Foals between 1 and 6 months of age frequently present with lower airway infection and is the primary cause of disease and
death in foals aged between 1 and 6 months of age. Foal pneumonia is primarily caused by bacterial infection and among all isolates, Streptococcus zooepidemicus and Rhodococcus equi are the most important. Several other aerobic bacterial species may also be involved including, Actinobacillus spp, Bordetella bronchiseptica, Escherichia coli, Klebsiella pneumoniae, Pasteurella spp, Pseudomonas spp, Salmonella spp and
Streptococcus zooepidemicus - Streptococcus zooepidemicus equi subsp. zooepidemicus is a beta hemolytic, gram-positive coccus that is a commensal organism colonizing the tonsil and nasopharyngeal mucosa of
healthy horses. However, it is also a recognized pathogen of the horse's respiratory tract. The exact mechanisms implicated
in the pathogenesis of S. zooepidemicus pneumonia in horses are not known. Opportunistic infection with S. zooepidemicus possibly occurs after the host defense mechanisms have been overwhelmed.
Rhodococcus equi - Rhodococcus equi is a pleomorphic gram-positive coccobacillus and a facultative intracellular pathogen of macrophages. It is a major cause
of pneumonia in foals aged between 1 and 6. Rhodococcus equi causes chronic pyogranulomatous pneumonia; however, foals may less commonly develop intestinal or abdominal lymph node abscessation,
osteomyelitis, uveitis, pahophthalmitis, cellulitis, subcutaneous abscesses, and hepatic and renal abscesses.
Although R. equi is found in the soil of most farms, pneumonia caused by this organism can be endemic, sporadic or unrecognized, depending
on the farm studied. Several factors may influence the incidence of the disease including the degree of contamination on the
farm, density of horses, climatic conditions and virulence of the isolate. The infection is acquired through inhalation. Environmental
conditions appear to play a role in the pathogenesis of the disease with warm, dry and windy conditions favoring multiplication
and aerosolizing of the organism. The key to the pathogenesis of R. equi pneumonia is related to the ability of the organism to survive and replicate within alveolar macrophages by inhibiting phagosome-lysosome
fusion after phagocytosis. Immunity to R. equi infection in foals, although not fully understood, probably involves both humoral and cell-mediated immunity. The role of
antibodies has been shown by the protective effect of prophylactic administration of R. equi-specific hyperimmune plasma [36-38] or purified immunoglobulins against VapA and VapC. Studies in mice have shown that CD4+
T lymphocytes are the most important cells involved in immunity against R. equi with a T helper-1 response allowing clearance of the infection and a T helper-2 response being detrimental.
Parascaris equorum - In foals, Parascaris equorum is a common parasite and because its life cycle involves migration through the lung, which can potentially cause signs of
respiratory disease. Parasite-free foals infected experimentally with P. equorum developed a mild to severe cough at the time of migration of the parasite through the lung.
Early clinical signs include, coughing especially during eating or exercise, respiratory rate above 30 breaths per minute,
an increased respiratory effort, depression or failure to nurse/eat, growth retardation, mucopurulent nasal discharge (inconsistently),
or elevated rectal temperature. Later in disease, wheezes or crackles may be present with thoracic auscultation. Labored breathing
and cyanosis can occur in the most severe cases with extensive pulmonary involvement. Lymph node enlargement may be noted.
The intestinal form of the disease may manifest itself by fever, depression, anorexia, weight loss, colic or diarrhea. Foals
with immune-mediated polysynovitis will present with multiple joint distension accompanied by mild or no apparent lameness.
Heat, pain and severe lameness are characteristics of R. equi septic arthritis or osteomyelitis.