PATHOGENESIS, PATHOLOGY AND IMMUNITY
Chlamydial infections usually produce well-balanced host—parasite relationships. Pathogenesis and the interaction between chlamydiae and the host are poorly understood. Infections of natural hosts usually cause relatively mild disease characterized by chronic, low-level persistent infections stimulating a relatively poor immune response in the host.
However, if latently infected hosts are stressed, for example by factors such as those listed earlier, larger numbers of chlamydiae are excreted and clinical disease may result. It was previously considered that avian chlamydial strains were similar, that strains differed in virulence and that the host cleared the pathogen following infection. Now it is believed that strains are highly host-specific and that disease in natural hosts is mild with long recovery periods or persistent infections. Strains that infect other hosts may produce clinical, occasionally severe, disease; however, persistence of infection is not a feature in secondary hosts(12). The intestinal tract is probably the natural habitat for chlamydiae; however, the organisms multiply in cells of the reticulo-endothelial system, epitheliae of the pharynx, conjunctivae, genital and intestinal tracts, in cells of the placenta and fetus, and in synoviocytes.Extrapolating from work with poultry, aerosol infections colonize air sacs after several hours, progressing to infection of lung and air sacs. At 48 hours post-infection, blood, spleen, liver and kidney are infected, and this then frequently progresses to infection of muscle, pericardium and bone marrow. Nasal glands, providing moisture for the nasal mucus, and possibly responsible for aerosolized excretions, are infected for prolonged periods. Cells in
TABLE 26.1 Characteristics of Chlamydiaceae infections (modified according to Everett, 2000)(1).
| Chlamydophila | Chlamydia | |||||||
| psittaci | abortus | pecorum | pneumoniae | felis | caviae | suis | muridarum | |
| Host(s) | Birds, mammals, humans | Ruminants, wild boar, other mammals, humans, reptiles | Ruminants, koala, pigs | Humans, koala, horses, reptiles, amphibians | Domestic cat, reptiles | Guinea pig | Domestic pigs, wild boar | Mice, hamsters |
| Route of entry | Pharynx, eye, genital tract | Oral, genital | Oral | Pharynx, eye | Pharynx, eye, genital tract | Pharynx, eye, urogenital tract | Pharynx | Pharynx, genital tract |
| Infected tissues | Conjunctiva, | Placenta, | Conjunctiva, | Lung, brain, | Conjunctiva, | Conjunctiva, | Conjunctiva, | Genital, |
| lung, | spleen, | bladder, joints, | arteries, | lung, genital, | lung, | lung, | lung, | |
| genital, liver, spleen, brain, intestine | fetal liver, intestine | intestine, brain, prostate | joints | brain | genital, bladder | intestine | liver, kidney, spleen, intestine | |
| Typical disease presentation | Respiratory, enteritis | Abortion | Respiratory, conjunctivitis, encephalomyelitis, polyarthritis | Respiratory | Respiratory, conjunctivitis | Conjunctivitis | Respiratory, conjunctivitis, enteritis | Respiratory |
these tissues develop inclusions filled with RB. There is increasing evidence that the host’s immune response in persistently infected animals significantly contributes to the tissue damage seen(13).
Characteristics of Chlamydiaceae infections are given in Tables 26.1 and 26.2.The range of pathological lesions include exudative serositis, pneumonia, enteritis, splenomegaly, hepatomegaly, endocarditis, bronchopneumonia, airsacculitis and encephalitis1-16); however, these lesions are considered to be non-specific. Common features are necrotizing lesions in spleen, liver, pericardium and the respiratory tract. Severity of lesions varies with the virulence of strain, the susceptibility of the host, route of infection and the presence of concurrent disease. Concurrent disease, such as metabolic bone disease, trichomonosis and helminthosis was described in three species of wild columbiforms with chlamydiosis(5). Pericarditis, pneumonia, perihepatitis, peritonitis and airsacculitis may be found in combination and are lesions characteristic of overwhelming systemic infections. In natural hosts infected by an endemic strain of chlamydia, the lungs rarely show lesions; however, air- sacculitis is frequently present.
Microscopic examination confirms the appearance of gross lesions; however, there is a greater appreciation of the variation in the severity of these lesions (Table 26.2). Multi- focal splenic and hepatic necrosis is seen. Splenic lymphocytes are depleted and replaced by swollen macrophages. At the periphery of the necrotic lesions, basophilic inclusion bodies can be seen in the cytoplasm of hepatocytes, capillary epithelia and bile duct cells(12). Inclusion bodies are present in the cytoplasm of cells within serosal exudates. The organisms may be found in tissues without histopathological lesions in sites such as intestinal epithelium and pancreas. Fibrino-purulent airsacculitis is usually present, sometimes with fibrinous pericarditis. In the lungs there may be a severe inflammatory response with destruction of tissue and occlusion of air spaces with cell debris and fibrinous exudates.
Induced immunity following infection includes systemic, mucosal, humoral and cellular responses and an IgA response to infection in epithelial cells.