Brain Infarction: Rare Neurological Presentation of African Bee Stings

Abstract

Bee stings are commonly encountered worldwide. Various manifestations after bee sting have been described including local reactions which are common, systemic responses such as anaphylaxis, diffuse intravascular coagulation and hemolysis. We report a case of a 74-year-old man who developed neurologic deficit 5 hours after bee stings, which was confirmed to be left frontal infarction on brain CT-scan. The case does not follow the reported  pattern  of hypovolemic or anaphylactic shock, hemolysis and/or  rhabdomyolysis, despite the potentially lethal amount of venom injected. Diverse mechanisms have been proposed to give an explanation to all the clinical manifestation of both toxic and allergic reactions secondary to bee stings. Currently, the most accepted one state that victims can develop severe syndrome characterized by the release of a large amount of cytokines.

Introduction

Africanized  honey  bees, known  colloquially as "killer bees", are some hybrid varieties of the Western honey bee species (Apis mellifera) and are particularly aggressive. They have been imported from tropical zones in America where a large number  of deaths have been reported [1].Bee stings are commonly encountered worldwide. Various manifestations after bee sting have been described. Local reactions are common.  Unusually, manifestations  like vomiting, diarrhea,  dyspnea, generalized edema,  acute  renal failure, hypotension and collapse may occur. Rarely vasculitis, serum sickness, neuritis and encephalitis have been described which generally develop days to weeks after a sting [2]. We report a case of a 74-year-old man who developed neurologic deficit 5 hours after bee stings, which was confirmed to be left frontal infarction on brain CT-scan.

Case Report

A 74-year-old male patient, with previous history of arterial hypertension; since a week, in the early morning, the patient was stung by Africanized race bees, up to 200, during roof cleaning, in a rural area of the Colombo-Venezuelan frontier. 5 hours later, the patient posteriorly experienced general malaise, and paresthesia of the right hand with language alteration during 5 minutes.After that time, the patient recovered completely and called for help to his physician, who prescribed paracetamol and rest. Two days after, the patient  experienced sudden right hemiparesia with inability to speak and comprehend. In the physical examination in the emergency department, relevant data obtained were: blood pressure: 150/100mmHg, cardiac sounds were rhythmic without murmurs, and lung fields were clear. Murmur  in the left common carotid   artery.  In   the   neurological  examination, the patient was alert with global aphasia (sensitive- motor), facial paralysis of the right lower quadrant. Paresis of in the  right  superior  (2/5)  and  inferior (4/5) limbs with hyperactive reflexes, with ipsilateral pathological reflexes such as Hoffman’s, Trommer’s and Babinski’s, plus right hemicorporal hypoesthesia. Coordination   and   gait  could  not   be  evaluated. The brain  CT-scan (Figure 1)  showed left frontal hypodensity suggestive of brain regional infarction. The patient was managed during hospitalization with intravenous  fluid replacement  and  corticoids. Due to satisfactory evolution the patient was discharged 10 days after. The outpatient controls had evidenced positive evolution of the right hemiparesis and hypoesthesia.

Fig. 1.

Brain CT-scan showing left frontal hypodensity suggestive of brain regional infarction.

Discussion

In 1956, Africanized bees began to spread in the American  continent  from  southern Brazil, where original  African  bees  mated  with  European  bees [3].  The presence of Africanized bees had produced positive effects on south-american economy, negative impacts-such as swarming, aggressive behavior, and the ability to mass attack-resulting in serious and fatal envenomation with humans and animals, can also be produced [3].

Diverse mechanisms have been proposed to give an explanation to all the clinical manifestation of both toxic and allergic reactions secondary to bee stings. Currently, the most accepted one state that victims can develop severe envenomation syndrome characterized by the release of a large amount of cytokines, mainly interleukins  (IL), e.g., IL-1, IL-6, IL-8, and  tumor necrosis factor (TNF); which subsequently, lead to acute inflammatory response triggering adverse effects on skeletal muscles; bone marrow; hepatic and renal functions; and cardiovascular, central nervous, and immune systems.

The  main  clinical manifestations  of  bee  venom poisoning are local allergic reactions at the site of the  sting such as edema, erythema, and  burn-like sensation and generalized reactions that include pruritus, urticarial, angioedema, and, in extreme cases, anaphylactic shock. Systemic toxic reactions due to venom compounds are observed usually after 50 to 100 bee bites [1].

Although adults can tolerate more than 1000 bee bites, sensitive individuals may develop mortal anaphylactic reaction after one. Sometimes life-threatening  allergic reactions  can occur due to bee stings, being the most important one the anaphylaxis. The incidence of anaphylaxis due to bee sting ranges between 0.4% and 5%. With high mortality rate associated with severe allergic reactions mainly before the age of 20 years and being twice common in male population [4].

Some unusual neurologic complications such as myasthenia gravis, peripheral neuritis, encephalomyelitis, optic neuritis, cerebral infarction, parkinsonism, trigeminal neuralgia, pontine hematoma, and thalamic and mesencephalic hemorrhages as well as the Guillain-Barré syndrome can also be related to bee stings [5].

We describe a case of multiple African bee stings in  which  the  exceptionally high dose  suggests a direct effect of hymenoptera venom on brain vessels. The case does not  follow the  reported  pattern  of hypovolemic or anaphylactic shock, hemolysis and/ or rhabdomyolysis, despite the potentially lethal amount  of  venom  injected. Diverse authors  have reported similar neurological alterations. Rajendiran et al. reported  a case of  a 25-year-old male who developed  left  sided  monoparesis  and   transient visual loss following multiple bee stings, with evidence supporting involvement of both the anterior circulation and posterior circulation territory to the brain, in our case the was involvement of the anterior left circulation [6]. Bilir et al. reported  a case of a 35-year-old man  who developed neurologic deficit 6 hours after a bee sting, which was confirmed to be left parietooccipital infarction on magnetic resonance imaging scan [1]. Dikici et al., [5] reported the case of a 49-year-old male patient presenting generalized tonic clonic seizure and loss of consciousness after an hour of wild bee bite from the anterior abdomen in a rural area. The cranial computed tomography taken in the emergency department  was normal; control cranial  computed   tomography  at  the  36th  hour after  admission  was consisted  with  subarachnoid hemorrhage  (SAH). The patient  was diagnosed as SAH due to exposure to bee stings. The patient was treated  for a month  in an intensive care unit and discharged in a vegetative state. Treatment  in these circumstances implies limiting the inflammatory cascade triggered by bee stings and the  management  of  secondary organ  injuries, i.e., intracranial  hemorrhage,  stroke,  acute  myocardial infarction, among others. Thus recurring to corticoids, antihistaminic drugs are useful in diminishing local and systemic allergic reactions, and for organ injuries, should  be applied a rationale treatment  approach. In  the  case of severe complications  such as brain ischemia/infarction or hemorrhage, rapid recognition and collaboration with experienced clinicians is the best way to facilitate specialized treatment protocols. In conclusion,  the  exact mechanism  that  drives to  brain   ischemia  are  not   fully comprehended, thus  further  studies  are  needed  to  elucidate  the pathogenetic mechanism  involved and  to  prevent organ damage as there is no complete cure for stroke [7].

Conflict of Interest: None declared.