Case Report: Late-Onset Pneumonitis after Apoica pallida (Insecta: Hymenoptera) Sting with Anaphylactic Reaction in the Brazilian Amazon

ABSTRACT.

Hymenopteran venoms, inoculated during stings by ants, bees, and wasps, are the most frequent cause of an IgE-mediated systemic hypersensitivity reaction in adults, which is a key process in drastic manifestations of anaphylaxis. Respiratory involvement is usually caused by pulmonary edema but is rarely described as including interstitial pneumonitis or acute respiratory distress syndrome. Here, we describe a case of severe allergic reaction after a sting by Apoica pallens with late-onset pulmonary involvement, including signs of vasoplegia (pleural effusion) and interstitial pneumonitis with mild rhabdomyolysis. The presence of late onset of pulmonary involvement after a severe allergic reaction after a sting by A. pallens shows the importance of keeping a patient with severe reactions under medical care for a minimum of 5 days to avoid serious late complications outside the hospital environment.

INTRODUCTION

Hymenopteran venoms, inoculated during stings by ants, bees, and wasps, for example, are the most frequent cause of an IgE-mediated systemic hypersensitivity reaction in adults, which is a key process in drastic manifestations of anaphylaxis.^1,2 The clinical presentation of wasp envenomation is related to the components of the venom that contain phospholipase A1, hyaluronidase, antigen 5, melittin, amines such as histamine and serotonin and kinins, apamin and acetylcholine.³ Acute renal failure, nephrotic syndrome, renal tubular acidosis, myocarditis, myocardial infarction, arrhythmias, centrilobular necrosis, pericolangitis, stroke, acute encephalopathy, hemolysis, disseminated intravascular coagulation, thrombocytopenia, and vasculitis are the main manifestations of a severe envenomation. A case’s severity is related to the amount of toxin inoculated, and severe cases are generally associated with massive stings by wasps.^3–6 Respiratory involvement usually includes pulmonary edema, and stings have been described, although rarely, as a cause of interstitial pneumonitis and acute respiratory distress syndrome (ARDS).^4–6 Here we describe a case of severe allergic reaction to Apoica pallens in the field without massive attacks that evolved to pleural effusion and interstitial pneumonitis with mild rhabdomyolysis or acute kidney injury.

CASE REPORT

A 25-year-old female biologist with no health problems was working in a field in a periurban area of Manaus, Western Brazilian Amazon, when she received a painful wasp sting on her neck. The wasp was sent to the health unit and later identified as Apoica pallida (Figure 1). Approximately 90 minutes after the wasp sting, she noticed increasing swelling of her lips, pruritus, wheals, and shortness of breath. Figure 2 summarizes the timeline from the accident to the patient’s discharge.

Figure 1.

Apoica pallens identified as the cause of the anaphylactic reaction of the reported case. This figure appears in color at www.ajtmh.org.

Figure 2.

Timeline from the accident to the patient's discharge. This figure appears in color at www.ajtmh.org.

The patient was taken by family members to a general hospital in the city of Manaus at 8:25 pm and was admitted 1 hour and 30 minutes after the sting. Before arrival at the hospital, her companions reported that the patient had a lowered level of consciousness, urticarial plaques throughout the body, abdominal pain, diarrhea, and convulsive episodes lasting < 5 minutes, with spontaneous resolution. On admission to the hospital, the patient was sleepy, disoriented, presented angioedema, hypotension (69/48 mm Hg), tachycardia (130 bpm), had normal breathing, 52% saturation in room air, warm body extremities, capillary refill time > 3 seconds, and capillary blood glucose of 201 mg/dL. Epinephrine was administered intramuscularly (1 dose of 0.3 mL and after 5 minutes 0.5 mL), hydrocortisone 500 mg, venous hydration 20 mL/kg, and O₂ via nasal catheter. Due to desaturation and lowering of consciousness, she required orotracheal intubation.

At 8 am on day 2 (∼10 hours after sting), she was on vasopressor support with adrenaline at 60 mL/hour, blood pressure 105/55 mm Hg, cold extremities, capillary refill time > 4 seconds, pale 3+/4+. Gasometry was as follows: pH 7.195, pO₂ 159, pCO₂ 29.5, bicarbonate 11.1, base excess –15.6, and lactate 8.30. Volume expansion with 1,500 mL Ringer lactate was performed at 1:30 pm (∼15 hours after sting), correction of metabolic acidosis using ketamine 0.5 mg/kg/hour, hydrocortisone 100 mg every 8 hours, and promethazine 25 mg intramuscularly.

Eleven hours after hemodynamic improvement, the patient was progressively weaned off mechanical ventilation, blood pressure was 135/85 mm Hg. Gasometry was as follows: pH 7.234, pCO₂ 24.4, bicarbonate 10.5, base excess –15.4, and lactate 6.69. Intravenous hydration was maintained with 1,000 mL Ringer lactate for 1 h.

At 2:00 pm on day 3, the patient no longer needed vasopressor support, maintained blood pressure at 147/92 mm Hg, heart rate of 107 bpm, without sedation, Glasgow coma scale 8T (ocullar operture [OA]: 3, motor response [MR]: 5). Gasometry was pH 7.380, pCO₂ 20.4, bicarbonate 11.9, base excess 11.3, and lactate 2.02. After 24 hours of therapeutic measures (day 4), she was transferred to a tertiary referral hospital specialized in treating accidents caused by venomous animals. On admission to the ICU, the patient was using a mask with a non-reinhalant reservoir with a flow of 10 L/minute, denied having dyspnea and had no complaints. She was discharged from the ICU 1 day later (day 5) without supplemental oxygen. Eight hours after discharge, the patient presented dyspnea, respiratory distress, tachypnea (RR 41 bpm), and physiological vesicular murmur with snoring.

Her chest radiograph showed bilateral opacities (Figure 3A), and her chest tomography revealed patterns of cryptogenic organizing pneumonia with bilateral pleural effusion, diffuse ground glass opacity, bronchial wall thickening, and arcade-like sign (Figure 3B–E). Her transthoracic echocardiogram was normal. No central nervous system imaging was performed due to rapid neurological improvement. Laboratory findings included leukocytosis, high DHL and creatine kinase levels that gradually came back to normal values (Table 1). Levofloxacin 500 mg/day associated with corticosteroid therapy with methylprednisolone was administered. Hemoculture for aerobes, sputum examination for mycobacterial infections, and a COVID-19 test were all negative.

Figure 3.

Radiograph (A) and chest tomography (B–F) show patterns of cryptogenic organizing pneumonia. A) bilateral opacities, B) bilateral pleural effusion and bronchial wall thickening, C) diffuse ground glass opacity, D) Arcade-like sign (dotted arrow) and reverse halo sign (full arrow), E) patterns of cryptogenic organizing pneumonia and F) pneumonia resolution. Figures A), B), C), D) show the radiological findings on day 5 and figure F) on day 10.

Table 1.

Follow-up of clinical parameters and laboratory tests.

	Day 4	Day 5	Day 6	Day 7	Day 8	Day 9	Day 10
AP (mm Hg)	138/72	151/96	140/95	141/88	183/86	163/97	163/97
Temp. (°C)	36.5	36.3	36.6	36.2	36.5	38.9	36.8
HR (bpm)	79	114	97	99	81	78	91
Ventilatory support	AA	NO	AA	AA	AA	AA	AA
Saturation	97%	98%	96%	98%	97%	94%	94%
Fluid balance (mL)	–	−2.309	+599	−432	+695	+530	–
Creatine phosphokinase (IU/L)	940	223	–	–	–	–	–
Creatinine (mg/dL)	–	–	–	0.7	–	–	–
LDH (IU/L)	840	598	–	448	355	372	–
ASO (IU/L)	86	52	–	–	–	–	–
AST (IU/L)	95	82	–	–	–	–	–
WBC (103/mm3)	35.5	20.15	25.7	27.88	19.85	16.92	–

AA = ambient air; AP = arterial pressure; ASO = antistreptolysin; AST = aspartate aminotransferase; HR = heart rate; LDH = lactate dehydrogenase; NO = nasal oxygen; WBC = white blood cell count.

After the patient’s return to the ICU (day 5), she remained for another 7 days. During her stay, she presented instability in clinical parameters (Table 1). She improved and was discharged from the ICU to the hospital ward, with improvement in the initial condition and resolution of pulmonary abnormalities (Figure 3F).

This study received ethical approval (CAAE: 30390613.9.0000.5016).

DISCUSSION

Hymenoptera envenomation, usually through multiple bites or stings, is a serious condition. Although wasp stings are common, serious clinical conditions appear to be underreported.^3–7 Wasp venoms are responsible for serious medical conditions. Components of wasp venoms are well documented and include allergens, enzymes, bioactive peptides, and amine substances that in general can act on the circulatory, immune, and nervous systems of their predators or an individual that causes them potential danger. The proteinous components from wasp venoms can cause tissue damage or allergic reactions in organisms.^8,9 However, clinicians should recognize wasp stings as an important public health problem, in addition to improving clinical management strategies, because serious conditions and death can be associated with envenomation. In view of this, developing a knowledge base on potential complications, the effect of the venom on homeostasis, and the evaluation of different therapeutic regimens to reverse the disorders in the physiological processes after wasp envenomation are essential.⁶

Although they are rare, severe clinical manifestations may occur as a result of Hymenoptera envenomation and include important organ dysfunction, such as intravascular hemolysis, rhabdomyolysis, as well as renal, pulmonary, and hepatic dysfunction.^3–6 Clinicians should be aware of the risk of interstitial pneumonitis and the risk of ARDS in cases with tachypnea and desaturation. Pneumonitis, ARDS, and rhabdomyolysis are rare conditions but can occur as a result of the toxic effects of wasp venom even in the absence of a serious allergic reaction.^5,8 The pathogenic mechanisms involved in lung alterations and injuries associated with wasp stings are not well known; thus, studies are needed to understand the pathophysiological mechanisms involved, as well as the use of adequate methods and therapies for lung injuries. According to Sirithep and Chinarooncha⁵ and Kularatne et al.,⁶ microvascular permeability in the lungs with fluid leakage into the alveolar spaces is responsible for acute pulmonary edema and other respiratory complications. In addition, acute kidney injury and accumulation of toxic metabolites can contribute to pulmonary edema, myocardial dysfunction, and metabolic acidosis, all of which are associated with fatal outcomes.⁶

Kularatne et al.⁶ reported the development of ARDS 2 days after a wasp sting to a patient with an acute kidney injury, followed by death 39 hours after the event. In the present study, late-onset interstitial pneumonitis without rhabdomyolysis or acute kidney injury was observed approximately 9 days after the sting by Apoica pallens. Although, the immunological mechanisms that cause the histamine-releasing action after Hymenoptera stings are type I hypersensitivity with anaphylaxis or rapid anaphylactoid reaction, occasionally late reactions due to type III hypersensitivity immune response may occur. However, it is necessary to consider that death and other complications that happen hours or days after wasp stings can be due to various conditions that are often unpredictable.^1,3

Thus, the presence of late-onset pulmonary involvement after a severe allergic reaction to a sting by Apoica pallens shows the importance of keeping a patient with severe reactions under medical care for a minimum of 5 days to avoid serious late complications outside the hospital environment. In addition, it is important that clinical staff, especially emergency physicians, are aware of the possibility of delayed reactions after wasp envenomation because these can be potentially fatal in the absence of intensive clinical management.