# Haemophilus agni / Histophilus ovis Infection in Sheep: Polyarthritis and Pleuritis

## 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](/knowledge/bacteria/livestock-bacteria/histophilus-somni-bovine-thrombotic-meningoencephalitis-brd)*, 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](/knowledge/bacteria/livestock-bacteria/histophilus-somni-feedlot-cattle-pathogenesis-diagnostic-detection)* 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](/knowledge/bacteria/livestock-bacteria/histophilus-somni-bovine-thrombotic-meningoencephalitis-brd)* 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](/knowledge/bacteria/livestock-bacteria/histophilus-somni-feedlot-cattle-pathogenesis-diagnostic-detection)* 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](/knowledge/bacteria/livestock-bacteria/histophilus-somni-bovine-thrombotic-meningoencephalitis-brd)* 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](/knowledge/bacteria/livestock-bacteria/mycoplasma-bovis)* and *[Mycoplasma agalactiae](/knowledge/bacteria/livestock-bacteria/mycoplasma-agalactiae-contagious-agalactia-sheep-goats)*), *[Erysipelothrix rhusiopathiae](/knowledge/bacteria/livestock-bacteria/erysipelothrix-rhusiopathiae-swine-erysipelas-arthritis-diamonds)*, *Chlamydia pecorum*, *Streptococcus* spp., and *[Trueperella pyogenes](/knowledge/bacteria/livestock-bacteria/trueperella-pyogenes)* [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. Respiratory presentations must be differentiated from *[Mannheimia haemolytica](/knowledge/bacteria/livestock-bacteria/mannheimia-haemolytica)* pneumonic pasteurellosis and *Bibersteinia trehalosi* infection [<a href="#ref-2">2</a>].

```mermaid
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](/knowledge/bacteria/livestock-bacteria/histophilus-somni-feedlot-cattle-pathogenesis-diagnostic-detection)* 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>].

## References

<a id="ref-1"></a>[<a href="#ref-1">1</a>] Quinn PJ, Markey BK, Leon FC, Leonard ES, Hartigan PJ. *Veterinary Microbiology and Microbial Disease*. 2nd ed. Wiley-Blackwell; 2011.

<a id="ref-2"></a>[<a href="#ref-2">2</a>] Radostits OM, Gay CC, Hinchcliff KW, Constable PD. *Veterinary Medicine: A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats*. 10th ed. Saunders Elsevier; 2007.

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