AIRBORNE SPREAD OF BRUCELLOSIS

AIRBORNE SPREAD OF BRUCELLOSIS

Arnold F. Kaufmann, Marshall D. Fox, John M. Boyce, Daniel C. Anderson,

Morris E. Potter, William J. Martone, and Charlotte M. Patton

Bacterial Diseases Division Bureau of Epidemiology

Center for Disease Control Atlanta, Georgia 30333, U.S.A.

INTRODUCTION

Brucellosis is a zoonotic disease that is transmitted from its animal reservoirs to humans by three primary routes: skin and conjunctival contact, ingestion, and inhalation of infectious aerosols. The relative importance of each route varies with the epidemiologic setting. Our discussion focuses on the respiratory route.

In his classic 1897 monograph summarizing the history of bruce tlosis, Hughes claimed that most patients were infected from breathing air contaminated with the causative bacterium arising from fecally polluted soil.' His theory was probably based more on the ancient concept of miasmas than on scientific observation. The role of domestic livestock in the epidemiology of brucellosis was not discovered until almost a decade later.

In reviewing the occurrence of brucellosis among Naval personnel stationed on Malta, Dudley described a shipboard outbreak of a protracted pulmonary disease with low m~rtal i ty .~ '~ He theorized that the disease was caused by Brucella melitensis adapted to growth in the human lung and transmitted person-to-person via aerosols in the ship's crowded living quarters. His hypothesis is interesting, but no convincing experimental or epidemiologic evidence for person-to-person transmission via aerosols has been subsequently developed to support it.

Aerosol transmission of brucellosis is widely accepted as a potential bioha- zard in lab~ratories.~.~ The largest single laboratory-associated epidemic of 45 cases (one fatal) occurred in Michigan in the period December 1938-February 1939.7 Most of the patients were students taking courses on the second and third floor of a building containing a brucellosis laboratory in the basement. All modes of transmission except airborne were ruled out by the investigators.

More recently, Hendricks et al. described a large brucellosis epidemic in an abattoir which apparently involved airborne transmission.' The disparate attack rates for workers doing comparable work on different floors were best explained by differences in exposure to aerosols generated in the kill department. Brucella suis was isolated from air in the kill department of this abattoir?

Experimental studies with guinea pigs show that brucellosis can be readily transmitted by Only a few more brucella organisms are required to infect guinea pigs by respiratory challenge than by subcutaneous challenge. Although brucellae readily invade through the lung, the respiratory challenge does not result in a primary pneumonia. The lesions caused by respiratory and subcutaneous challenge of guinea pigs are comparable with two exceptions." More pronounced cervical and mediastinal lymphadenopathy occurs and epi- didymitis is less frequent following respiratory challenge.

Although brucellosis can certainly be transmitted by aerosols, the respiratory 105

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106 Annals New York Academy of Sciences

route of infection has not been traditionally considered to be epidemiologically signifi~ant. '~, '~ This interpretation is probably correct in countries where brucellosis is predominantly acquired through consumption of unpasteurized dairy products and on farms and ranches. In the United States, however, brucellosis is now most prevalent among abattoir ~ 0 r k e r s . I ~ We will present evidence from a series of abattoir-associated brucellosis outbreaks that airborne transmission is important for this occupational group.

Potential Routes of Infection for Abattoir Workers

Potential routes of infection for abattoir-associated brucellosis include: (1) Direct contact of the conjunctiva or broken skin with animals, tissues, or contaminated fomites, (2) inhalation of infectious aerosols with invasion occurring through the mucous membranes of the upper respiratory tract or the lung, and (3) ingestion of tissues or fluids containing brucella organisms.

Ingestion appears to be of minor importance for abattoir-associated brucellosis in the United States. Workers interviewed in multiple outbreak investigations have reported that fresh animal tissues from processing lines, whether raw or cooked, were not commonly eaten. Also, experimental studies with guinea pigs indicate that significantly higher challenge doses are required to produce infection by ingestion than by the skin contact or respiratory route^.'^^'^ Experimental studies of adult men have also shown that humans are readily infected by exposing broken skin to brucella organisms but that infection is difficult to produce by oral challenge.'6

Assessing the relative importance of the contact and the inhalation routes of infection is more difficult because abattoir workers would seem to be exposed by both routes. However, analysis of exposure potential by slaughter process stage shows that risk varies by job location.

Slaughtering and processing of animals can be divided into three stages (FIGURE 1). In the first stage, the animals are sequentially immobilized and bled out. Hair is removed from the carcasses of swine in this processing stage. Employees who immobilize and bleed animals have contact with live animals and may be splattered with blood. Those who dehair swine have contact only with the skin of the unopened carcass. While the dehairing process may result in the generation of aerosols, they should contain few brucellae.

In stage 11. the carcasses are beheaded and eviscerated. The hide is normally removed in this processing stage from all animals except swine. At the end of this processing stage, the carcasses are split with a power saw and washed before being chilled. Persons involved in stage I1 processing have continuous contact with freshly opened animals. Their hands and forearms are often bathed continuously with blood, tissue fluids, and water. In addition, their faces are frequently splattered with these fluids. Numerous operations in stage 11, such as removing viscera and sawing and washing opened carcasses, may generate aerosols containing brucellae. Thus, stage I1 processing employees have signifi- cant exposure to both the contact and airborne routes of infection.

In stage 111. the chilled carcasses are processed into wholesale and retail cuts, sausage, and canned or smoked products. This stage also includes processing of viscera and other tissues that have been chilled or cooked. Employees involved in processing carcasses after chilling frequently have intimate tissue contact; however, the carcasses and tissues processed in stage 111 are relatively free of lymphatic tissues and free-flowing blood and tissue fluids, and they should be

Kaufmann et a].: Airborne Brucellosis 107

less hazardous to persons in contact with them. The potential for generating aerosols during stage I11 is generally minimal; therefore, the respiratory route of infection should be unimportant in this stage.

Thus, stage I workers should be at minimal risk of brucellosis, stage I1 workers are at risk of infection by both the airborne and contact routes, and stage I11 workers are primarily at risk of infection by the contact route. These differences in exposure potential are dependent on physical separation of each processing

Stage I

Imobi l i za t ion

Dehairyg (Swine)

Stage I1

Head Table

Hide Removal' (Cattle & Sheep)

Evisceration

Processing of Viscera (Casings, Offal, Inedible)

Spl i t t ing & Cleaning

1

Further Processing stage I11

Further Processing (fresh pork cuts sausage, canned and smoked products)

FIGURE 1. Schematic representation of the procedures followed in the slaughter of animals by processing stage.

stage. However, as we shall discuss, the relative separation of these stages varies in individual abattoirs.

Case Distribution in Abattoir-Associated Outbreaks

Six abattoir-associated brucellosis outbreaks investigated by the Center for Disease Control in collaboration with state health departments in the period


1960-1976 were selected for analysis on the basis of comparability of investiga- tive approach. Four abattoirs slaughtered only swine, one slaughtered cattle and swine, and vne slaughtered cattle, swine, and sheep. The slaughtering and processing procedures were similar at the abattoirs, although the physical separation of the various processing stages and the air flow patterns in the buildings differed. These variations resulted in a series of naturally occurring experiments on the importance of the respiratory route of infection for abattoir- associated brucellosis.

A total of 387 clinical cases of brucellosis occurred in the six outbreaks with attack rates ranging from approximately one to 11 percent. Case distribution by processing stage varied by abattoir (TABLE 1). The differences in case distribution correlated well with relative separation of processing stages and air flow patterns at the abattoirs (FIGURE 2).

Abattoir A

I f contact exposure is the most important route of infection in the abattoir setting, the brucellosis attack rate should be similar for groups of employees with

TABLE 1 DISTRIBUTION OF BRUCELLOSIS CASES I N SIX ABATTOIRS BY PROCESSING STAGE

Processing Stage* Abattoir I 11 111 Misc.t Total

A 16 (13%) 73 (57% ) 32 ( 2 5 7 ~ ) 7 (570) 128 B - 30 ( 3 8 7 ~ ) 23 (437< ) 10 (197") 53 C 3 (7% ) 40 (89% ) 1 ( 2 6 ) 1 ( 2 7 0 ) 45 D - 8 (57% ) - 6 (43% ) 14 E 16 (23% ) 44 ( 6 2 7 ~ 1 6 (8'h) 5 (770) 71 F a ( 1 1 7 ~ ) 54 (717~ ) 9 (12% ) 5 (770) 76

Total 43 ( 1 1 % ) 234 (60%) 71 (18% ) 39 (107o) 387

*Approximate distribution of workers by processing stage is: Stage 1-470, Stage 11-15Oh.

tlncludes maintenance, sanitation, management and other personnel who do not have Stage 111-57%, and MisceIlaneous-24T~.

primary meat or by-product processing duties.

comparable contact exposure, regardless of exposure to aerosols generated in the stage I1 processing area. However, the attack rate for employees who were exposed to aerosols from the stage I1 processing area at abattoir A was significantly higher than for unexposed control groups with similar contact exposure.8

At abattoir A, processing stages I and I1 were on the fourth floor of the building except that the head-trim department was located on the third floor. Stage I11 processing was conducted on both the third and fourth floors. Persons who worked on the fourth floor and had contact with carcasses and viscera before they were chilled (stages I and 11) had a significantly higher ( p < 0.001) attack rate of brucellosis than did head-trim department employees on the third floor (TABLE 2). If contact was the most important factor in the epidemiology of brucellosis in this setting, employees working in the head-trim department

Kaufmann et al.: Airborne Brucellosis 109

ABATTOIR A

4 t h Floor 16.4%

S t a g e I11 Stage IIt

1.8% 7.4% 3rd Floor

MATTOIR B

S t a g e 11 S t a g e I11

2 . 5 %

ABATTOIR C ABATTOIR U

11.3% 0.0%

FIGURE 2. Schematic relationship of air-flow patterns and the brucellosis attack rates in selected employee groups at four abattoirs. Arrows indicate direction of air-flow, *is the percent attack rate and t. the head-table department.

should have had the highest attack rate because B. suis infections are frequently localized in the mandibular and retropharyngeal lymph nodes of wine.'^,'^

Stage I processing employees, as discussed earlier, should be at minimal risk of acquiring infection: yet this group, located on the fourth floor, also had a significantly higher attack rate (p < 0.001] than did employees in the head-trim department. The only adequate explanation is that head-trim department employees on the third floor were separated from aerosols generated in the stage 11 processing area on the fourth floor. The attack rate for the fourth floor stage I employees was comparable to that for stage I1 employees located on the same floor, again indicating that work location is more important than degree of contact exposure.

Equally striking was the comparison of attack rates for stage I11 employees who processed chilled carcasses. This processing was done on both the third and the fourth floors, and stage I11 employees on both floors had essentially similar contact exposure to chilled tissues; however, employees on the fourth floor who worked in an area adjacent to the stage I1 processing area and were exposed to

TABLE 2 BRUCELLOSIS ATTACK RATES IN PROCESSING STAGE I, 11, AND 111 WORKERS

BY FLOOR, ABATTOIR A

Processing Stage Floor I I1 I11 Total

3rd Floor - 4/54 (7.4%)* 3/159 (1.8%) 7/213 (3.3%) 4th Floor 16/54 (29.6%) 64/206 (31.1% J 27/161(16.4%) 107/421 (25.4%)

Total 16/54 (29.6%) 68/260 (26.2%) 30/320 (9.4%) 114/634 (18.0%)

*No. brucellosis cases/no. workers at risk (701.


air from the stage I1 area had an attack rate of 16.4 percent, and employees on the third floor, who were not exposed to air from stage 11, had a significantly lower attack rate of 1.8 percent ( p < 0.001) (TABLE 2).

The various rooms of this plant were well-lighted. had high ceilings, and appeared to be well-ventilated. While the air-flow pattern was not confirmed with smoke candles, from on-site observations it appeared that the only air flow between floors was from the third to the fourth floor. The hot, humid air in the fourth floor stage I1 processing area could be seen rising and exiting through a large open skylight in the roof. The fourth floor also had exhaust fans, and the third floor did not. There was no active input of fresh air into the fourth floor. Also, the only direct connections between the floors were several chutes for conveying animal tissues. Brucellae were isolated from air in the fourth floor stage 11 processing area, and guinea pigs exposed to air exhausted from this area contracted brucellosis, confirming the presence of an etiologic agent in aerosol^.^

Because the attack rate for employees exposed to aerosols from the fourth floor stage I1 processing area was significantly higher than for employees not exposed to stage I1 but with similar contact exposure, airborne transmission seemed a likely explanation of the case distribution in this epidemic."

Abattoir B

If exposure to stage I1 aerosols is important in transmitting brucellosis to abattoir employees, forcing air from the stage I1 area into stage I11 processing areas should result in comparable attack rates in both areas. This distribution pattern occurred at abattoir B.

Abattoir €3, which had approximately 2,700 employees, was composed of a complex series of directly adjoining processing buildings for the slaughter of swine, calves, cattle, and sheep. The stage I1 processing area for swine was maintained under positive air pressure relative to other areas in the plant. Air-flow studies with smoke candles showed that during normal plant operation, air was forced out of the swine kill floor (stage 111 through various openings into many of the stage 111 processing areas and into the men's locker room.

In contrast to the other five epidemics, most employees involved in this outbreak worked in stage I11 processing on other floors and in buildings contigu- ous to the stage I1 swine processing area. The attack rates for the various stage I11 areas appeared to correlate with the amount of air they received from the swine kill floor (stage 111.

A comparison of the attack rates for stage I and I1 swine processing employees (excluding casing, offal, and inedible departments] and for employees in the pork cut and boning departments (stage 111) serves as an example. Fifteen of the 409 stage I and I1 employees (3.7 percent) had clinical brucellosis. The attack rate was comparable in the cut and boning departments, where 10 of 405 employees (2.5 percent) were affected. The cut and boning department employees were exposed to aerosols coming from the stage I1 area while working and while using the men's locker room.

Attempts to document the presence of airborne brucella organisms both by air sampling and by exposure of sentinel guinea pigs were unsuccessful at abattoir R. However, three patients had no contact with animal tissues and had not entered the kill area for many months to years before becoming ill. Two of these patients made cardboard boxes, and the third was a welder in the plant boiler room. All three were exposed to air being exhausted from the roof of the stage 11 processing

Kaufmann et a).: Airborne Brucellosis 111

area. A reasonable explanation for their brucellosis was exposure to airborne organisms.

Abattoir C

If the distribution of cases in an epidemic of abattoir-associated brucellosis correlates with exposure to air from the stage I1 processing area, putting stage I1 in a building separate from stage 111 processing areas should reduce the number of stage 111 workers who are infected. The epidemic at abattoir C supports this hypothesis.

Abattoir C, with about 400 employees for slaughtering cattle and swine, comprised several adjacent buildings. Processing stages I and I1 of both the cattle and swine slaughtering operations were done in the same building and involved about 130 employees. The other 270 employees, who were engaged in stage 111 processing and clerical operations, worked in other buildings.

In a 13 month period, 45 workers had br~cellosis. '~ All but one worked in the building housing the stage I and I1 processing areas. Brucella suis was isolated from the air in this building on several occasions.

Abattoir D

If complete physical separation from the stage I and I1 processing areas virtually eliminates brucellosis among stage 111 workers, maintaining the stage I1 area under strong negative air pressure should have a similar effect. At abattoir D. the design of the plant resulted in such a situation.

Abattoir D consisted of a single large building. The stage I1 processing area at one end of the building was separated by a large cooling room from the stage 111 processing area. The stage I1 processing area was under negative air pressure that caused a strong in-flow of air from all surrounding areas. Air was exhausted from the stage I1 area through large roof fans and did not re-enter other areas of the building.

In the period 1970-1971, 14 of the 365 employees of this plant contracted brucellosis. Eleven of the 97 people working in the stage I1 processing area were sick. None of the 18 workers in the stage I area or the 110 workers in the cut department (stage 111) where carcasses are processed immediately after chilling were affected 1 p < 0.0004).

The three patients who did not work in the stage I1 processing area were two clerks in the shipping department and a man who assembled cardboard boxes. None of these three patients handled animal products as part of their job but routinely walked through the stage I1 processing area to reach their work location.

Abattoirs E and F

The review of the first four abattoir-associated brucellosis epidemics shows that distribution of cases correlates to a large degree with distribution of air from the stage I1 processing area. Data from our next two naturally occurring epidemiologic experiments show that the same case distribution pattern applies to and is reproducible for endemic brucellosis.


Abattoirs E and F were virtually identical. They were located on adjacent premises, slaughtered only swine obtained from the same geographic area, and had similar sized work forces. The slaughtering and processing procedures at both plants were comparable. Also. the air from the kill department (stages I and 11) at both plants was primarily exhausted through large ceiling fans over the stage I work area. Little air from the kill department entered stage 111 processing areas.

Brucellosis was endemic in the workers at both plants but did not occur in discrete epidemics. In the period 1968-1974, 71 cases occurred at abattoir E, whose average daily work force was 873, and 76 cases occurred at abattoir F, whose average work force was 997. Fifty-four of the 71 (82%) cases at abattoir E were among stage I and I1 workers, as were 62 of the 76 (82%) cases at abattoir F [TABLE 3).

TABLE 3 DISTRIBUTION OF BRUCELLOSIS CASES IN Ai3A’rrOIRS E AND F BY PROCESSING

STACE AND DEPARTMENT. 1968-1974

Abattoir F - Abattoir E

Cases Cases Annual 7-Year Mean Daily Annual 7-Year Mean Daily

Stane DeDartment Mean Total Work Force Mean Total Work Force I Kill 2.3 16 I1 Kill 5.4 38

Inedible 0.3 2 Lard 0.6 4

I11 c u t 0.3 2 Curing 0.1 1 Fresh Pack 0.1 1 Other 0.3 2

Misc. Maintenance 0.3 2 Other 0.4 3

41 114

8 9

89 45 29

316 61

161

___

11 8 6.9 48 0.6 4 0.3 2 0.4 3 0.3 2 0.3 2 0.3 2 0.3 2 0 6 3

34 108 10

8 124 41 31

357 63

221

Total 10.1 71 a73 10.9 76 997

The attack rate for stage I and I1 workers was comparable at both plants. If tissue contact was of paramount importance, stage I workers who do not contact the deep raw tissues of the carcass should have had a lower attack rate. The fact that air from stage I1 moved past these workers enroute to the exhaust may explain the comparable attack rates. The incidence of brucellosis among stage 111 and nonprocessing workers was significantly lower. Extensive serosurveys of workers at these abattoirs confirmed these observations but did not provide any further epidemiologic insights.

DISCUSSION

The airborne route of infection clearly plays a role in abattoir-associated brucellosis. The distribution of cases in abattoirs correlates better with distribution of air from the stage I1 processing area than with degree of worker’s skin contact to potentially infectious materials. Persons are also infected who are

Kaufmann et a].: Airborne Brucellosis 113

exposed to air from the stage I1 processing area but have no contact with animal tissues.

The kill department (stage 11) of an abattoir is organized chaos centered on a rapidly moving carcass disassembly line. The splashing of viscera, hectic cutting operations, washing and carcass sawing generate aerosols at numerous points. Brucellae survive well in aerosols and resist drying." Thus, their potential for transmission in this environment is great.

Brucellae have been isolated from the air in abattoir kill departments in three investigations. A single colony forming unit (CFU) of B. suis was isolated from 13,592 liters of air sampled over a 5 day period at abattoir A.' Four CFUs of B. suis were isolated from 84,664 liters of air sampled over a 30-day period at abattoir C." In a third abattoir, air sampling was conducted while 136 swine from a brucellosis infected herd were being slaughtered." Two CFUs of B. suis were isolated from 849 liters of air sampled over a 90-minute period.

The low yield of brucellae from kill department air and the evidence that airborne transmission of infection does occur suggest that the minimum infecting dose by the respiratory route is low for humans. The minimum oral infective dose of B. abortus and B. suis for guinea pigs is about lo6 to lo7 organisms;'' experimental evidence suggests a comparable minimum oral infective dose for humans.'' The minimum infecting dose by aerosol or subcutaneous injection of guinea pigs, however, is less than 100 organisms." If a comparable disparity exists for humans, the minimum respiratory infecting dose may also be less than 100 organisms.

Controlling abattoir-associated brucellosis is difficult. Designing abattoirs to avoid spreading aerosols generated from stage I1 processing will reduce risk for workers in other departments but will not prevent the possibility of transmission by skin contact. Also, this approach will not affect risk for stage I1 processing workers, who already have the highest case incidence. The disease probably must be eradicated from domestic livestock or an effective human brucellosis vaccine must be developed in order to eliminate this occupational hazard.

SUMMARY

Review of epidemic and endemic brucellosis at six abattoirs demonstrates a correlation between case distribution and flow of air from the kill department [stage 11) to other areas within an abattoir. Air from the kill department dissemi- nated to nearby departments led to abnormally high brucellosis attack rates for persons who worked in these areas at two abattoirs. Complete physical separation or maintaining negative air pressure in the kill department was associated with reduced risk for workers in other areas at four abattoirs. Cases in persons who had exposure to kill department air but no contact with animal tissues provide strong evidence for airborne transmission of infection. Brucellosis is also contracted through skin contact with infectious animal tissues, but this route of transmission appears less important than formerly believed.

REFERENCES

1.

2 .

HLIGHES, M. L. 1897. Mediterranean, Malta or Undulant Fever. Macmillan and Co.

DLIDLEY, S. F. 1931. Some lessons of distribution of infectious diseases in the Royal London.


3.

4.

5.

6.

7.

8.

9.

10.

11. 12.

13.

14.

15.

16.

17.

18.

19.

20.

Navq'. Lecture I l l . The history of undulant fever in the Royal Navy. Lancet 1: 683-691.

DIIFILEY, S. F. 1935. On the biological approach to the study of epidemiology. President's address. Proc. R. Snc. Med. 29: 1-14.

DALRyMpLE-CtiAh~PNEYs. W. 1960. Brucellosis Infection and Undulant Fever in Man. Oxford University Press. London.

MEYER. K. F. & B. EDDIE. 1941. Laboratory infections d u e to brucella. 1. Infect. Dis. 68: 74-32.

TREVER, R. W.. L. E. CLIIFF. R. N. PEELER & 1. L. BENNETT. 1959. Brucellosis. 1. Laboratory acquired acute infection. Am. Med. Assoc. Arch. Int. Med. 103: 381-397.

H ~ J ~ F I L E S O N . I . F. & M. MLINCER. 1940. A study of an epidemic due to Brucella melitensis. Am. 1. Public Health 3 0 944-954.

Brucellosis outbreak in a n Iowa packing house. Am. 1. Public Health 5 2 1166-1178.

Brucella suis from air of slaughterhouse. Public Health Reports 77: 602-604.

Dis. 45: 271 -282.

HENDRICKS. S. L.. 1. H . BORTS, R. H. HEEREN. W. J. HALJSLER & 1. R. HELD. 1962.

HARRIS. M. M., s. L. HENDRICKS. G. w . GORMAN & 1. R. HELD. 1962. Isolation O f

ELBERG. S. S. & D. W. HENDERSON. 1948. Respiratory pathogenicity of brucella. I. Infect.

HENDERSON. D. W. 1960. Bacterial interference. Ract. Rev. 24: 167-176. BIICHANAN, T. M., S. L. HENDRICKS. C. M. PATTON & R. A. FELDMAN. 1974. Brucellosis

in the United States, 1960-1972. An abattoir-associated disease. Part 111. Epidem- iology and evidence for acquired immunity. Medicine 53: 427-439.

SPINK. W. W. 1956. The Nature of Brucellosis. The University of Minnesota Press. Minneapolis.

Fox. M. D. & A. F. KAIJFhlANN. 1977. Brucellosis in the United States. 1965-1974. 1 . Infect. Dis. 1 3 6 312-316.

H.4RDY. A. V.. M. G. H ~ J D S O N & C. F. ~ O R D A N . 1929. The skin a s a portal of entry in B. melitensis infections. 1. Infect. Dis. 45: 271-282.

MORALES-C~ERO. P. 1930. Brucella abortus in Porto Rico. Porto Rico 1. Public Health Trop. Med. 6: 3-88.

HLITCHINCS. L. M. 1950. Swine brucellosis. In Brucellosis Symposium. American Association for the Advancement of Science.: 188-198. Waverly Press. Washington, D.C.

MCCLILLOIIGH. N. B.. C. W. EISELE & E. PAVELCHEK. 1951. Survey of brucellosis in slaughtered hogs. Public Health Reports 66: 205-208.

WHITE. P. C.. E. F. BAKER, A. J. ROTH. W. 1. WILLIAMS & T. S. STEPHENS. 1974. Brucellosis in a Virginia meat-packing plant. Arch. Environ. Health 28: 263-271.

ROSEHURY. T. 1947. Experimental Airborne Infection. Williams & Wilkins Co. Balti- more.

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