The epidemic of cynanche angina (also known as angina maligna or malignant quinsy) that appeared in Guilford in 1769 and has spread through a series of Connecticut towns has most recently caused increased deaths in Litchfield. The colonial surveillance system based on reporting of burials by selected religious societies identified excess mortality last year in Guilford, Hartford, and Middletown (Table 1) but until earlier this year Litchfield was spared. The relationship of the angina epidemic to the spreading malady of prim, the popular hedge in Connecticut that began mysteriously to die in 1770, continues to be a cause of speculation. Likewise, whether the increase in the epidemic is related to the meteor of 1775 is unknown (1).

Fear has been expressed that the angina epidemic may reach the proportions of the epidemic of 1735-1740. That epidemic began in Kingston, New Hampshire, in May 1735 and was fatal to the first 40 persons afflicted. Spread was slow, the disease taking 3 months to reach Boston. The disease gradually travelled westward and was 2 years in reaching the river Hudson, distant from Kingston about 200 miles in a strait line. By 1740 many thousands had died including half the children of Haverhill, Massachusetts.

First reported in the colonies by Cotton Mather in 1659 (as "the Malady of Bladders in the Windpipe"), angina maligna has affected mostly children and persons less than 20 years of age. Its symptoms generally are a swelled throat with white or ash-colored specks, an efflorescence of the skin, great debility of the whole system, and a tendency to

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George Washington Custis

At 3:00 AM January 26, 4 family members became ill; the father's illness began 4 hours later. Symptoms included diarrhea and abdominal cramps (100%) and nausea (60%).

Remaining portions of each meal item were obtained from the family's refrigerator on January 26. Cultures were made of all food items except the roli and butter; all were negative except for the gravy, which had 5.8x105 Clostridium perfringens per gram. A package of chicken gravy mix, obtained from the restaurant, contained <102 C. perfringens per gram. Since the dry gravy mix is combined at the restaurant with water and cracklings, a sample of cracklings was also tested and found to contain <102 C. perfringens per gram.

Stool specimens from 2 patients were negative for salmonella and shigella but both contained C. perfringens.

International Notes

These organisms and those from the gravy were non-typable by CDC's laboratory. C. perfringens organisms from the gravy and from 1 patient sporulated sufficiently in vitro to produce enterotoxin.

It was the restaurant's practice to save remaining gravy for use the next day. Failure to properly reheat the gravy before placing it on the steam table presumably led to this outbreak.

Reported by PJ Pace, City of Milwaukee Health Dept; CL Duncan, PhD, Food Research Institute, University of Wisconsin, Madison; KO Bjorklund, HG Skinner, MD, State Epidemiologist, Wisconsin State Dept of Health and Social Services; Enterobacteriology Br, Bacteriology Div, Bur of Laboratories, and Enteric Diseases Br, Bacterial Diseases Div, Bur of Epidemiology, CDC.

Three episodes of milk-borne Salmonella virchow infection occurred in 1 local authority area of England in a 12-month period.

In June 1974 a veterinary surgeon reported that he suspected that a specimen of bovine feces contained salmonellae. Examination of milk filters from the farm showed S. virchow. The farmer had a herd of 55 milk-producing cows, which produced 120 gallons per day; 48 untreated (unpasteurized) gallons were bottled daily on the farm and sold retail by the farmer's son. The farmer, his wife, and their 2 sons submitted fecal specimens, and all were positive for S. virchow, although none of these people gave a history of any bowel upset. It was reported that 18 cows had been ill with diarrhea, but the farmer did not agree to fecal swabs being taken from the herd until October, at which time 3 swabs were positive for S. virchow. Fecal specimens were again taken from the family. One young boy's specimen was positive for S. virchow; those from the other members of the family were negative. Again, none gave a history of bowel upsets. However, the farmer's grandchild, who lived nearby, had been ill with gastroenteritis, and S. virchow was recovered from her feces. The farmer made no attempt to clear the herd of infected animals but agreed to send all his own milk for heat treatment and not to supply his son again with untreated milk.

In March 1975 a married couple in the area was reported to be suffering from diarrhea and vomiting. S. virchow was

isolated from the feces of both patients. They were found to drink untreated milk from a local farmer. An examination of milk filters on the farm revealed S. virchow and S. saint-paul. The dairy herd consisted of 75 cattle, and rectal swabs were positive for S. virchow in 11 and for S. saint-paul in 1. The farmer himself was found to have S. virchow in a fecal specimens but denied having had symptoms.

In April 1975 notification was received that S. virchow had been isolated from the feces of an 83-year-old man, a patient at a hospital. On investigation it was found that he also was supplied with untreated milk at his home. Subsequently, S. virchow was isolated from milk filters taken from the farm that supplied the milk. The farmer was found to have S. virchow in a fecal specimen, but all rectal swabs taken from the herd were negative. S. virchow was later isolated from 3 customers who had been ill with gastroenteritis. The 83-year-old man died in the hospital; the cause of death was stated to be bronchopneumonia.

Subsequent investigation of these 3 separate outbreaks of milk-borne S. virchow infection by staff of the veterinary service failed to show any common source of infection.

From notes based on reports to the Public Health Laboratory Service from public health and hospital laboratories in the United Kingdom and the Republic of Ireland, published in the British Medical Journal, October 18, 1975.

Three cases of human infection caused by monkeypox virus were detected in Zaire during 1975-1976. Since discovery of the first human case in August 1970, 21 cases have been diagnosed; 13 occurred in Zaire, 4 in Liberia, 2 in Nigeria, and 1 each in Ivory Coast and Sierra Leone. The reservoir of this virus is still unknown. Despite the fact that the patients were in contact with large numbers of susceptible persons, a secondary case occurred on only 2 occasions, once in Nigeria and once in Zaire. In 2 other in

stances, cases occurred simultaneously in one locale, 3 in one outbreak in Liberia (1970) and 2 in Zaire (1972).

In the belief that perhaps additional cases of monkeypox have been occurring but are not being detected, special surveys were undertaken during 1975 by joint national-WHO teams in Liberia, Nigeria, Sierra Leone, and Ivory Coast. All inhabitants of villages where a monkeypox case had occurred and residents of surrounding villages were carefully examined for vaccination scars and for facial pockmarks