Paralytic Shellfish Poisoning - Continued

The last reported outbreak occurred July 18, when a local physician in Haines performed mouth-to-mouth resuscitation and an emergency tracheotomy on a 39-year-old male and treated 3 other members of the patient's family, all of whom had symtoms of PSP including oral numbness, vomiting, double vision, loss of equilibrium, and varying degrees of respiratory paralysis after consuming a meal of local mussels. The family was immediately air-evacuated to Juneau for treatment and hospitalization. The father was placed on a respirator for 48 hours. Recovery was slow with muscular weakness persisting for several days. The 3 other family members were released after 2 days. PSP was the admitting diagnosis and confirmed by mouse bioassay of the stomach contents of the father with a report of 370 micrograms of PSP toxin per 100 grams of sample.

The family, from Whitehorse, Yukon Territory, had gathered mussels during a holiday cruise of the Lynn Canal area. The father had eaten about 2 dozen of the sautéed mussels; the mother and 2 children had consumed lesser amounts. Within 15 minutes after eating, the father had begun to experience numbness of the mouth with rapid development of other symptoms. The family rushed into

Haines and was taken to the Juneau Hospital. Samples of the mussels from the same beach location were later obtained and tested; 6,107 micrograms of PSP toxin per 100 grams of meat were found.

Reported by D Gerber, Southeastern Regional Laboratory, Juneau; K Ballentine, M Bixby, PHN, J Cladouhos, R Fraser, MD, G Markham, JP Middaugh, MD, Acting State Epidemiologist, and FP Pauls, DrPH, Alaska State Dept of Health and Social Services; and Enteric Diseases Br, Bacterial Diseases Div, Bur of Epidemiology, CDC.

Editorial Note: Although PSP has been recognized in Alaska for at least 167 years, the incidence and severity of the phenomena increased dramatically during the summer of 1976. The majority of the cases involved non-residents of the state.

PSP is caused by ingestion of bivalve mollusks contaminated with neurotoxin (termed saxitoxin) produced by species of the dinoflagellate Gonyaulax. Saxitoxin, a heatstable molecule, is thought to act by blocking the propagation of nerve and muscle action potential (1).

References

1. Hughes JM, Merson MH: Fish and Shellfish Poisoning. New Engl J Med 295:1117-1120, 1976

Haemophilus influenzae, type b, resistant to chloramphenicol, was recovered from blood and cerebrospinal fluid (CSF) of a 9-month-old male from Philadelphia, Pennsylvania on November 4, 1976.

The infant had never traveled from Philadelphia. He was a normal child in good health until November 2, 1976, when he fell, hitting his head. About 6 hours after the fall he became lethargic and febrile to 102 F. At a local hospital he was noted to have an occipital fracture and a large occipital hematoma; he was hospitalized for observation. The following day his fever rose to 104 F, and a lumbar puncture was performed which revealed a CSF with a protein of 116 mg %, glucose of 28 mg %, 1800 neutrophils /mm3, 440 mononuclear cells/mm3, 100 red blood cells/ mm3, and a gram stain which revealed gram-negative pleomorphic rods. Cultures of blood and CSF were obtained before he was given intravenous ampicillin and transferred to another hospital.

On admission to the referral hospital, the patient was stuperous, had paresis of the right arm and a temperature of 104 F. Another blood culture was obtained, and he was begun on intravenous ampicillin at 400 mg per kg per day and intravenous chloramphenicol at 100 mg per kg per day. H. influenzae, type b, was isolated from CSF and from both blood cultures. The infant remained stuperous with a temperature to 103 F through the fifth day of therapy. On the sixth day of therapy a repeat lumbar puncture was performed which revealed CSF with a protein of 54 mg %, glucose of 65 mg %, and 166 white blood cells/mm3 of which 32% were neutrophils and 68% were mononuclear cells. CSF culture was negative. On the seventh day of therapy a computer axial tomography scan of the skull revealed fluid over the right hemisphere with shift of midline structures to the left. Seventy cubic centimeters of sterile, non-purulent hemorrhagic fluid was drawn from the right subdural space. After completing 7 days of ampicillin and chloramphenicol, the patient was switched to intravenous chloramphenicol alone. By the eleventh day of therapy he had become afebrile, and his neurologic symptoms gradually improved. Chloramphenicol was discontinued after 24 days of therapy. A third lumbar puncture was performed 5 days after completion of antibiotic therapy; it revealed a protein of

17, a glucose of 51, and 50 white blood cells/mm3 of which 90% were mononuclear cells and 10% were neutrophils. He has remained afebrile while off antibiotics and is being observed.

H. influenzae, type b, organisms isolated from initial blood cultures and initial cerebrospinal fluid cultures were sensitive to ampicillin but resistant to chloramphenicol. The minimum inhibitory concentration as performed by CDC was 32 μg per ml of chloramphenicol, 32 μg per ml of tetracycline, and 0.25 μg per ml of ampicillin, as determined by micro tube dilution technique.

Reported by S Long, MD, S Phillips, PhD, St. Christopher's Children's Hospital, Philadelphia; W Parkin, DVM, Acting State Epidemiologist, Pennsylvania State Dept of Health; Clinical Bacteriology Br, Bacteriology Div, Bur of Laboratories; and Special Pathogens Br, Bacterial Diseases Div, Bur of Epidemiology, CDC.

Editorial Note: There have been 3 previously reported isolates of H. influenzae resistant to chloramphenicol. The first isolate was a type b organism recovered in Texas from a child with meningitis, but it was not confirmed (1). The second, from the throat of a 4-year-old Dutch girl with leukemia (2), and the third, from the blood, sputum, and conjunctiva of a 38-year-old Connecticut woman with agammaglobulinemia, were non-typable strains (3). This is the first H. influenzae, type b, isolated from a child with meningitis which CDC has confirmed to be resistant to chloramphenicol.

Chloramphenicol has been recommended for initial therapy in documented or suspected severe H. influenzae, type b, infections because of the occurrence of ampicillin-resistant type b isolates (4). Intravenous ampicillin and chloramphenicol have been recommended as initial therapy for purulent meningitis in childhood (5).

Regimens that may be effective in treatment of meningitis caused by H. influenzae resistant to ampicillin, tetracycline, and chloramphenicol include intrathecal streptomycin and the combination of trimethoprim and sulfamethoxazole given orally (6).

References

1. Barrett FF, Taber LH, Morris CR, et al: A 12-year review of the antibiotic management of Hemophilus influenzae meningitis: Comparison of ampicillin and conventional therapy including chloramphenicol. J Pediatr 81:370-377, 1972