In April 1998, an annual 2-day animal farm sale was held in Hodmezovasarhel
y, where 500 to 600 visitors consumed unpasteurized milk. The first signs o
f disease began 2 days after the end of the sale. Fifty-two people from a w
ide age range fell ill, primarily with inflammatory enteritis. These cases
included 34 with Campylobacter positivity: 30 with Campylobacter jejuni and
4 with Campylobacter coli. Environmental samples (raw milk, udder swabs, a
nd rectal swabs from 12 cows in the suspected herd) were tested 2 weeks aft
er the first signs of the disease, and two rectal swabs were found to be po
sitive for C. jejuni.. Initially, the epidemic seemed to be sporadic and, a
ccordingly, only 26 human and 2 animal Campylobacter isolates were reserved
for randomly amplified polymorphic DNA analysis. This comparative analysis
verified that fecally contaminated milk was the source of the outbreak. Th
e DNA-banding patterns of 20 C. jejuni isolates (19 human and 1 animal) wer
e identical. The antibiotic susceptibilities of the Campylobacter isolates
were determined, and only six C. jejuni (human) isolates, one C. coli (huma
n) isolate, and one C. jejuni (animal) isolate were resistant to tetracycli
ne, both by disk diffusion and by E test (antimicrobial gradient strip for
the quantitative determination of susceptibility or resistance of microorga
nisms). No plasmid was detected in these tetracycline-resistant isolates. T
he endotoxin production of Campylobacter isolates was examined via the cyto
pathogenic effect on the Vero cell line. This effect exhibited various degr
ees of positivity in 19 cases. Only two human C. jejuni isolates displayed
++++ positivity. Both isolates were from patients who had required antibiot
ic therapy and hospital care.