopathology reveals an ulcerated epidermis with or without hyperkeratosis and an inflammatory infiltrate composed of lymphocytes and neutrophils with eosinophils, fibroblasts, histiocytes, basophils, mast cells, plasma cells, and Langerhans cells within the dermis and subcutis.¹¹

There are various approaches to treating furuncular myiasis, with the goal of complete removal of the larva and prevention of secondary infection. One treatment option is to apply a toxic substance to the larva, effectively killing it. Another approach is to force the larva to emerge via localized hypoxia, which can be done by occluding the punctum of the lesion for at least 24 hours. A complication of this method is suffocation of the larva without migration, leading to incomplete extraction and secondary infection.¹ A third method is to surgically remove the larva, which allows for debridement of necrotic tissue surrounding the lesion if present.¹² Ultrasonography also can be used therapeutically to aid in the removal of the larvae. The last method is to inject lidocaine into the base of the lesion, forcing the larva out of the punctum via fluid pressure.¹³ Oral treatments such as ivermectin are not recommended because they can result in the death of larvae within the lesion, leading to an inflammatory response.⁸

Furuncular myiasis is a form of cutaneous larvae infestation not commonly seen in individuals who do not live or travel in endemic, tropical, and subtropical regions. Diagnosis is based on clinical presentation, with imaging and laboratory studies available to supplement in unclear or atypical manifestations. Treatment involves complete removal of the larva, typically through forced evacuation via hypoxia or through surgical removal. Most cases resolve without notable scarring or other sequelae; however, in those who do have complications, the most common is secondary bacterial infection. Our patient’s absence of notable travel history and frequent environmental exposure in Michigan led us to believe the organism was from a domestic source. Our case underlines the importance of a thorough history and clinical examination of furuncular lesions including the use of dermoscopy to yield an appropriate diagnosis and treatment plan.

To the Editor:

Cutaneous myiasis is a skin infestation with dipterous larvae that feed on the host’s tissue and cause a wide range of manifestations depending on the location of infestation. Cutaneous myiasis, which includes furuncular, wound, and migratory types, is the most common clinical form of this condition.¹ It is endemic to tropical and subtropical areas and is not common in the United States, thus it can pose a diagnostic challenge when presenting in nonendemic areas. We present the case of a woman from Michigan who acquired furuncular myiasis without travel history to a tropical or subtropical locale.

A 72-year-old woman presented to our clinic with a chief concern of a burning, pruritic, migratory skin lesion on the left arm of approximately 1 week’s duration. She had a medical history of squamous cell carcinoma, keratoacanthoma, and multiple tick bites. She reported that the lesion started on the distal aspect of the left arm as an eraser-sized, perfectly round, raised bruise with a dark pepperlike bump in the center. The lesion then spread proximally over the course of 1 week, creating 3 more identical lesions. As one lesion resolved, a new lesion appeared approximately 2 to 4 cm proximal to the preceding lesion. The patient had traveled to England, Scotland, and Ireland 2 months prior but otherwise denied leaving the state of Michigan. She reported frequent exposure to gardens, meadows, and wetlands in search of milkweed and monarch butterfly larvae that she raises in northeast Michigan. She denied any recent illness or associated systemic symptoms. Initial evaluation by a primary care physician resulted in a diagnosis of a furuncle or tick bite; she completed a 10-day course of amoxicillin and a methylprednisolone dose pack without improvement.

Physical examination revealed a 1-cm, firm, violaceous nodule with a small distinct central punctum and surrounding erythema on the proximal aspect of the left arm. Dermoscopy revealed a pulsating motion and expulsion of serosanguineous fluid from the central punctum (Figure 1). Further inspection of the patient’s left arm exposed several noninflammatory puncta distal to the primary lesion spaced at 2- to 4-cm intervals.

Gross examination of a 6-mm punch biopsy from the primary inflammatory nodule uncovered a small, motile, gray-white larval organism in the inferior portion of the specimen (Figure 2). Histopathology revealed superficial and deep eosinophil-rich inflammation, fibrosis, and hemorrhage. There was a complex wedge-shaped organism with extensive internal muscle bounded by a thin cuticle bearing rows of chitinous hooklets located at one side within the deep dermis (Figure 3). The findings were consistent with a diagnosis of cutaneous myiasis. No further treatment was required, as the organism was completely excised with the biopsy.

The most common causative agents of furuncular myiasis obtained from travelers returning from Mexico and Central and South America are Dermatobia hominis and Cordylobia anthropophaga. Cases of furuncular myiasis acquired in the United States without recent foreign travel are rare. Most of these cases are caused by larvae of the Cuterebra species (also known as the rabbit botfly or rodent botfly).² In a 2003 literature review by Safdar et al³ on 56 cases of furuncular myiasis in the United States, the median age of patients was 14 years, 87% of cases occurred in August and September, and most involved exposure in rural or suburban settings; 53% of cases presented in the northeastern United States.

Furuncular myiasis occurs when the organism’s ova are deposited on the skin of a human host by the parent organism or a mosquito vector. The heat of the skin causes the eggs to hatch and the dipteran larvae must penetrate the skin within 20 days.¹ Signs of infection typically are seen 6 to 10 days after infestation.³ The larvae then feed on human tissue and burrow deep in the dermis, forming an erythematous furunculoid nodule containing one or multiple maggots. After 5 to 10 weeks, the adult larvae drop to the ground, where they mature into adult organisms in the soil.¹

The most reported symptoms of furuncular myiasis include pruritus, pain, and movement sensation, typically occurring suddenly at night.⁴ The most common presentation is a furunclelike lesion that exudes serosanguineous or purulent fluid,¹ but there have been reports of vesicular, bullous, pustular, erosive, ecchymotic, and ulcerative lesions.⁵Dermatobia hominis usually presents on an exposed site, such as the scalp, face, and extremities. It may present with paroxysmal episodes of lancinating pain. Over time, the lesion usually heals without a scar, though hyperpigmentation and scarring can occur. The most reported complication is secondary bacterial infection.⁴ Local lymphadenopathy or systemic symptoms should raise concern for infection. Staphylococcus aureus and group B Streptococcus have been cultured from lesions.^6,7

The differential diagnosis for myiasis should include furuncle, insect bite, insect prurigo, pyoderma, inflamed cyst, and tungiasis. Myiasis also can present similarly to severe soft tissue infections or cellulitis. If located on the breasts, it can be mistaken for periductal mastitis, a benign mass with microcalcification, or inflammatory carcinoma. Lastly, due to pain, erythema, pruritus, small vesicles, and crusting, it may be confused for herpes simplex virus.¹

Furuncular myiasis typically is diagnosed based on clinical presentation, especially in endemic regions. In nonendemic areas, the patient’s history may reveal recent travel or predisposition to myiasis. In cases where there is uncertainty, dermoscopy may be used to identify the maggot in the lesion, or ultrasonography can be used to confirm myiasis through the detection of larval movement.⁸ Dermoscopy will reveal a furuncular lesion with a central opening surrounded by dilated blood vessels and a yellowish structure with black barblike spines.⁹ Within the dermis is a fibrous cystic sinus tract containing the dipteran larva. Laboratory studies typically are unremarkable. In chronic cases, a complete blood cell count and other laboratory tests may show systemic inflammation, peripheral eosinophilia, and elevated IgE.¹⁰ Biopsies of furuncular myiasis are not necessary for diagnosis. Histopathology reveals an ulcerated epidermis with or without hyperkeratosis and an inflammatory infiltrate composed of lymphocytes and neutrophils with eosinophils, fibroblasts, histiocytes, basophils, mast cells, plasma cells, and Langerhans cells within the dermis and subcutis.¹¹

There are various approaches to treating furuncular myiasis, with the goal of complete removal of the larva and prevention of secondary infection. One treatment option is to apply a toxic substance to the larva, effectively killing it. Another approach is to force the larva to emerge via localized hypoxia, which can be done by occluding the punctum of the lesion for at least 24 hours. A complication of this method is suffocation of the larva without migration, leading to incomplete extraction and secondary infection.¹ A third method is to surgically remove the larva, which allows for debridement of necrotic tissue surrounding the lesion if present.¹² Ultrasonography also can be used therapeutically to aid in the removal of the larvae. The last method is to inject lidocaine into the base of the lesion, forcing the larva out of the punctum via fluid pressure.¹³ Oral treatments such as ivermectin are not recommended because they can result in the death of larvae within the lesion, leading to an inflammatory response.⁸

Furuncular myiasis is a form of cutaneous larvae infestation not commonly seen in individuals who do not live or travel in endemic, tropical, and subtropical regions. Diagnosis is based on clinical presentation, with imaging and laboratory studies available to supplement in unclear or atypical manifestations. Treatment involves complete removal of the larva, typically through forced evacuation via hypoxia or through surgical removal. Most cases resolve without notable scarring or other sequelae; however, in those who do have complications, the most common is secondary bacterial infection. Our patient’s absence of notable travel history and frequent environmental exposure in Michigan led us to believe the organism was from a domestic source. Our case underlines the importance of a thorough history and clinical examination of furuncular lesions including the use of dermoscopy to yield an appropriate diagnosis and treatment plan.

To the Editor:

Cutaneous myiasis is a skin infestation with dipterous larvae that feed on the host’s tissue and cause a wide range of manifestations depending on the location of infestation. Cutaneous myiasis, which includes furuncular, wound, and migratory types, is the most common clinical form of this condition.¹ It is endemic to tropical and subtropical areas and is not common in the United States, thus it can pose a diagnostic challenge when presenting in nonendemic areas. We present the case of a woman from Michigan who acquired furuncular myiasis without travel history to a tropical or subtropical locale.

A 72-year-old woman presented to our clinic with a chief concern of a burning, pruritic, migratory skin lesion on the left arm of approximately 1 week’s duration. She had a medical history of squamous cell carcinoma, keratoacanthoma, and multiple tick bites. She reported that the lesion started on the distal aspect of the left arm as an eraser-sized, perfectly round, raised bruise with a dark pepperlike bump in the center. The lesion then spread proximally over the course of 1 week, creating 3 more identical lesions. As one lesion resolved, a new lesion appeared approximately 2 to 4 cm proximal to the preceding lesion. The patient had traveled to England, Scotland, and Ireland 2 months prior but otherwise denied leaving the state of Michigan. She reported frequent exposure to gardens, meadows, and wetlands in search of milkweed and monarch butterfly larvae that she raises in northeast Michigan. She denied any recent illness or associated systemic symptoms. Initial evaluation by a primary care physician resulted in a diagnosis of a furuncle or tick bite; she completed a 10-day course of amoxicillin and a methylprednisolone dose pack without improvement.

Physical examination revealed a 1-cm, firm, violaceous nodule with a small distinct central punctum and surrounding erythema on the proximal aspect of the left arm. Dermoscopy revealed a pulsating motion and expulsion of serosanguineous fluid from the central punctum (Figure 1). Further inspection of the patient’s left arm exposed several noninflammatory puncta distal to the primary lesion spaced at 2- to 4-cm intervals.

Gross examination of a 6-mm punch biopsy from the primary inflammatory nodule uncovered a small, motile, gray-white larval organism in the inferior portion of the specimen (Figure 2). Histopathology revealed superficial and deep eosinophil-rich inflammation, fibrosis, and hemorrhage. There was a complex wedge-shaped organism with extensive internal muscle bounded by a thin cuticle bearing rows of chitinous hooklets located at one side within the deep dermis (Figure 3). The findings were consistent with a diagnosis of cutaneous myiasis. No further treatment was required, as the organism was completely excised with the biopsy.

The most common causative agents of furuncular myiasis obtained from travelers returning from Mexico and Central and South America are Dermatobia hominis and Cordylobia anthropophaga. Cases of furuncular myiasis acquired in the United States without recent foreign travel are rare. Most of these cases are caused by larvae of the Cuterebra species (also known as the rabbit botfly or rodent botfly).² In a 2003 literature review by Safdar et al³ on 56 cases of furuncular myiasis in the United States, the median age of patients was 14 years, 87% of cases occurred in August and September, and most involved exposure in rural or suburban settings; 53% of cases presented in the northeastern United States.

Furuncular myiasis occurs when the organism’s ova are deposited on the skin of a human host by the parent organism or a mosquito vector. The heat of the skin causes the eggs to hatch and the dipteran larvae must penetrate the skin within 20 days.¹ Signs of infection typically are seen 6 to 10 days after infestation.³ The larvae then feed on human tissue and burrow deep in the dermis, forming an erythematous furunculoid nodule containing one or multiple maggots. After 5 to 10 weeks, the adult larvae drop to the ground, where they mature into adult organisms in the soil.¹

The most reported symptoms of furuncular myiasis include pruritus, pain, and movement sensation, typically occurring suddenly at night.⁴ The most common presentation is a furunclelike lesion that exudes serosanguineous or purulent fluid,¹ but there have been reports of vesicular, bullous, pustular, erosive, ecchymotic, and ulcerative lesions.⁵Dermatobia hominis usually presents on an exposed site, such as the scalp, face, and extremities. It may present with paroxysmal episodes of lancinating pain. Over time, the lesion usually heals without a scar, though hyperpigmentation and scarring can occur. The most reported complication is secondary bacterial infection.⁴ Local lymphadenopathy or systemic symptoms should raise concern for infection. Staphylococcus aureus and group B Streptococcus have been cultured from lesions.^6,7

The differential diagnosis for myiasis should include furuncle, insect bite, insect prurigo, pyoderma, inflamed cyst, and tungiasis. Myiasis also can present similarly to severe soft tissue infections or cellulitis. If located on the breasts, it can be mistaken for periductal mastitis, a benign mass with microcalcification, or inflammatory carcinoma. Lastly, due to pain, erythema, pruritus, small vesicles, and crusting, it may be confused for herpes simplex virus.¹

Furuncular myiasis typically is diagnosed based on clinical presentation, especially in endemic regions. In nonendemic areas, the patient’s history may reveal recent travel or predisposition to myiasis. In cases where there is uncertainty, dermoscopy may be used to identify the maggot in the lesion, or ultrasonography can be used to confirm myiasis through the detection of larval movement.⁸ Dermoscopy will reveal a furuncular lesion with a central opening surrounded by dilated blood vessels and a yellowish structure with black barblike spines.⁹ Within the dermis is a fibrous cystic sinus tract containing the dipteran larva. Laboratory studies typically are unremarkable. In chronic cases, a complete blood cell count and other laboratory tests may show systemic inflammation, peripheral eosinophilia, and elevated IgE.¹⁰ Biopsies of furuncular myiasis are not necessary for diagnosis. Histopathology reveals an ulcerated epidermis with or without hyperkeratosis and an inflammatory infiltrate composed of lymphocytes and neutrophils with eosinophils, fibroblasts, histiocytes, basophils, mast cells, plasma cells, and Langerhans cells within the dermis and subcutis.¹¹

There are various approaches to treating furuncular myiasis, with the goal of complete removal of the larva and prevention of secondary infection. One treatment option is to apply a toxic substance to the larva, effectively killing it. Another approach is to force the larva to emerge via localized hypoxia, which can be done by occluding the punctum of the lesion for at least 24 hours. A complication of this method is suffocation of the larva without migration, leading to incomplete extraction and secondary infection.¹ A third method is to surgically remove the larva, which allows for debridement of necrotic tissue surrounding the lesion if present.¹² Ultrasonography also can be used therapeutically to aid in the removal of the larvae. The last method is to inject lidocaine into the base of the lesion, forcing the larva out of the punctum via fluid pressure.¹³ Oral treatments such as ivermectin are not recommended because they can result in the death of larvae within the lesion, leading to an inflammatory response.⁸

Furuncular myiasis is a form of cutaneous larvae infestation not commonly seen in individuals who do not live or travel in endemic, tropical, and subtropical regions. Diagnosis is based on clinical presentation, with imaging and laboratory studies available to supplement in unclear or atypical manifestations. Treatment involves complete removal of the larva, typically through forced evacuation via hypoxia or through surgical removal. Most cases resolve without notable scarring or other sequelae; however, in those who do have complications, the most common is secondary bacterial infection. Our patient’s absence of notable travel history and frequent environmental exposure in Michigan led us to believe the organism was from a domestic source. Our case underlines the importance of a thorough history and clinical examination of furuncular lesions including the use of dermoscopy to yield an appropriate diagnosis and treatment plan.

THE CASE

A 25-year-old woman presented to an infectious diseases (ID) physician with a 4-day history of symptoms following receipt of a quadrivalent influenza vaccine. Two hours after receiving the vaccine, the patient experienced abdominal pain. One hour later, she felt warm and developed diffuse urticaria and rigors. Because of her worsening condition, she presented to the emergency department, where she was given intravenous methylprednisolone 40 mg, ondansetron 8 mg, diphenhydramine 25 mg, and normal saline. Her urticarial rash resolved within 45 minutes, and she was discharged home.

Three days later, she sought additional medical care because of persistent chest tightness, new-onset bronchospasm, pleuritic chest pain, nausea, diarrhea, facial swelling, urticaria, and anorexia. The patient’s vital signs were within normal limits. The oropharynx lacked erythema or obstruction. The lungs were clear to auscultation bilaterally, and heart sounds were regular, with no ectopy or murmurs. Her abdomen was soft, nontender, and nondistended. The patient demonstrated dermatographism on her back.

Historically, the patient had received the influenza vaccine without difficulty. She tolerated latex but had concerns about egg allergy due to vomiting with egg-yolk exposure.

THE DIAGNOSIS

The ID physician, suspecting anaphylaxis and sustained allergic response to the influenza vaccine, arranged for immediate follow-up with an allergist. Multiple tests were done. A negative result on epicutaneous testing to egg was inconsistent with an immunoglobulin (Ig) E-mediated food allergy.

Intradermal testing with the flu vaccine (diluted 1:100) was subsequently performed with appropriate controls. A positive intradermal result is typically a wheal ≥ 5 mm larger than the control. The patient had a 5-mm/15-mm wheal-and-flare response to the flu vaccine, compared to a negative response to saline (FIGURE). (Since the vaccine did not contain gelatin, this was not tested.)

Based on the positive response to flu vaccine and negative response to egg, it was determined that the patient had experienced an anaphylactic reaction to the vaccine itself.

DISCUSSION

In adults, the most common adverse reactions to quadrivalent flu vaccine include pain, headache, and fatigue. IgE-mediated reactions to the influenza vaccine, especially anaphylactic reactions, are rare. A Vaccine Safety Datalink study found 10 cases of anaphylaxis after more than 7.4 million doses of inactivated flu vaccine were given, for a rate of 1.35 per 1 million doses.¹

Continue to: Don't blame eggs

Don’t blame eggs. It was previously believed that reactions to the flu vaccine were due to egg allergies, because the vaccine may contain a tiny amount of ovalbumin, a protein found in egg. However, multiple studies have supported the safety of injectable influenza vaccine in patients with an egg allergy because the amount of ovalbumin contained in each dose is very low and thus not likely to evoke an allergic response.^2,3

How and when to test for allergy. For patients who have a severe allergic reaction or anaphylaxis after immunization, immediate-type allergy skin testing should be performed by an allergist to establish whether the reaction was IgE mediated and to determine the causative agent.

Wait 4 to 6 weeks after an anaphylactic reaction before doing skin testing, as earlier testing can lead to false-negative results.

It’s best to wait 4 to 6 weeks after an anaphylactic reaction before doing skin testing, as earlier testing can lead to false-negative results.⁴ The vaccine should first be tested by using the prick method. If this test is negative, an intradermal test with the vaccine diluted 1:100 should be performed with appropriate controls.⁵

Should the patient receive future vaccinations?

If skin testing is positive, there are several ways to proceed. A vaccine to which the patient has previously had an allergic reaction and positive skin test can still be administered, with caution.⁵ With emergency supplies, medication, and equipment immediately available, medical personnel can administer the influenza vaccine in titrated doses. If the full vaccine dose is normally a volume of 0.5 mL, the patient is first given 0.05 mL of a 1:10 dilution and then, at 15-minute intervals, given full-strength vaccine at doses of 0.05, 0.1, 0.15, and finally 0.2 mL, for a cumulative dose of 0.5 mL.⁵

Alternatively, the patient can forego the vaccination, although this decision has its own risks. In a patient who has previously had an anaphylactic reaction but has negative skin tests—meaning it is unlikely that the patient has IgE antibody to the vaccine—the vaccine can be administered and followed with an observation period of at least 30 minutes.⁵z Our patient was counseled on both options and decided to forego the vaccine.

THE TAKEAWAY

Anaphylaxis is a life-threatening allergic reaction requiring immediate treatment. Anaphylaxis after vaccine receipt is exceedingly rare.⁶ Most IgE-mediated allergic reactions post vaccination are attributed to added or residual substances in the vaccine, rather than the immunizing agent itself.⁶ While common local reactions and fever post vaccination do not contraindicate future vaccination, rare anaphylactic reactions need to be further evaluated, with a referral to an allergist to determine if the patient is, in fact, allergic to additive ingredients within the vaccine vs allergic to the vaccine itself.

CORRESPONDENCE
Kathleen Dass, MD, 24601 Coolidge Highway, Oak Park, MI 48237; kathleen.j.dass@gmail.com

THE CASE

A 25-year-old woman presented to an infectious diseases (ID) physician with a 4-day history of symptoms following receipt of a quadrivalent influenza vaccine. Two hours after receiving the vaccine, the patient experienced abdominal pain. One hour later, she felt warm and developed diffuse urticaria and rigors. Because of her worsening condition, she presented to the emergency department, where she was given intravenous methylprednisolone 40 mg, ondansetron 8 mg, diphenhydramine 25 mg, and normal saline. Her urticarial rash resolved within 45 minutes, and she was discharged home.

Three days later, she sought additional medical care because of persistent chest tightness, new-onset bronchospasm, pleuritic chest pain, nausea, diarrhea, facial swelling, urticaria, and anorexia. The patient’s vital signs were within normal limits. The oropharynx lacked erythema or obstruction. The lungs were clear to auscultation bilaterally, and heart sounds were regular, with no ectopy or murmurs. Her abdomen was soft, nontender, and nondistended. The patient demonstrated dermatographism on her back.

Historically, the patient had received the influenza vaccine without difficulty. She tolerated latex but had concerns about egg allergy due to vomiting with egg-yolk exposure.

THE DIAGNOSIS

The ID physician, suspecting anaphylaxis and sustained allergic response to the influenza vaccine, arranged for immediate follow-up with an allergist. Multiple tests were done. A negative result on epicutaneous testing to egg was inconsistent with an immunoglobulin (Ig) E-mediated food allergy.

Intradermal testing with the flu vaccine (diluted 1:100) was subsequently performed with appropriate controls. A positive intradermal result is typically a wheal ≥ 5 mm larger than the control. The patient had a 5-mm/15-mm wheal-and-flare response to the flu vaccine, compared to a negative response to saline (FIGURE). (Since the vaccine did not contain gelatin, this was not tested.)

Based on the positive response to flu vaccine and negative response to egg, it was determined that the patient had experienced an anaphylactic reaction to the vaccine itself.

DISCUSSION

In adults, the most common adverse reactions to quadrivalent flu vaccine include pain, headache, and fatigue. IgE-mediated reactions to the influenza vaccine, especially anaphylactic reactions, are rare. A Vaccine Safety Datalink study found 10 cases of anaphylaxis after more than 7.4 million doses of inactivated flu vaccine were given, for a rate of 1.35 per 1 million doses.¹

Continue to: Don't blame eggs

Don’t blame eggs. It was previously believed that reactions to the flu vaccine were due to egg allergies, because the vaccine may contain a tiny amount of ovalbumin, a protein found in egg. However, multiple studies have supported the safety of injectable influenza vaccine in patients with an egg allergy because the amount of ovalbumin contained in each dose is very low and thus not likely to evoke an allergic response.^2,3

How and when to test for allergy. For patients who have a severe allergic reaction or anaphylaxis after immunization, immediate-type allergy skin testing should be performed by an allergist to establish whether the reaction was IgE mediated and to determine the causative agent.

Wait 4 to 6 weeks after an anaphylactic reaction before doing skin testing, as earlier testing can lead to false-negative results.

It’s best to wait 4 to 6 weeks after an anaphylactic reaction before doing skin testing, as earlier testing can lead to false-negative results.⁴ The vaccine should first be tested by using the prick method. If this test is negative, an intradermal test with the vaccine diluted 1:100 should be performed with appropriate controls.⁵

Should the patient receive future vaccinations?

If skin testing is positive, there are several ways to proceed. A vaccine to which the patient has previously had an allergic reaction and positive skin test can still be administered, with caution.⁵ With emergency supplies, medication, and equipment immediately available, medical personnel can administer the influenza vaccine in titrated doses. If the full vaccine dose is normally a volume of 0.5 mL, the patient is first given 0.05 mL of a 1:10 dilution and then, at 15-minute intervals, given full-strength vaccine at doses of 0.05, 0.1, 0.15, and finally 0.2 mL, for a cumulative dose of 0.5 mL.⁵

Alternatively, the patient can forego the vaccination, although this decision has its own risks. In a patient who has previously had an anaphylactic reaction but has negative skin tests—meaning it is unlikely that the patient has IgE antibody to the vaccine—the vaccine can be administered and followed with an observation period of at least 30 minutes.⁵z Our patient was counseled on both options and decided to forego the vaccine.

THE TAKEAWAY

Anaphylaxis is a life-threatening allergic reaction requiring immediate treatment. Anaphylaxis after vaccine receipt is exceedingly rare.⁶ Most IgE-mediated allergic reactions post vaccination are attributed to added or residual substances in the vaccine, rather than the immunizing agent itself.⁶ While common local reactions and fever post vaccination do not contraindicate future vaccination, rare anaphylactic reactions need to be further evaluated, with a referral to an allergist to determine if the patient is, in fact, allergic to additive ingredients within the vaccine vs allergic to the vaccine itself.

CORRESPONDENCE
Kathleen Dass, MD, 24601 Coolidge Highway, Oak Park, MI 48237; kathleen.j.dass@gmail.com

THE CASE

A 25-year-old woman presented to an infectious diseases (ID) physician with a 4-day history of symptoms following receipt of a quadrivalent influenza vaccine. Two hours after receiving the vaccine, the patient experienced abdominal pain. One hour later, she felt warm and developed diffuse urticaria and rigors. Because of her worsening condition, she presented to the emergency department, where she was given intravenous methylprednisolone 40 mg, ondansetron 8 mg, diphenhydramine 25 mg, and normal saline. Her urticarial rash resolved within 45 minutes, and she was discharged home.

Three days later, she sought additional medical care because of persistent chest tightness, new-onset bronchospasm, pleuritic chest pain, nausea, diarrhea, facial swelling, urticaria, and anorexia. The patient’s vital signs were within normal limits. The oropharynx lacked erythema or obstruction. The lungs were clear to auscultation bilaterally, and heart sounds were regular, with no ectopy or murmurs. Her abdomen was soft, nontender, and nondistended. The patient demonstrated dermatographism on her back.

Historically, the patient had received the influenza vaccine without difficulty. She tolerated latex but had concerns about egg allergy due to vomiting with egg-yolk exposure.

THE DIAGNOSIS

The ID physician, suspecting anaphylaxis and sustained allergic response to the influenza vaccine, arranged for immediate follow-up with an allergist. Multiple tests were done. A negative result on epicutaneous testing to egg was inconsistent with an immunoglobulin (Ig) E-mediated food allergy.

Intradermal testing with the flu vaccine (diluted 1:100) was subsequently performed with appropriate controls. A positive intradermal result is typically a wheal ≥ 5 mm larger than the control. The patient had a 5-mm/15-mm wheal-and-flare response to the flu vaccine, compared to a negative response to saline (FIGURE). (Since the vaccine did not contain gelatin, this was not tested.)

Based on the positive response to flu vaccine and negative response to egg, it was determined that the patient had experienced an anaphylactic reaction to the vaccine itself.

DISCUSSION

In adults, the most common adverse reactions to quadrivalent flu vaccine include pain, headache, and fatigue. IgE-mediated reactions to the influenza vaccine, especially anaphylactic reactions, are rare. A Vaccine Safety Datalink study found 10 cases of anaphylaxis after more than 7.4 million doses of inactivated flu vaccine were given, for a rate of 1.35 per 1 million doses.¹

Continue to: Don't blame eggs

Don’t blame eggs. It was previously believed that reactions to the flu vaccine were due to egg allergies, because the vaccine may contain a tiny amount of ovalbumin, a protein found in egg. However, multiple studies have supported the safety of injectable influenza vaccine in patients with an egg allergy because the amount of ovalbumin contained in each dose is very low and thus not likely to evoke an allergic response.^2,3

How and when to test for allergy. For patients who have a severe allergic reaction or anaphylaxis after immunization, immediate-type allergy skin testing should be performed by an allergist to establish whether the reaction was IgE mediated and to determine the causative agent.

Wait 4 to 6 weeks after an anaphylactic reaction before doing skin testing, as earlier testing can lead to false-negative results.

It’s best to wait 4 to 6 weeks after an anaphylactic reaction before doing skin testing, as earlier testing can lead to false-negative results.⁴ The vaccine should first be tested by using the prick method. If this test is negative, an intradermal test with the vaccine diluted 1:100 should be performed with appropriate controls.⁵

Should the patient receive future vaccinations?

If skin testing is positive, there are several ways to proceed. A vaccine to which the patient has previously had an allergic reaction and positive skin test can still be administered, with caution.⁵ With emergency supplies, medication, and equipment immediately available, medical personnel can administer the influenza vaccine in titrated doses. If the full vaccine dose is normally a volume of 0.5 mL, the patient is first given 0.05 mL of a 1:10 dilution and then, at 15-minute intervals, given full-strength vaccine at doses of 0.05, 0.1, 0.15, and finally 0.2 mL, for a cumulative dose of 0.5 mL.⁵

Alternatively, the patient can forego the vaccination, although this decision has its own risks. In a patient who has previously had an anaphylactic reaction but has negative skin tests—meaning it is unlikely that the patient has IgE antibody to the vaccine—the vaccine can be administered and followed with an observation period of at least 30 minutes.⁵z Our patient was counseled on both options and decided to forego the vaccine.

THE TAKEAWAY

Anaphylaxis is a life-threatening allergic reaction requiring immediate treatment. Anaphylaxis after vaccine receipt is exceedingly rare.⁶ Most IgE-mediated allergic reactions post vaccination are attributed to added or residual substances in the vaccine, rather than the immunizing agent itself.⁶ While common local reactions and fever post vaccination do not contraindicate future vaccination, rare anaphylactic reactions need to be further evaluated, with a referral to an allergist to determine if the patient is, in fact, allergic to additive ingredients within the vaccine vs allergic to the vaccine itself.

CORRESPONDENCE
Kathleen Dass, MD, 24601 Coolidge Highway, Oak Park, MI 48237; kathleen.j.dass@gmail.com