Rhodococcal pneumonia is the most important life-threatening
lower respiratory disease in young foals. The causative
agent is Rhodococcusequi, a facultative intracellular
pathogen with virulent and avirulent strains, is a common
soil organism, and is also present in the intestinal tract
of (healthy) horses. The major route of transmission is
aerosolization via dust particles, occasionally followed
by secondary intestinal infection due to swallowing of sputum
containing the organism. However, a minor route of infection
is primary intestinal infection which may lead to secondary
hematogenous pulmonary infection. Concurrent helminthic
infection of the intestine predisposes to intestinal infection
with Rhodococcusequi. R. equi preferentially
targets macrophages where it is able to survive and multiply,
presumably by inhibition of phagosome-lysosome fusion and
triggering the premature release of lysosomal contents.
R. equi infection is primarily observed in 2-4
month old foals. At this age, maternal antibodies wane,
making foals susceptible to infection. In addition, foals
with coprophagic behavior are predisposed to infection since
R. equi depends on volatile fatty acids in herbivore
manure for optimal multiplication. In addition, R. equi
is capable of multiplication in the intestinal tracts of
foals up to 12 weeks of age which allows the organisms to
concentrate on farms where foals are raised. Although most
farms are infected with R..equi, disease occurrence
ranges from nonexistent on most farms to sporadic or endemic.
Variable infection rates are associated with several factors,
including environmental temperature, soil pH, strain virulence,
and management factors.
Clinical findings Most cases of rhodococcal pneumonia
occur in foals between two and four months of age.
Disease onset is insidious, and foals are generally able
to compensate for the progressive loss of pulmonary function,
making early clinical diagnosis difficult. Despite the
chronicity of lung lesions, foals usually present with an
acute onset of respiratory distress and/or sudden death.
Observed clinical signs include anorexia, lethargy, slight
mucopurulent nasal discharge, fever (101.50 -1040F),
tachypnea, increased respiratory effort, and lack of response
to common antibiotics. On auscultation, wheezes and crackles
may be present and percussion may reveal areas of dull resonance
associated with chronic abcessation. Coughing, if present,
varies from moist to nonproductive, and may be intermittent
or frequent.
Approximately 50% of pneumonic foals also present with
ulcerative colitis. Clinical signs in foals with severe
gastrointestinal involvement include diarrhea, weight loss
and ascites. Immune-mediated polysynovitis is seen in approximately
1/3 of foals with lung lesions. In these foals, effusion
is most common in the tarsal and stifle joints, and is not
associated with lameness. An agent is rarely cultured from
synovial fluid. Other uncommon manifestations of R.
equi include septic arthritis and osteomyelitis, subcutaneous
abcesses, and uveitis.
Clinical diagnosis: Clinical signs suggestive of
R. equi infection include age of the foal, presence
of fever, and lack of nasal discharge. Hyperfibrinogenemia
is the most consistent laboratory finding. Thoracic radiographic
findings include a prominent alveolar pattern characterized
by discrete nodular or cavitary lesions consistent with
abscesses.
Serologic tests that have been used in diagnosis include
agar gel immunodiffusion (AGID), ELISA, and synergistic
hemolysis inhibition. A major problem with serologic diagnosis
is the widespread exposure of foals to R. equi in
the environment, resulting in antibody production which
is not necessarily associated with infection. The presence
of maternal antibodies may further confound interpretation,
resulting in additional false positive tests.
Definitive diagnosis of Rhodococcal pneumonia is based
on PCR, bacterial culture, and cytology of transtracheal
wash (TTW) fluid. Presence of large gram positive pleomorphic
organisms in TTW cytology is consistent with R. equi
infection. Organisms are usually present in low numbers.
R. equi can be isolated by aerobic culture, generally
within 48 hours. RCR is a new method which is more rapid
than bacterial culture and can differentiate between virulent
and avirulent strains.
Postmortem diagnosis: Gross pulmonary lesions are
consistent with multifocal to coalescing pulmonary abcesses
and/or granulomas with consolidation and congestion of lung
parenchyma; airways in affected regions may be clogged with
mucopurulent exudates. Similar abcesses and/or granulomas
may be found within tracheal lymph nodes. Histologically,
lesions are composed of a necrotic central core with a collar
of degenerate neutrophils. An outer zone of macrophages,
occasional giant cells, and lymphocytes surrounds the core.
The amounts of intralesionalneutrophils is variable and
is increased in older lesions. Lesions within the adjacent
parenchyma include infiltration of bronchi, bronchioli,
and alveolar spaces with macrophages and neutrophils in
varying amounts.
Almost ˝ of necropsied foals will show multifocal ulcerative
typhlocolitis, often associated with abcesses and/or granulomas
within mesenteric lymph nodes. On gross examination, the
mucosa is thickened by infiltration with (numerous) macrophages,
giant cells and neutrophils. There are sharply demarcated
foci of coagulation necrosis with ulceration of the mucosal
surface.
Gram-positive and partial acid-fast small rod-shaped
bacteria consistent with R. equi can be detected
within the cytoplasm of macrophages and giant cells by use
of the special stains Brown and Brenn and Ziehl Nelson.
Prevention and treatment: Screening methods to
detect early disease on farms with a history of rhodococcal
pneumonia include frequent physical examination, twice daily
rectal temperature measurement, thoracic auscultation, and
diagnostic imaging to detect early pulmonary lesions. Frequent
removal of manure from foaling stalls and paddocks may help
decrease environmental contamination and exposure to foals.
Efforts to reduce population density and dust in the environment
should be considered on large breeding farms with endemic
R. equi pneumonia.
Transfusion of hyperimmune plasma, preferably in the
first few days after birth and again in the third week of
life, is the only method proven, though not failsafe, to
prevent R. equi pneumonia. Oral administration of
colostrums from immunized mares is not protective and effective
vaccinations are currently not available.
Standard treatment of rhodococcal pneumonia is the combination
of erythromycin and rifampin. The combination has synergistic
activity and excellent penetration of pulmonary alveolar
macrophages. Dosages range from 5-10 mg/kg of oral rifampin
twice daily, and 10-37.5 mg/kg of oral erythromycin 3 times
daily. Length of treatment may last from 30-60 days, depending
on clinical response, return to normal laboratory values,
and resolution of radiographic changes. Additional supportive
therapy includes intravenous fluids, nasal oxygen for foals
with respiratory distress, NSAIDS, and a cool environment.
-by Kim, Maratea, Class of 2003
-edited by Dr. Sandra Schoeniger, ADDL Graduate student
References
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with Rhodococcusequi. Equine Internal Medicine,
970-980.
2. CohenND,
Chaffin MK, and RJ Martens, 2000. Control and prevention
of Rhodococcusequi pneumonia in foals. CompendContinEducPract
Vet, 22: 1062-1069
3. Giguere, S. and JF Prescott, 1997. Clinical manifestations,
diagnosis, treatment, and prevention of Rhodococcusequiinfection
in foals. Vet Microbiol, 56: 313-334.
4. Prescott, JF, 1991. Rhodococcusequi:
an animal and human pathogen. ClinMicrobiolRev 4: 20-34.
5. Prescott
JF and AM Hoffman, 1993. Rhodococcusequi,
Vet Clin North Am Equine Pract. 375-384
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