Mycoplasma, Chlamydia, and Q Fever Pneumonias
Of these organisms, mycoplasma are most frequently isolated and of the greatest economic importance.
Several species of mycoplasma have been shown to cause pneumonia in goats (Hudson et al.
1967; Ojo 1987; Nicholas 2002a, b). Some of these (belonging to the Mycoplasma mycoides cluster) cause specific syndromes known as CCPP and pleuropneumonia, and are discussed separately. Because of changes in classification schemes, it is very difficult to interpret the older literature and to know exactly which organism was involved in a given report (Moulton 1980).Mycoplasma are generally fragile outside the host animal. They are easily inactivated by heat, sunlight, and disinfectants. Mycoplasma have been isolated from the external ear canal of goats (Ribeiro et al. 1997). Ear mites have been proposed as possibly disseminating the infection (Cottew and Yeats 1982; DaMassa 1983; DaMassa and Brooks 1991).
Non-specific Mycoplasma Pneumonia
Several species are isolated sporadically from goats, either alone or in conjunction with other causes of pneumonia.
Etiology and Pathogenesis
Mycoplasma Ovipneumoniae can be isolated from the trachea and lungs of healthy goats. When found in pneumonic lungs, the numbers of organisms present do not correlate with the severity of the lesion (Bolske et al. 1989). Fever and subacute fibrinous pleuritis have been produced experimentally with M. ovipneumoniae (Goltz et al. 1986), and natural cases also have been reported in goats, often in combination with pasteurellosis (Livingston and Gauer 1979; Jones and Wood 1988; Gonqalves et al. 2010; Rifatbegovic et al. 2011). Production of a capsule may contribute to this organism's pathogenicity (Niang et al. 1998a). It lacks the “fried egg” colony appearance typical of other mycoplasmas when grown on solid medium (DaMassa et al. 1992). Note that M. ovipneumoniae may accompany other mycoplasma species that are more pathogenic, but also more difficult to isolate.
Mycoplasma agalactiae, which typically causes mastitis in sheep and goats, has been shown to be capable of causing pneumonia in kids (Guha and Verma 1987). Mycoplasma arginini is isolated occasionally, but appears to have low pathogenicity (Goltz et al. 1986; DaMassa et al. 1992). Mycoplasma bovis has been isolated from the lungs of goats, and could potentially have been acquired by consumption of milk from infected cows (DaMassa et al. 1992).
Associated Clinical Syndromes
In addition to respiratory disease, other conditions associated with mycoplasma include polyarthritis, mastitis, conjunctivitis, and keratitis (see Table 4.4). This combination of clinical signs has been termed the MAKePS syndrome, standing for mastitis, arthritis, keratitis, pneumonia, and septicemia (Thiaucourt and Bolkse 1996). The differential diagnoses of these syndromes are considered elsewhere in this text.
Diagnosis
Thoracocentesis has been suggested for the diagnosis of mycoplasmal pneumonia in living goats. Pleomorphic coc- coid, ring, and filamentous organisms can be seen with the dark-field microscope or, alternatively, after staining with a 5% nigrosin solution (Ojo 1987). Although special media are required, the MAKePS mycoplasmas (including those that cause pleuropneumonia, see below) grow on modified Hayflick’s mycoplasma medium (Rosendal 1994). It is relatively easy to isolate mycoplasma from acute cases, but difficult or impossible to culture the organism from chronically infected goats. Swabs should be shipped in transport media (without charcoal), refrigerated but not frozen. Tissue samples from the interface between consolidated and unconsolidated areas are chopped or pulverized in culture medium.
Peribronchiolar lymphocytic infiltrations and diffuse non-suppurative pleuritis at necropsy are suggestive of mycoplasma, but secondary pasteurellosis complicates the diagnosis. Serologic tests are not available for many mycoplasmal species, and in fact few laboratories are capable of typing mycoplasma isolates to determine if a known pathogenic species is present.
Therapy
Penicillin and related drugs are ineffective because mycoplasma lack a cell wall. Tylosin (10-20 mg/kg once daily) and tiamulin (20 mg/kg once daily; Ojo et al. 1984) are considered to be superior to tetracycline in the treatment of pulmonary mycoplasmosis. Adverse reactions associated with intramuscular injection of these drugs include lameness and collapse. Side effects may be reduced by diluting the drug with an equal quantity of sterile saline solution just before injection or administering the drug SC. The newer macrolide drug tulathromycin, which has a prolonged pulmonary half-life after a single injection (Romanet et al. 2012), has been found to be quite useful for caprine pneumonias where mycoplasma are suspected.
The drug is given SC at 2.5 mg/kg, but is not appropriate for dairy goats, as milk residues persist for at least 45 days (Grismer et al. 2014). Isolation of infected animals is desirable, but very difficult in free-ranging systems, especially where communal water holes are used. Control measures used for pleuropneumonia are applicable if herd outbreaks occur.
Contagious Caprine Pleuropneumonia
CCPP is a disease that naturally infects goats, and less commonly sheep (OIE 2018). Lesions are confined to the respiratory tract (Harbi et al. 1983). The disease is notifiable to the World Organization for Animal Health (OIE).
Etiology and Pathogenesis
Mycoplasmologists have reclassified the etiologic agent several times (Martin 1983). In the 1980s the organism was specified as the highly fastidious F38 biotype Mycoplasma (McMartin et al. 1980), but currently it is named Mycoplasma capricolum subsp. Capripneumoniae (Thiaucourt and Bolkse 1996). Previously, M. mycoides subsp. capri was cited as the cause of CCPP, but now the disease associated with the latter organism is designated as pleuropneumonia, as discussed below. Although not identified in the Western Hemisphere, CCPP is prevalent in Africa, Turkey, the Middle East, and Asia (Thiaucourt and Bolkse 1996).
The organism is transmitted by aerosol during cohabitation and is highly contagious. The incubation period is typically 6-10 days or longer. All ages are affected.Clinical Signs and Diagnosis
In countries where this infection occurs, the signs are considered to be specific enough to permit an easy clinical diagnosis (Ojo 1987). These signs include fever, cough, and a painful respiration, with grunting and the forelimbs held widely separated. The head is held low, there may be a frothy nasal discharge and salivation, and the goat is unwilling to move. Death occurs within 2-10 days after onset of clinical signs. Typically there is a 100% morbidity rate and as much as 50-100% mortality rates in a susceptible flock (Ojo 1977).
Necropsy Findings and Diagnosis
Serofibrinous pleuritis results in accumulation of strawcolored pleural fluid. Pneumonia usually causes hepatization of entire lobes and is often unilateral. The lung appears granular or variegated, with red, yellow, white, and gray foci. Several reports include color photographs (Kaliner and MacOwan 1976; Thiaucourt et al. 1996; Nicholas 2002a). There is extensive bronchoalveolar cellular exudate. In contrast to the findings in goats with pleuropneumonia caused by other organisms, there is no thickening of the interlobular septa (Thiaucourt et al. 1996; Nicholas 2002a).
The isolation of the CCPP mycoplasma is difficult and requires special media. Techniques have been described elsewhere (Rosendal 1994; OIE 2018). The agent can be identified by immunofluorescence, growth inhibition, or metabolism inhibition tests (United States Animal Health Association, Committee on Foreign Animal Diseases 2008). Serologic cross-reactions and similarity in biochemical tests can cause confusion in distinguishing M. capricolum subsp. Capripneumoniae from M. capricolum subsp. capricolum (Jones 1989). Paired serology with samples taken three to eight weeks apart is useful for diagnosing the disease in animals that recover, but in acute cases death typically occurs before seroconversion (OIE 2018).
A latex agglutination test for field detection of antibodies to M. capricolum subsp. capripneumoniae polysaccharide antigen has been reported to be specific for CCPP in goats (Rurangirwa et al. 1990). A PCR testing scheme, when available, is considered conclusive (Hotzel et al. 1996; OIE 2018), unless the disease has not been diagnosed in the country before. A very important advantage of PCR testing is that a sample of pleural fluid from an untreated sacrificed animal can be allowed to dry on filter paper and then transported to a reference laboratory without having to maintain a constant “cool chain.”In countries where CCPP exists, the disease must be differentiated from other or coexisting infections such as pleuropneumonia caused by other mycoplasma infections, PPR, pasteurellosis, heartwater, and goat pox.
Treatment and Control
As with other mycoplasma, treatment with tylosin, tetracycline (El Hassan et al. 1984), tiamulin, or streptomycin (30 mg/kg) (Rurangirwa et al. 1981) is recommended. When tylosin (11 mg/kg), oxytetracycline (15 mg/kg), chloramphenicol (22 mg/kg), and penicillin plus streptomycin (dose per kg not indicated) were compared experimentally, tylosin caused more rapid recovery than oxytetracycline, while fevers were more persistent and some deaths occurred with the other two treatments (Onoviran 1974). More recently, fluoroquinolones have also been found to be effective against caprine mycoplasmas (Al-Momani et al. 2006), but their veterinary use is discouraged or forbidden in food animals because of the importance of the antibiotic class in human medicine.
Treatment should be continued for five days or pro - vided with a long-duration product (Thiaucourt et al. 1996). The prognosis for recovery with prompt treatment is approximately 87% (Rurangirwa et al. 1981; El Hassan et al. 1984). Animals recovered from clinical disease may remain carriers (El Hassan et al. 1984) and spread the disease to other herds. One study found that dihydrostreptomycin-treated goats did not remain carriers (Rurangirwa et al.
1981), but use of this antibiotic is discouraged because of rapid development of resistance (Lefevre and Thiaucourt 2004). Farmers usually retain animals that survive the infection.An experimental vaccine showed good protection for as long as one year after a single immunization (Rurangirwa et al. 1987). Vaccination of 10 000 goats in Kenya with an inactivated F38 vaccine was followed by cessation of reported losses to CCPP after three weeks. None of 400 closely monitored goats showed any evidence of clinical CCPP during the six-month period after vaccination (Litamoi et al. 1989). Commercial killed vaccines are now widely available. Recommendations for production of a safe and effective vaccine have been described (OIE 2018; Jores et al. 2020).
Pleuropneumonia
Etiology
Currently several different species of mycoplasma (M. mycoides subsp. capri, M. mycoides subsp. mycoides large-colony [LC] or caprine type, and M. capricolum subsp. capricolum) are believed to cause very similar syndromes known as pleuropneumonia (Pearson et al. 1972; Nicholas 2002b; United States Animal Health Association, Committee on Foreign Animal Diseases 2008), usually accompanied by involvement of other organ systems. Earlier reports of M. mycoides subsp. capri from the United States probably reflect a misidentification of M. mycoides subsp. mycoides LC (DaMassa et al. 1984). Mycoplasma mycoides subsp. capri has been isolated from a high-mortality respiratory outbreak in goats in Mexico (Hernandez et al. 2006). To add to the confusion, M. mycoides subsp. mycoides LC is now classified as a serovar of M. mycoides subsp. capri (Manso-Silvan et al. 2009).
A closely related species, M. mycoides subsp. mycoides small-colony type (the cause of contagious bovine pleuropneumonia), has been isolated from pneumonic lungs of goats in Africa (Kusiluka et al. 2000).
Clinical Signs
Incubation is from 2-28 days, depending on virulence. Clinical signs include high fever, cough, painful dyspnea, increased nasal secretion, ear droop, and anorexia. Morbidity rates are near 100%, but mortality rates vary with the organism, less than 40% for the LC type and close to 100% for the M. mycoides subsp. capri. Since the discovery of M. capricolum subsp. Capripneumoniae (F38 biotype), mortality rates attributed to M. mycoides subsp. capri have been questioned (Jones 1989).
Oral administration of M. capricolum (M. capricolum subsp. capricolum) causes acute pneumonia and polyarthritis in kids via the septicemic route (DaMassa et al. 1983b, 1992; Bolske et al. 1988; Taoudi et al. 1988). The pneumonia is only rarely accompanied by pleurisy. The organism can then spread to contact kids, probably via respiratory secretions.
Diagnosis
In the pleuropneumonia caused by M. mycoides subsp. mycoides LC, which is common in California, the organism is easily isolated from many internal organs and from joints and milk. The lungs of fatal cases are enlarged and firm. There is hepatization of cardiac and diaphragmatic lobes and marked pleural effusion and fibrinous pleuritis (Thigpen et al. 1981; DaMassa et al. 1986, 1992; Rodriguez et al. 1995). Both subspecies of M. mycoides cause similar histopathologic changes; pulmonary edema is extensive and interlobular septa are distended and pale. Arterial and arteriolar vasculitis with necrosis of vessel walls and thrombi formation are seen (Jones 1989).
Mycoplasma mycoides subsp. mycoides LC is less fastidious in its growth requirements than many mycoplasma and can be isolated on blood agar. Growth is slow, beta hemolysis appears by day six or seven, and colonies have a “fried egg” appearance (DaMassa et al. 1983a). Biochemical characteristics and antisera can be used to differentiate the various mycoplasma causing pleuropneumonia and CCPP, but a PCR scheme has also been devised for differentiating these organisms (Hotzel et al. 1996).
Treatment and Prevention
Kids are often infected by ingestion of milk, and the entire kid crop may be infected by pooled colostrum or milk (DaMassa et al. 1983a). Pasteurization of milk is routinely suggested to control an outbreak. Kids should be raised isolated from adults. Burning or deep burial of placentas and stillborn kids is also important. Tylosin (11 mg/kg intramuscularly for five days to two weeks) has been reported to be more rapidly effective for treatment than oxytetracycline at 15 mg/kg.
Ear mites, which may spread mycoplasma to additional animals or herds, can be controlled with ivermectin (see Chapter 2).
Chlamydiosis
The role of chlamydia in caprine pneumonia is very unclear. A serious outbreak of pneumonia in goats in Japan seemed to originate with goats imported from the United States after World War II (Omori et al. 1953; Saito 1954). Elementary bodies of various sizes were seen in bronchial epithelial cells and stained by the Machiavello stain. An agent was isolated in embryonated eggs that caused mild chronic respiratory signs such as slight cough, nasal discharge, and fever after intratracheal inoculation, although secondary bacterial infections were often fatal. Experimentally infected goats were successfully treated with tetracycline (7 mg/kg intramuscularly for 11 days; Ishii et al. 1954). A cough without dyspnea or nasal discharge developed in 2 of 11 goats experimentally inoculated with an abortion strain of Chlamydophila abortus (Chlamydia psittaci) and persisted one to two months in another study (Rodolakis et al. 1984).
Texas researchers have proposed that chlamydia are usually primary, with Pasteurella and mycoplasma causing a secondary pneumonia (Sharp et al. 1982). This theory does not seem to be commonly espoused, except perhaps in India. Fluorescent antibody tests, as have been used for diagnosis of abortion caused by chlamydio - sis, would be a useful tool for additional study of the importance of the organism in pneumonia outbreaks. In a slaughterhouse study in India involving 3799 apparently healthy goats, chlamydia were identified from 14 of 218 (6.4%) pneumonic lungs by fluorescent antibody tests (Rahman and Singh 1990). Special stains identified elementary bodies in only 8 of these cases. Gross lung lesions were mostly cranioventral. Histologically, there was an interstitial pneumonia and macrophage-filled alveoli. Additional slaughterhouse studies have identified chlamydia in lung lesions of unknown clinical rele - vance by special stains or fluorescent antibody tests (Chauhan and Singh 1971; Patnaik and Nayak 1984; Kumar et al. 2004).
Too little is known about the condition to formulate control programs. Different chlamydia serotypes are incriminated from those included in anti-abortion vaccines. Long-lasting oxytetracycline would be appropriate for therapy if involvement of this agent were suspected in field cases of pneumonia.
Q Fever
Q fever, caused by Coxiella burnetti, is occasionally associated with abortion in sheep and goats, but is otherwise considered to be non-pathogenic for livestock. Its importance is as a zoonosis. However, experimental intrapulmonary or intranasal inoculation has produced febrile bronchopneumonia in goats (Caminopetros 1948). Kids from an abortion outbreak have also shown non-suppurative interstitial pneumonia (Moore et al. 1991).