Chlamydial infections

Chlamydial

infections

Elaine Larson, R.N., Ph.D., F.A.A.N. Irving Nachamkin, Dr.P.H., M.P.H. Philadelphia,

Pennsylvania

Chlamydiae

are small bacteria that have a unique life cycle. There are two species, and C. truckomatis, which cause a wide spectrum of clinical disease, including neonatal conjunctivitis and pneumonia, sexually transmitted disease, psittacosis, and trachoma. The importance of chlamydial disease in public health is being increasingly recognized, and the incidence in developed countries seems to be increasing. An understanding of chlamydial disease, its prevention and t::eatment, is essential for the infection control practitioner, who can play a significant role in patient education. (AM J INFECT CONTROL 13: 259-268, 1985.) Ckhnydia

psittaci

Chlamydial infection was described as early as 2700 BC by the Chinese. Trachoma, a disease caused by certain strains of Chlamydia trachomatis, was prevalent in the Middle Ages among crusaders in Palestine and was again introduced into Europe in the late eighteenth century during the Napoleonic Wars. Only in recent times, however, has the order Chlamydiales been accurately identified and classified. We now know that there are two species of Chlamydia, and thlzre are many serotypes that cause a variety of disease manifestations. THE ORGANRSM Chlamydia are bacteria that undergo a unique developmental cycle in contrast to most bacterial species and are obligate intracellular parasites. According to the most recent classification schema, ChZamydia belong in the order Chlamydiales and the family Chlamydiaceae as described in Elergey’s Manual of Systematic Bacteriology.’ Two species are presently recognized in the genus: C. psittaci and C. trachomatis. HuFrom the School and Laboratory Reprint Terrace,

of Nursing,* and the Department of Pathology Medicine of the University of Pennsylvania.

requests: Elaine Larson, Cabin John, MD 20818

R.N.,

Ph.D.,

6428

Wishbone

*Views expressed in this article are those of the authors and no official endorsement of the Robert Wood Johnson Foundation is intended or should be inferred.

mans are the natural host for C. trachomatis. In addition, this species causes a latent respiratory infection in mice. Birds, domestic animals, and wild mammals are natural hosts for C. psittaci. Chlamydia have cell walls similar to more common gram-negative bacteria except for their lack of muramic acid. These bacteria are nutritionally dependent upon the host cell and cannot be grown in cell-free media. Chlamydia are unable to synthesize their own high-energy compounds and have thus been described as “energy parasites.“’ The cell cycle involves two morphologically distinct forms described as elementary bodies (EB) and reticulate bodies (RB). EB are nonmultiplying cells specialized for extracellular transit and entry into new host cells, whereas RB are noninfectious cells specialized for intracellular multiplication.’ The first stage in the developmental cycle is attachment of EB and entry into the host cell, where they reorganize into RB. Penetration of chlamydiae into the host cell is an active process induced by the organism. In some manner, the organisms prevent fusion of the phagosomal vacuole with lysosomes and are able to grow within the cell. After entry and transformation into RB, the RB multiply by binary fission. At some stage in this multiplication, the RB convert into newly formed EB and are released from the host cell for subsequent attachment 259

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Table 1. Spectrum of disease and manifestations associated with chlamydial serotypes Speoies

c. psittaci C. trachomatis

Disease and manifestations

S-type

Psittacosis(atypiL-l,

L-2, L-3

A, B, Ba, C D-K

cal pneumonia) Lymphogranuloma venereum Trachoma Neonates: conjunctivitis, pneumonia Adults: ocular and genital infections

and reentry into new cells.‘v2 The cell cycle takes approximately 48 to 72 hours after infection. ChZumydia are inhibited by several antimicrobial agents such as tetracyclines, erythromycin, and rifampin when tested in vitro. C. truchomatis can be differentiated from C. psittuci on the basis of sulfonamide susceptibility: C. truchomutis is susceptible to sulfonamides in vitro whereas C. psittuci is resistant. In addition, cells infected with C. truchomutis produce inclusions that contain glycogen whereas C. psittuci inclusions do not.3 All chlamydiae share a common genus-specific antigen.2 However, there are 15 recognized serotypes of C. truchomutis. The spectrum of infection for lymphogranuloma venereum (LGV) is sufficiently different from that caused by other serotypes of C. truchomutis to consider LGV serotypes as a different species. Immunologic differences also occur in C. psittaci strains.4 EPIDEMIOLOGY AND CLINICAL MANIFESTATIONS

The three major areas clinically affected by various serotypes of C. truchomutis and by C. psittuci are genital, ocular, and respiratory (Table 1). Genital

infection

Worldwide. Genital disease in developed countries is caused by serotypes D through K of C. truchomutis. In addition, serotypes L-l, L-2, and L-3 cause LGV, a sexually transmitted disease (STD) that occurs worldwide, but primar-

ily in individuals in the tropics.

of lower socioeconomic

status

In developed countries. C. truchomutis is the most common cause of STD in developed countries.S-s Although it is not a highly invasive organism and infection often goes undiagnosed, it is several times more common than infection with the gonococcus or Trichomonus vaginalis. Hence, it represents a significant public health problem. In the United States annually, there are an estimated three million cases of chlamydial genital infection.7, ’ The epidemiology of chlamydial genital infections parallels that of other STD; its occurrence is more common during ages 20 to 40 years, among individuals with multiple sex partners, and in conjunction with other STD.‘O C. truchomutis has been demonstrated in numerous reports to be significantly associated with gonorrhea1 infection,‘1-‘4 but the prevalence of chlamydial antibody in tested populations is higher than the prevalence of antibody to herpes virus or to Neisseriu gonorrhoeue.‘, ‘3-‘5

The primary site of infection in women is the cervix and in men, the urethra.16 Although infection is often asymptomatic, sequelae occur most frequently and are more serious in women. The most common clinical manifestations of chlamydial infection in women are cervicitis, salpingitis, bartholinitis, pelvic inflammatory disease (PID), and postpartum endometritis; in men, urethritis, epididymitis, and proctitis.7, 17-lpIt has been estimated that Chlumydiu may be responsible for as much as half of cases of acute salpingitis,p*‘3f20 which in turn increases the risk of ectopic pregnancy and infertility. 2o,21 In addition, C. truchomutis is responsible for about one fourth of PID in the United States, Great Britain, and Scandinavia. I** 13r**, 23 Some have speculated that Chlumydiu may be related to cervical neoplasia.1*r24 Approximately half of cases of nongonococcal urethritis (NGU) in men are associated with C. truchomutis.25, 26 Both sexes can acquire venereal Reiter’s syndrome (urethritis, polyarthritis, and conjunctivitis or uveitis). The incubation period for genital infections is 7 to 28 days, usually approximately 2 weeks. If symptoms develop, they are most frequently mild dysuria and mucopurulent urethral dis-

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1985

Fig. 1. Giemsa

stain of infected

McCoy cells show characteristic

charge in men and vaginal discharge, mild dysuria, urinary frequency, pelvic pain, and pain with sexual intercourse in women.26 Sometimes more severe symptoms such as fever and acute abdominal palin occur.“.” There are no pathognomonic symptoms indicative of infection with C. twachomatis. Lymphograttuloma venereum. LGV is an STD primarily occurring in tropical and subtropical climates (India, Indonesia, East Africa, Central and South America). LGV is rare in developed countries: < 1000 cases are reported annually in the United States, mostly among individuals who have hasd sexual exposure in foreign endemic areas.;13 Fewer than 20 cases were reported in Scandinavia in 1980.27 The clinical disease is approximately 20 times more common in men than in women. LGV strain:5 are the most invasive strains of ChZamydia and generally infect macrophages and other mononuclear cells.*’ However, symptoms are usually limited to the genitalia and to the inguinal ;and pelvic lymph nodes. Clinical disease can be divided into three stages. The first stage occurs after an incubation period of 3 to 30 days as a painless papule or vesicle in the exposed region, usually the penis or vagina, but rarely in the rectum, tongue, or even finger. EIecause this primary sore is painless, it goes unrecognized in approximately 75% of cases and heals in a few days. After several weeks the secondary stage of

cytoplasmic

261

inclusion.

lymph node involvement occurs. The lymphadenopathy is usually unilateral, involving the inguinal or femoral lymph nodes. If untreated, the swollen lymph nodes (called buboes) rupture, resulting in suppurating fistulae. The affected individual will often have systemic symptoms such as fever, chills, headache, and muscle and joint aches. Scars formed by healing lesions impair lymph drainage. This can result in the elephantiasis of lower limbs often associated with LGV. The tertiary stage occurs 5 to 10 years after untreated infection, as a result of the progressive spread of infection to adjacent lymph nodes. In this stage, destruction of the urethra, vulvar-perineal-rectal fistulae, chronic genital ulcers, and intestinal strictures are seen. Damage caused by such tertiary lesions often requires surgical correction. LGV strains have also been reported to cause cervical lymphadenopathy, proctitis, aseptic meningitis, conjunctivitis, and have been associated with hepatic and cardiac involvement.*7, 29 Little is known about the development of immunity against the LGV agent. Ocular

infection

In developed countries. Ocular infection caused by C. trachomatis (called inclusion conjunctivitis or paratrachoma) is acquired when infected material from the genital tract is transferred to the eyes. It is most common in new-

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262

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and Nachamkin

INFECTION

Journal

of

CONTROL

Fig. 2. Infected McCoy cells stained with a fluorescein tagged-monoclonal antibody (MicroTrak, Syva Company, Palo Alto, Calif.) show fluorescent cytoplasmic inclusion. borns, who acquire the infection from the mother during birth, but it also occurs in adults. Si rice the first isolation of C. truchomatis from an infant’s eyes and the mother’s cervix in 1959,3c’ it has become clear that infants who pass through an infected birth canal have an approximately 70% risk of acquiring chlamydial infection. From one fourth to one half of infected infants have clinical conjunctivitis and in 10% to 20%, chlamydial pneumonia develops. 3’ An estimated 5% to 30% of all neonatal conjunctivitis is caused by C. trachomatis.“2 After a:n incubation period of 3 to 14 days, infection in neonates is usually manifested by a mild, acute purulent conjunctivitis, sometimes associated with swelling of the eyelids. Untreated cases can continue to be symptomatic for weeks or months, but the course is usually benign; conjunctival and cornea1 scarring is rare.14, .‘2 There is nothing clinically distinctive about the symptoms. Because the incubation period is usually longer than a neonate’s hospital stay after birth, diagnosis is not often made in the hospital. However, once eye infection develops, Chlamydia are shed profusely, and sprea.d between siblings has been documented.32, 33Therefore, it seems reasonable that a hospitalized infant with chlamydial infection should be placed in barrier isolation. Chlamydial eye infection in adults is also mild, causing tearing, purulent drainage, red-

ness, a sense of a foreign body in the eye, photophobia, and eyelid swelling. C. trachomatis is probably responsible for ~20% of adult keratoconjunctivitis in developed countries, and may even be spread in swimming pools when infected genital secretions are present3’ Unlike trachoma, chlamydial ocular disease caused by serotypes D through K does not result in blindness. Worldwide. Trachoma, caused by serotypes A, B, Ba, and C of C. truchomatis, is a local infection of the epithelial cells of the eye and sometimes the nasopharynx. Unlike eye infections caused by serotypes D through K, it is not an STD but is spread by direct eye-hand-eye contact, by indirect contact with contaminated articles, and probably by a fly vector. In endemic areas-North Africa, the Middle East, Southeast Asia, and India-most children are infected before the age of 2 years. Trachoma is the leading cause of blindness in the world. For example, almost 800/100,000 people in rural southern Africa have been blinded by trachoma.34 The estimated worldwide prevalence of trachoma is about 500 million people.35 About 1000 cases per year of a mild form of the disease are reported among American Indians.23 Although trachoma is an ancient disease, described in China before Christ, isolation of the trachoma agent was not reported until 1957.3” Trachoma is a familial disease; young chil-

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1985

dren are the primary source of infection. Infection usually occurs within the first 6 weeks of life. Genital ‘carriage of C. truchomatis is uncommon in areas where trachoma is endemic.-)’ The infecting Chlumydia cause bilateral inflammation of the conjunctiva that is ordinarily selflimited. Sometimes, however, keratitis, cornea1 vascularization and infiltration of leukocytes (called pannus formation), and scarring of the conjunctiva and cornea occur. Blindness results from severe scarring and fibrosis and by deformity of the eyelids that causes the lashes to turn in and produce cornea1 abrasion. The disease varies in severity and all degrees of severity can be seen in the same community.35 Improvement in hygiene and living conditions is the best method for control of trachoma and has been shown to result in a significant reduction in the incidence.34. 37 Respiratory

infection

Although genital strains of C. truchomatis are not common causes of pneumonia in adults, they cause almost half of pneumonias in infants <6 months of age.33 The incidence is approximately B/1000 live births in the United States. Disease usually manifests itself in the second or third month of life. It is slow in onset. Although the infants usually have no fever, they have a rapid respiratory rate, crepitant rales, and a protracted, staccato cough similar to that heard with whooping cough (except for the absence of the inspiratory “whoop”). There is recent but inconclusive evidence that C. trachomatis may be responsible for ~20% of pharyngitis in adults.38 Caused by C. psittaci. C. psittuci causes an infectious atypical form of pneumonia called psittacosis (obsolete terms are parrot fever and ornithosis), which is transmitted by at least 130 species of birds, including parrots, parakeets, pigeons, canaries, gulls, and even domestic poultry such as chickens, ducks, and turkeys.39 Outbreaks of psittacosis were reported during the late 18OOs, but it was not until 1930 that the causative agent was discovered. Although the disease occurs worldwide, it is rare in the United States: approximately 50 to 100 cases are reported each year.23 Young birds are infected by contact with contaminated excreta. If they survive the disease, Caused by C. trachomatis.

2Q3

they become healthy carriers. Transmission to humans results from inhalation of organisms from infected bird excreta, handling of infected birds (whose tissues and feathers are also infectious) or excreta, or bite wounds. The organisms settle in lung alveoli and reticuloendothelial cells, resulting in patchy inflammationandpneumonitis.Aftera l- to3-week incubation period, symptoms may occur gradually or suddenly and may be mild or fulminating. Most commonly there is a dry, unproductivecough, bradycardia, fever, andinfluenzalike symptoms. Recovery is prolonged and gradual. If untreated, psittacosis can have a mortality rate of ~30%.*~, 4o Although the primary manifestation of psittacosis is pneumonia, Guillain-Barre syndrome has been associated with the infection in at least one case,4’ and possibly even spontaneous abortion.23 Because person-to-person spread by infectious sputum (and venereally) has been reported, and sputum carriage of the organism for a period as long as 8 years has been documented, hospitalized patients with psittacosis should be placed in a private room with secretion precautions, and should wear a mask when out of the room .42 LABORATORY

DIAGNOSIS

There are two major approaches to diagnosing chlamydial- infections: direct observation and cultural isolation. In either case, proper sample collection is extremely important and cannot be overemphasized. Without a properly collected specimen, the use of other optimal identification systems will fail to provide useful information. Sample

collection

In order to isolate C. truchomatis from clinical specimens, proper collection and the use of a suitable transport medium are essential. Several transport media have been evaluated. Sucrose-phosphate (2-SP) and sucrose-phosphateglutamate (SPG) have been used successfully.43 After the sample is collected, the swab should be placed into the medium and shipped to the laboratory for immediate processing.44 Samples should be transported to the laboratory at 4” C (on ice) and stored at refrigerator temperature if they are to be processed within 72 hours.

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Table 2. Acceptable specimens for diagnosis of chlamydial infections Type of infection

Conjunctivitis Genital tract Proctitis Lymphogranuloma Respiratory tract

venereum

Speolmen

Scraping of conjunctival epithelium Urethral swab, cervical scraping or swab Rectal mucosa (swab or biopsy) Lymph node aspirate Nasopharyngeal aspirate or swab

Freezing and thawing appear to be deleterious to the organisms. Smith et a1.45 found that inactivation of C. trachomatis was less when specimens were stored at 4” C rather than stored frozen at -70” C and thawed for processing. Studies by Aarnae et a1.46 suggest that 2-SP medium supplemented with serum or albumin may help to prevent loss of infectivity of organisms in the sample during storage.46 Specimen collection media usually contain antimicrobial agents (commonly vancomycin, gentamicin, and amphotericin B) that are active against other bacteria and fungi. Thus, it is important to recognize that if causative agents other than chlamydiae are also suspected, additional samples should be collected and transported in other media. Some swab materials are toxic to chlamydial organisms.45, 47 For example, swabs with wooden sticks should never be used for collection of specimens when chlamydial infection is suspected because wood is toxic to the organism. Calcium alginate, Dacron, rayon, or cotton-tipped swabs have been used, but the laboratory performing chlamydial isolation should check the types of swabs used for toxicity.48 Certain lubricants used for instrumentation during vaginal or rectal examinations may have toxic effects on genital tract pathogens.49 Osborn and Johnson found that KY jelly was less toxic to chlamydial organisms than other lubricants and analgesics tested.” Because chlamydiae are associated with host cells, it is important to collect samples that contain the cellular material, not purulent drainage or other exudative material (Table 2). For specimens from the eye, cells from the con-

junctival surface should be collected. For urethral samples, swabs should be inserted approximately 3 to 5 cm into the urethra. For cervical specimens, the cervix should be cleansed to remove drainage material, the swab inserted in the endocervical canal, and cells collected from the wall of the canal. For upper respiratory tract infections, posterior nasopharyngeal samples can be collected.4’ Stamm et a1.51 found that nasopharyngeal aspirates were slightly more sensitive than swabs for detecting infection. Lymph node aspirates should be collected with needle and syringe if LGV is suspected. Lesions of the gastrointestinal tract should be visualized before samples are collected. Diagnostic

tests

(Table 3)

Direct detection. Cytologic diagnosis is one of the more rapid means of diagnosing C. trachomatis infections, but diagnosis is very dependent on adequate specimen collection. Several hundred cells from the suspected area of infection are necessary for successful examination (Fig. 1). Giemsa stain of cell scrapings from the conjunctiva of neonates is extremely sensitive (approximately 95%), but is not as useful in adults (approximately45%).3 In adults, fluorescent antibody staining of scrapings is the preferred technique for detecting inclusions. Giemsa staining of cells from the male urethra and female cervix is not very sensitive, detecting ~50% of samples that are positive by culture, and is not recommended. PapanicoZaou (Pap) smear has been thought to be useful for diagnosis of chlamydial infection, but the stain lacks the sensitivity to detect inclusions specific to ChZamydia.48* 49 Fluorescent monoclonal antibody has recently become commercially available, incorporated into tests for direct detection of Chlamydia in genital specimens. 51-53Tam et a1.52evaluated the MicroTrak, Chlamydia trachomatis Direct Specimen Test (Syva Company, Palo Alto, Calif.), which employs a monoclonal antibody conjugated with fluorescein isothiocyanate (FITC). Urethral or cervical specimens are collected with swabs and a smear is made on a glass slide. After air drying, the smear is fixed and stained with the FITC-monoclonal antibody, and ex-

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Table 3. Laboratory tests for diagnosis of chlamydial infections Test

Advantages

detectiorl Giemsa stain

(cytology)

Papanicolaou smear Fluorescent antibody Cell culture

(Pap)

Direct

Serology Complement

Disadvantages

Least expensive; rapid; good for neonatal conjunctivitis May incidentally reveal infection in test for other disease Sensitive compared with culture; excellent specificity; same day results Reference method; cost-effective if processing large volumes

monoclonal

fixation

Useful

Micro-immunofluorescence -

for LGV

More sensitive; studies; can tears)

and

psittacosis

good for seroepidemiologic test different secretions

amined by means of fluorescence microscopy for the presence of EB. Typical organisms with characteristic morphology and applegreen color indicate a positive test result. The test procedure takes approximately 30 minutes. Compared with several cultural confirmation procedures, the MicroTrak direct immunofluorescence was s93% sensitive and 97% specific. Stamm et a1.5’ demonstrated a sensitivity of 92% and 96% specificity in symptomatic males. In females, sensitivity and specificity were 92% and 96%, respectively. Uyeda et a1.53 evaluated the test in a population of asymptomatic women attending pregnancy or planned parenthood clinics and found similarly excellent results, with 96% sensitivity and 99% specificity. Taylor et al.54 recently tested this fluorescent reagent in the detection of experimental eye infection in a monkey model and found encouraging results, although evaluation of this reagent in human eye infections has not yet been reported (see Fig. 2). Enzyme immunoassay. Jones et al.” recently reported preliminary information regarding an enzyme immunoassay developed by Abbott Laboratories. This test had a sensitivity of 80.5% and a 98.1% specificity. Although further improvements in the test are needed to achieve greater sensitivity, this enzyme immunoassay may offer another approach to testing clinical samples and may be easier to use in laboratories performing large numbers of assays.

(e.g.,

Not sensitive Least

sensitive;

nonspeciftc

Expensive, requires fluorescent and experienced personnel Expensive; requires expensive and experienced personnel; several days to get results Not good for trachoma genital infections Antibodies may persist specificity; not good

or ocular

microscope equipment takes

and

for years; low for psittacosis

Cell culture. Isolation of chlamydiae requires cell cultures; because the organisms are obligate intracellular parasites, they cannot be grown on standard bacteriologic media. Cultural isolation is usually limited to C. truchomatis.. Isolation of C. psittuci should be restricted to specialized laboratories that have sufficient containment facilities, since this species is highly infectious and has been known to cause laboratory-acquired infection. Cell culture requires a high level of technical expertise, special equipment, and cell culture facilities. Sensitivity depends on many factors such as type of cell line and growth conditions, method of sample collection, and transport. However, cell culture remains the reference method, the “gold standard.“56 Specimens are inoculated onto cell culture monolayer cells and the organisms are brought into close contact with the cells by centrifugation to maximize cell-to-cell contact and infectivity. The monolayer cells are treated with antimetabolites such as cycloheximide to inhibit replication of the cell culture cells. After incubation of the cells for 24 to 72 hours, the cells are stained for the detection of chlamydial inclusions. Two methods available for detection are iodine staining and immunofluorescence. Iodine staining is the least sensitive method but is useful when fluorescent microscopy is not available. Serology. Diagnosis of C. psittaci infections

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Table 4. Treatment

of chlamydial

disease

DiSeaSS Genital C. trachomatis,

types

Lymphogranuloma

Treatment

D-K

venereum

Ocular C. trachomatis neonatal conjunctivitis Trachoma Respiratory C. trachomatis pneumonia, infants Psittacosis

Journal of CONTROL

and infection

control

Long course of systemic tetracyclines (substitutes: erythromycin, sulfonamides); less than 2 weeks may be sufficient for nongonococcal uretheritis and mucopurulent cervicitis Long course of systemic tetracyclines, erythromycin, or sulfonamides Surgical correction Topical tetracycline or erythromycin Improved hygiene Long course of topical or systemic tetracyclines or sulfonamides Surgical correction of deformed lids Erythromycin, sulfonamides

(tetracycline contraindicated)

Eliminate avian carriers (tetracycline in bird feed, quarantine imported birds) Systemic tetracycline

is usually based on serologic evidence rather than culture. Complement-fixing antibodies to a common group chlamydial antigen (heat-stable) can be detected by the complement fixation (CF) test. However, there may be cross-reactions in patients with LGV infection. As with any serologic test, a fourfold or greater increase in antibody titer should be demonstrated to support a clinical diagnosis of psittacosis.39 Serologic tests for the diagnosis of genital infection caused by C. truchomatis have not proved useful because of the high prevalence of antibody in sexually active populations at high risk for acquiring infection.3* 48 Several procedures for detecting antibodies have been used, including microimmunofluorescence (MIF) and CF. MIF is more useful for epidemiologic and etiologic studies than for diagnosis, although antibody titers in patients with systemic complications may be high compared with titers found during uncomplicated infections?’ Neither MIF nor CF are useful in nongonococcal urethritis because results are unreliable. In trachoma, the CF test is of little value. Moderate levels of IgG may be detected by MIF; IgM may or may not be present. Complement fixation has been found useful for supporting a clinical diagnosis of LGV. The CF test may be positive in LGV infection 1 to 2 weeks after infection, with titers as high as 1: 128. IgM anti-

bodies are not usually present in LGV infection?’ MIF can also be used to detect IgM to C. truchomatis in infants with pneumonia?’ Schachter et a1.5’ found that organisms could be isolated more often from infants who were IgM positive than from those in whom no IgM could be detected. Infants with conjunctivitis do not usually have’high levels of IgM antibodies.58 Enzyme immunoassays for detecting antibodies have also been reporteds9em but are not routinely in use at this time. TREATMENT

The treatment of choice for all chlamydial disease is either tetracyclines, erythromycin, or sulfonamides (Table 4). C. psittuci is resistant in vitro to sulfonamide. Infection is usually difficult to eradicate because the organisms are protected by host cells. Therefore, long-term therapy, as long as 2 or 3 weeks, may be necessary. Several courses of systemic antimicrobial agents may be necessary with LGV. Trachoma presents particularly difficult problems because long-term antimicrobial therapy has inherent risks and may be difficult to monitor in endemic areas. It is also difficult to assure compliance with topical therapy, especially since it is necessary for such long periods. Prevention by improved hygiene is the best method for control of trachoma. Field trials of

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trachoma vaccine have been unsuccessful; immunity is short-lived and subsequent infection results in more severe disease because of a sensitizing effect. Improved understanding of the role of immunity in chlamydial diseases may allow production of a protective vaccine in the future ! References JW, Hatch TP, Kuo CC, Schachter J, Storz J: In Holt JG, Krieg NR, editors: Bergey’s Manual of Systematic Bacteriology, vol 1. Baltimore, 1984, Willia.ms & Wilkins Co, pp 729-239. Schachter J, Grossman M: Chlamydial infection. Annu Rev Med 32:45-61, 1981. Schachter .I: Biology of Chlamydia truchomatis. In Holmes KK, Mardh PA, Sparling PF, Wiesner PJ, editors: Sexua;!ly transmitted diseases. New York, 1984, McGraw-Hi I1 Inc, pp 243-257. Eb F, Orfila J: Serotyping of Chlamydia psittuci by the microimmu nofluorescence test: Isolates of ovine origin. Infect Immun 37:1289-1291, 1982. Paavonen J, Vesterinen E: Chlamydia trachomatis in cervicitis and urethritis in women. Stand J Infect Dis 32(suppl):45-54, 1982. Ward ME: Chlamydial classification: Development and structure. Br Med Bull 39:109-115, 1983. Schachter J: Sexually transmitted Chlumydia trachomatis infection. Postgrad Med 72:60-62, 1982. National Imtitute of Allergy and Infectious Diseases: ChZam.ydia and nongonococcal urethritis. In: Sexually transmitted diseases: 1980 status report. Bethesda, 1981, U.S. Dlepartment of Health and Human Services, Government document No. 81-2213. Thompson SE, Washington AE: Epidemiology of sexually :transmitted Chlamydia tnzchomatis infections. Epidemiol Rev 5:96-123, 1983. Munda.y PE, Pritchard G, Harris JRW, Taylor-Robinson D: Prevalence of chlamydial infections in promiscuous women. Br J Vener Dis 59:103-104, 1983. Mohammed IVRS, McQuoid G, Hillary IB, Verling WH: Incidence of Chlamydia tmchomatis infection in patients a.ttending a Dublin venereal disease clinic. Ir Med J 77:102-105, 1984. Gunby P: Chlamydial infections probably most prevalent of sexually transmitted diseases. Arch Intern Med 143:1665, 1983. Sweet RL: Chlamydial salpingitis and infertility. Fert Steril 38:530.,533, 1982. Raucher HS, Newton MJ: New issues in the prevention and treatment of ophthalmia neonatorum. Ann Ophthalmol 15:1004-1009, 1983. Harrison HR, Alexander ER, Weinstein L, Lewis M, Nash M, Sim DA: Cervical Chlamydia trachomatis and mycoplasmal infections in pregnancy. JAMA 250: 172 l1727, 1983. Bowie WR: New pathogens: Chlamydia trachomatis. Asepsis 5:4-7, 1983. Sorbie J, O’Shaughnessy MV: Chlamydia trachomatis

18. 19. 20. 21.

1. Moulder

Chlamydia.

2. 3.

4. 5. 6. 7. 8.

9. 10. 11.

12. 13. 14. 15.

16. 17.

22. 23. 24. 25. 26. 27.

28. 29.

30. 31. 32. 33. 34. 35. 36. 37. 38. 39.

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