Haemophilus agni / Histophilus ovis Infection in Sheep: Polyarthritis and Pleuritis
By Dr. Zubair Khalid, DVM, MS, PhD ·
Key Takeaways
- Histophilus somni, formerly Haemophilus agni and Histophilus ovis, is a Gram-negative, pleomorphic coccobacillus responsible for polyarthritis and pleuritis in sheep, particularly affecting lambs aged 2-6 months.
- Transmission occurs via the respiratory route from carrier animals, with disease outbreaks frequently triggered by stressors such as weaning, transportation, or concurrent infections.
- Pathogenesis involves colonization of the respiratory mucosa, systemic dissemination via bacteremia, and a resulting neutrophilic vasculitis with thrombosis, leading to inflammation in joints and pleural cavities.
- Definitive diagnosis relies on isolation and identification of H. somni from affected tissues (synovial fluid, pleural exudate) via bacterial culture (requiring NAD supplementation) or molecular methods like PCR, which offers high sensitivity and specificity.
- Treatment involves early antimicrobial therapy with agents like florfenicol, oxytetracycline, or tulathromycin, with chronic cases having a guarded prognosis and requiring prolonged treatment.
- Prevention strategies focus on stress reduction, improved hygiene, avoiding overcrowding, and implementing all-in/all-out stocking; no specific ovine vaccine is widely available, though autogenous bacterins may be considered.
Etiology and Taxonomy
The causative agent of polyarthritis and pleuritis in sheep is a Gram negative, pleomorphic coccobacillus historically designated Haemophilus agni and Histophilus ovis [<a href="#ref-1">1</a>]. Current taxonomic consensus places this organism within the species Histophilus somni, which also includes the bovine pathogen formerly known as Haemophilus somnus [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. Histophilus somni is a member of the family Pasteurellaceae and is characterized by fastidious growth requirements, including a need for nicotinamide adenine dinucleotide (NAD) or other growth factors provided by blood or serum supplementation [<a href="#ref-1">1</a>]. On culture, colonies are small, smooth, and grayish, with a characteristic sweet or musty odor [<a href="#ref-2">2</a>]. The organism is nonmotile, non spore forming, and facultatively anaerobic [<a href="#ref-1">1</a>].
Epidemiology
Histophilus somni infection in sheep occurs worldwide, with seroprevalence studies indicating widespread exposure in many flocks [<a href="#ref-2">2</a>]. Disease is most commonly reported in lambs between 2 and 6 months of age, although older sheep can also be affected [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. Outbreaks often follow stressful events such as weaning, transportation, adverse weather, concurrent parasitic burdens, or intercurrent viral infections [<a href="#ref-2">2</a>]. Transmission occurs via the respiratory route through direct contact with nasal or ocular secretions from carrier or clinically affected animals [<a href="#ref-1">1</a>]. Carrier animals harbor the organism in the upper respiratory tract and tonsillar crypts, and stress induced immunosuppression can precipitate endogenous spread and clinical disease [<a href="#ref-2">2</a>]. Morbidity in affected flocks may reach 10-20%, with case fatality rates variable depending on the severity of systemic involvement [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>].
Pathogenesis and Virulence Factors
Following inhalation or aspiration of the bacterium, Histophilus somni colonizes the upper respiratory mucosa [<a href="#ref-1">1</a>]. The organism possesses several virulence factors that facilitate invasion and systemic dissemination. A major virulence determinant is the lipooligosaccharide (LOS), which exhibits endotoxic activity and contributes to inflammatory damage in vascular endothelium [<a href="#ref-2">2</a>]. Additionally, the bacterium expresses immunoglobulin binding proteins that interfere with opsonization and complement mediated killing [<a href="#ref-1">1</a>]. A fibronectin binding protein mediates adhesion to host extracellular matrix components, facilitating translocation across epithelial barriers [<a href="#ref-2">2</a>]. Once in the bloodstream, the bacterium can disseminate to multiple sites, including synovial membranes, pleural surfaces, and occasionally the central nervous system [<a href="#ref-1">1</a>]. The resulting inflammatory response, driven by cytokine release and neutrophil recruitment, leads to fibrinosuppurative exudation into joint spaces and pleural cavities [<a href="#ref-2">2</a>]. The hallmark lesion is a neutrophilic vasculitis with thrombosis, which underlies the development of polyarthritis and pleuritis [<a href="#ref-1">1</a>].
Clinical Signs
The incubation period following natural exposure ranges from 3 to 10 days [<a href="#ref-1">1</a>]. The disease can present acutely or peracutely. Affected lambs exhibit sudden onset of fever (40.5-42.0 degrees Celsius), depression, anorexia, and reluctance to move [<a href="#ref-2">2</a>]. Polyarthritis is the most prominent clinical feature, with hot, swollen, and painful joints, most commonly involving the carpi, tarsi, and stifles [<a href="#ref-1">1</a>]. Lambs may adopt a stilted gait or become recumbent [<a href="#ref-2">2</a>]. Pleuritis manifests as tachypnea, dyspnea, abdominal breathing, and a soft, productive cough [<a href="#ref-1">1</a>]. In some outbreaks, a fibrinous pericarditis and polyserositis accompany the thoracic involvement [<a href="#ref-2">2</a>]. Septicemic forms may present with sudden death without premonitory signs [<a href="#ref-1">1</a>]. Central nervous system signs, such as circling, head tilt, and nystagmus, are less common in sheep than in cattle but have been documented [<a href="#ref-2">2</a>].
Pathology and Lesions
At necropsy, the most consistent gross findings are fibrinous to fibrinopurulent polyarthritis and pleuritis [<a href="#ref-1">1</a>]. Joint capsules are distended with turbid, yellowish, or blood tinged synovial fluid containing flakes of fibrin [<a href="#ref-2">2</a>]. The articular cartilage may be eroded in chronic cases, with pannus formation [<a href="#ref-1">1</a>]. The pleural cavity contains variable amounts of fibrinous exudate, with adhesions between visceral and parietal pleura [<a href="#ref-2">2</a>]. The lungs may show areas of consolidation, atelectasis, and fibrinous pleuropneumonia [<a href="#ref-1">1</a>]. Additional lesions may include fibrinous pericarditis, peritonitis, myocarditis, and meningitis [<a href="#ref-2">2</a>]. Histologically, affected tissues exhibit a necrotizing vasculitis with thrombosis, fibrin deposition, and dense infiltrates of neutrophils and macrophages [<a href="#ref-1">1</a>]. The synovial membrane shows villous hypertrophy and fibrinocellular exudate [<a href="#ref-2">2</a>].
Diagnosis
A definitive diagnosis requires isolation or molecular detection of Histophilus somni from synovial fluid, pleural exudate, or other affected tissues [<a href="#ref-1">1</a>]. The table below outlines the primary diagnostic approaches.
| Diagnostic Method | Sample Type | Key Features | Sensitivity / Specificity |
|---|---|---|---|
| Bacterial culture | Synovial fluid, pleural swab, lung tissue | Requires NAD supplementation; colonies appear in 24-48 hours at 35-37 degrees Celsius in 5-10% carbon dioxide [<a href="#ref-1">1</a>] | Moderate; affected by prior antibiotic use [<a href="#ref-2">2</a>] |
| Polymerase chain reaction (PCR) | Synovial fluid, whole blood, tissue homogenate | Targets 16S rRNA or specific virulence genes; species specific [<a href="#ref-2">2</a>] | High sensitivity and specificity [<a href="#ref-1">1</a>] |
| Immunohistochemistry | Formalin fixed, paraffin embedded tissues | Detects bacterial antigens in situ [<a href="#ref-1">1</a>] | High specificity; useful for chronic cases [<a href="#ref-2">2</a>] |
| Serology (ELISA) | Serum | Detects antibodies against LOS or whole cell antigens; used for herd level screening [<a href="#ref-2">2</a>] | Moderate; cross reactivity with other Pasteurellaceae [<a href="#ref-1">1</a>] |
Differential diagnoses for ovine polyarthritis and pleuritis include Mycoplasma spp. (especially Mycoplasma bovis and Mycoplasma agalactiae), Erysipelothrix rhusiopathiae, Chlamydia pecorum, Streptococcus spp., and Trueperella pyogenes [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. Respiratory presentations must be differentiated from Mannheimia haemolytica pneumonic pasteurellosis and Bibersteinia trehalosi infection [<a href="#ref-2">2</a>].
flowchart TD
A["Lamb with fever, lameness, dyspnea"] --> B{"Clinical suspicion of Histophilus somni"}
B --> C["Collect sterile synovial fluid & pleural swab"]
C --> D["Perform Gram stain and culture on NAD-enriched media"]
D --> E["Gram-negative pleomorphic rods? Colonies after 24-48h?"]
E -->|"Yes"| F["Confirm by PCR or MALDI-TOF MS"]
E -->|"No"| G["Consider molecular testing directly from sample"]
G --> H["PCR positive?"]
H -->|"Yes"| I["Diagnosis confirmed: H. somni infection"]
H -->|"No"| J["Re-evaluate differentials: Mycoplasma, Chlamydia, Erysipelothrix"]
F --> I
I --> K["Antimicrobial susceptibility testing"]
K --> L["Initiate treatment: florfenicol, tetracyclines, or tulathromycin"]
L --> M["Monitor response; implement biosecurity measures"]Treatment
Antimicrobial therapy should be initiated as early as possible, ideally based on culture and susceptibility results [<a href="#ref-1">1</a>]. Empirical first line agents include florfenicol, oxytetracycline, and tulathromycin, all of which achieve good penetration into joint and pleural spaces [<a href="#ref-2">2</a>]. Ceftiofur and penicillin G may be effective but require careful dosing for acute cases [<a href="#ref-1">1</a>]. The duration of treatment is typically 5 to 7 days, but chronic arthritis often requires prolonged therapy (10 to 14 days) and has a guarded prognosis [<a href="#ref-2">2</a>]. Supportive care includes nonsteroidal anti inflammatory drugs to reduce fever and inflammation, as well as provision of soft bedding and easy access to feed and water [<a href="#ref-1">1</a>]. Severely affected lambs with irreversible joint damage should be culled [<a href="#ref-2">2</a>].
Control and Prevention
Control measures focus on reducing stress, improving hygiene, and limiting respiratory transmission [<a href="#ref-1">1</a>]. Management strategies include avoiding overcrowding, ensuring adequate ventilation in lambing sheds and feedlots, and implementing all in/all out stocking practices [<a href="#ref-2">2</a>]. Vaccines against Histophilus somni are available for cattle, but their efficacy in sheep is not well established, and no commercial ovine specific vaccine exists in most regions [<a href="#ref-1">1</a>]. Autogenous bacterins prepared from flock specific isolates may be considered when outbreaks are recurrent [<a href="#ref-2">2</a>]. Early identification and isolation of affected lambs, combined with prompt antimicrobial treatment, can reduce within flock spread [<a href="#ref-1">1</a>]. No carrier state eradication program is available, so ongoing biosecurity and monitoring are essential [<a href="#ref-2">2</a>].