Typhoid Fever - Continued

S. typhi on 3 occasions in June. Water samples of their homes also were negative.

Reported by L Berry, St. Edwards Hospital, Fort Smith, Arkansas; CH Floyd, MD, and JM Post Jr, MD, Fort Smith; C Cook, MD, Poteau, Oklahoma; PC White, Jr, MD, Arkansas State EpidemiInternational Notes

ologist, Arkansas State Board of Health; A Start, MD, Oklahoma State Epidemiologist, Oklahoma State Dept of Health. Editorial Note: Typhoid fever is rarely reported from Arkansas but, when diagnosed, it usually can be traced to elderly relatives who are carriers. There are 68 known carriers in the state with an average age of 70 years.

In the period July-September 1976, a few sporadic cases of fever with hemorrhagic manifestations were observed in the area of Nzara and Maridi in southern Sudan (MMWR 25 [40]). The first cases are believed to have occurred in households in an agricultural settlement. In September, 30 of 42 known cases in the Maridi hospital were staff members, suggesting direct person-to-person transmission. By October 9, 137 cases with 59 deaths had been reported from the area as a whole, including Nzara, Maridi, and Lirangu. The disease caused alarm locally, making it difficult to maintain surveillance of numerous contacts of primary cases. The outbreak is considered to be declining.

The patients' symptoms include acute fever, malaise, sore throat, muscular pain, vomiting, and diarrhea; upper respiratory tract symptoms are more common than gastrointentinal ones. Severe cases developed epistaxis, subconjunctival hemorrhages, hemoptysis, hematemesis, and melena. A body rash and tremors and convulsions, suggesting central nervous system involvement, were also observed in some instances. Fatal cases became very toxic with death occurring 7-14 days after onset of the disease.

The National Administration in collaboration with WHO is undertaking a systematic epidemiologic investigation of the outbreak and implementing the necessary control

measures.

In northern Zaire an outbreak of viral hemorrhagic fever with symptoms similar to those described for cases from Sudan has been reported from the zone of Bumba. Details of the number of cases are not yet available but the case fatality ratio is believed to have been high.

Reported by the World Health Organization in the Weekly Epidemiological record 51(42):327, 1976; and Bur of Laboratories, CDC.

Surveillance Summary

FIGURE 1. Electron micrograph of Marburg-like virus from first cell culture passage from human serum from Zaire. The virus is morphologically indistinguishable from Marburg virus but appears to be serologically unrelated. Approximately x 40,000 mag. Findings were confirmed simultaneously by 3 laboratories - CDC, the Institut de Médecine Tropicale Prince Léopold and the University of Antwerp, Belgium, and the Microbiological Research Establishment, Porton Down, Salisbury, England.

State and nationwide data sources generally report a decreasing incidence of Rh hemolytic disease and infant mortality and an increasing use of the preventive agent, Rh immune globulin (RhiG), according to the recently released CDC Rh Hemolytic Disease Surveillance Summary for 1974. In 5 of the 10 census divisions, however, the previously observed steady deciine in Rh disease mortality was absent.

Rh hemolytic disease of the newborn, which results from an Rh incompatible pregnancy of a previously sensitized Rh negative woman, is characterized by red blood cell hemolysis resulting in anemia, hyperbilirubinemia, and edema. Depending upon the amount of red blood cell destruction, the disease may range from mild anemia in newborn infants to severe hydrops in stillborn infants. The *Rh negative woman with an Rh positive fetus.

disease became preventable in the United States in 1968 when RhIG was licensed for use. If administered to Rh negative women with Rh positive fetuses within 72 hours of pregnancy termination, RhIG suppresses the maternal antiRh antibody response. The widespread and regular use of RhIG can virtually eliminate maternal Rh sensitization, thereby eradicating Rh hemolytic disease of the newborn.

According to the report, the nationwide Birth Defects Monitoring Prograrn (BDMP) registered a decline in the incidence of Rh hemolytic disease from 45 per 10,000 total births (live births and stillbirths) in 1970 to 23 per 10,000 total births in 1974, a 49% reduction in incidence. (BDMP is the largest single source of uniformly collected and coded hospital discharge data on newborn infants in this country.) If one assumes that the BDMP figures are representative of the entire United States population, an estimated 16 0

Rh Hemolytic Disease - Continued

infants were affected with Rh hemolytic disease in 1970 and 7,000 in 1974. Three states - California, Connecticut, and New Jersey - of the 4 with special programs for collecting and reporting data on Rh hemolytic disease incidence reported similar declines for the same period.

In the United States infant mortality caused by hemolytic disease of the newborn has declined consistently for over 2 decades. In 1950, the disease accounted for 2.4% (1), in 1968, 1.2% (2), and by 1974, only 0.6% of total infant mortality (3). Data from states' vital records show that nationwide infant mortality due to hemolytic disease of the newborn has declined from 941 deaths in 1968 (2.7 per 10,000 live births) to 320 (1.0 per 10,000 live births) in 1974 (Figure 2). However, in contrast to 1973, 3 of the 10 census divisions and 21 states reported increased rates in 1974. (The rates of 2 census divisions remained the same.)

While Rh hemolytic disease incidence and infant and fetal mortality have been declining, the number of eligible Rh negative women who have received Rh immune globulin has been increasing. According to data from 5 states with Rh disease surveillance programs, the RhIG utilization rate - the ratio of the number of RhIG doses distributed to the number of women who should have received RhIG has increased. Nationally, the estimated RhIG utilization rate † has increased from 79% in 1973 to 80% in 1974. The 1974 figure was based on data supplied by the 5 globulin producers, who distributed 357,814 doses of RhIG that year. Preliminary data show that 403,866 doses of RhIG were distributed in 1975.

Reported by Birth Defects Br, Cancer & Birth Defects Div, Bur of Epidemiology, CDC.

References

1. National Office of Vital Statistics: Vital Statistics in the United States, 1950. 1:169. Washington, Government Printing Office, 1954 2. Health Services and Mental Health Administration and National Center for Health Statistics: Vital Statistics of the United States, 1968, 2: Part A, Washington, Government Printing Office, 1972

**Since virtually all mortality from hemolytic disease is due to Rh incompatibility (rather than ABO or other blood incompatibilities) these data are useful in observing the national Rh hemolytic disease mortality trends.

↑ Includes use after abortions as well as after term deliveries.

A private physician in rural northeast Georgia reported in May 1976 that 4 persons from one 7-member family had been hospitalized with suspected Rocky Mountain spotted fever. Subsequent laboratory tests confirmed the diagnoses.

The index case was a 58-year-old man who became ill on May 4 with low grade fever and headache. Three days later he visited his physician complaining of chills, fever, myalgia, and a severe headache. At that time his temperature was 102.4 F, and tachycardia and a macular rash around the belt line and under the arms were noted. He gave a history of removing a tick from his hand on May 1.

The patient was hospitalized and penicillin therapy begun. By May 10, the rash had spread to his entire body and to the palms of his hands, and antibiotic therapy was changed to tetracycline (500 mg/6 hours). The clinical improvement was immediate, and the patient's recovery was uneventful. Complement fixation tests performed on acute and convalescent sera confirmed Rocky Mountain spotted fever as the cause of illness.

The second case was the first patient's 7-year-old son, who became ill on May 5 with a temperature of 102.4 F, myalgia, and a severe headache. A rash appeared on the axillary region the next day and spread by May 10 to the entire body and palms. The signs and symptoms persisted, and his condition worsened. He was semi-comatose when admitted to the hospital on May 11. The third and milder case was in the 46-year-old wife of the index case, who had onset May 5 of fever, chills, severe headache, diarrhea, and vomiting. A rash appeared at the belt line for 2 days, and she was hospitalized on May 12 with a fever of 102.4 F. The last case was the 12-year-old son, who became ill on May 19 with symptoms of anorexia, generalized myalgia,

dizziness, and a temperature of 104.8 F. The patient was admitted to the hospital the next day when a very light macular rash appeared on his lower extremities and face.

All 4 patients were treated with tetracycline, and all recovered. Ticks had been removed from 3 of the 4 family members on May 1. All 4 cases were laboratory confirmed by complement fixation tests as Rocky Mountain spotted fever. Tests for murine typhus were negative.

Tick collection was attempted in the family's home, a farmhouse in an unwooded area of the family's poultry farm. Two yard-dragging attempts both unsuccessful were undertaken, since the patients gave no history of travel into wooded areas. Three ticks were collected from the family's pet dog. These ticks, Dermacentor variabilis, were negative for rickettsia by hemolymph test. The first patient sprayed pesticide on approximately May 25 both inside his home and in the entire area within 50 feet of the house.

Reported by TB Gibson, MD, Winterville, Georgia; JK Larkins, District 10, Athens, JE McCroan, PhD, State Epidemiologist, and JD Smith, Georgia Dept of Human Resources; Viral Diseases Div, Bur of Epidemiology, CDC.

Editorial Note: Approximately 5% of Rocky Mountain spotted fever cases reported to CDC have associated cases in the same household. However, the combination of 4 cases from 1 household together with the temporal clustering in this outbreak are unusual.

Reported cases of Rocky Mountain spotted fever have continued to increase this year. To date, a total of 825 cases have been reported to CDC, compared with 776 cases in the corresponding period of 1975.

Five confirmed cases and 1 suspected case of serogroup A meningococcal meningitis or septicemia have been reported to the Alaska Division of Public Health since February 1976. There had been no serogroup A cases identified in the preceding 7 years. Three of the confirmed cases and the 1 suspected serogroup A case were adults, and 2 were children. There was 1 death. Two isolates have been tested

Rocky Mountain Spotted Fever Continued proximately 500 people. The case suspected to be caused by serogroup A was an adult household contact of 1 of the Anchorage cases; he had had meningococcal meningitis 3 weeks earlier. The other adult and 2 children lived in other cities, and there was no other known contact between

cases.

Reported by F Pauls, PhD, Section of Laboratories, JP Middaugh, MD, Acting State Epidemiologist, RI Fraser, MD, Alaska Division of Public Health; Special Pathogens Br, Bacterial Disease Div, Bur of Epidemiology, CDC

Editorial Note: In the last year there have been small outbreaks of group A meningococcal disease in Seattle, Washington, and Portland, Oregon (1,2). Most cases have occurred in the skid row communities of those cities in persons who are heavy alcohol users. There is a great deal

International Notes

of travel between Alaska and the rest of the northwest United States, which may have contributed to this unusual incidence of group A cases. However, no direct link between this outbreak and the earlier ones in Seattle and Portland has been demonstrated.

Group A meningococcal vaccine is available for control of meningococcal disease in populations with clearly demonstrated high risk. Household contacts of cases should receive chemoprophylaxis and, if the index case is known to have had serogroup A disease, the use of group A vaccine in household contacts should be considered (3). References

1. MMWR 25(15):123, Apr 23, 1976

2. MMWR 25(35):277-278, Sep 10, 1976

3. Advisory Committee on Immunization Practices: Meningococcal polysaccharide vaccines. MMWR 24(45):381-382, 1975