Arthritis and Fever: A Clinician's Guide to Differential Diagnosis

11.1. Introduction

In patients managing rheumatic diseases, the onset of fever necessitates a swift and comprehensive evaluation. The intersection of fever and arthritis presents a diagnostic challenge, as various conditions can manifest with both symptoms. While fever can be a manifestation of active rheumatic disease, observed in over half of Systemic Lupus Erythematosus (SLE) patients, it is crucial to consider infectious etiologies and post-infectious sequelae. The complexity is further amplified by the diverse range of infections that exhibit rheumatological symptoms. This chapter aims to clarify the intricate relationship between fever and arthritis, particularly in the context of differential diagnosis. Fever of Unknown Origin (FUO) will be explored, given its potential link to systemic rheumatic diseases. A critical dilemma arises when a patient with established arthritis presents with fever, prompting the question: What is the appropriate course of action? This chapter provides a structured, stepwise diagnostic approach to guide clinicians towards a definitive diagnosis in such scenarios.

A concise overview of rheumatological manifestations associated with various infections is included to broaden the differential diagnosis of fever and arthritis, emphasizing the importance of considering common viral infections. Furthermore, the often-overlooked aspect of vaccination in arthritis patients is addressed, highlighting its relevance in clinical practice.

The primary objective of this chapter is to present a systematic framework for evaluating patients presenting with both fever and arthritis, ensuring a comprehensive and evidence-based approach to differential diagnosis.

Specific learning objectives include:

Developing a systematic approach to patients with Fever of Unknown Origin (FUO).
Formulating a diagnostic strategy for patients with known rheumatological diseases who present with fever, with an emphasis on recognizing common infections in immunocompromised individuals.
Identifying the rheumatological manifestations of prevalent infectious diseases.
Establishing safe and effective vaccination protocols for patients with rheumatological diseases.

11.2. Fever of Unknown Origin (FUO)

11.2.1. Definition [28]

Fever of Unknown Origin (FUO) is clinically defined by the following criteria:

Documented temperature exceeding 38.3°C (100.9°F) on multiple occasions.
Fever duration of 3 weeks or longer.
Unsuccessful diagnosis after one week of thorough in-hospital investigation.

11.2.2. Epidemiology

The epidemiological landscape of FUO has evolved due to advancements in medical science and technology, including improved imaging techniques, enhanced pathogen identification, and a deeper understanding of connective tissue diseases. A multicenter prospective study investigating FUO etiology revealed the following distribution: connective tissue diseases (22%), infections (16%), malignancies (7%), miscellaneous causes (4%), and undiagnosed cases (51%).

Box 11.1 Initial Evaluation for FUO

The initial diagnostic workup for FUO should encompass a comprehensive approach, including:

Detailed Medical History: (Refer to Table 11.2) focusing on potential exposures, travel history, medications, and underlying conditions.
Thorough Physical Examination: (Refer to Table 11.2) to identify any localizing signs of infection or systemic disease.
Complete Blood Count (CBC) with Differential and Blood Film: To assess for leukocytosis, leukopenia, or atypical cells.
Electrolytes, Liver Function Tests (LFTs), Lactate Dehydrogenase (LDH), Erythrocyte Sedimentation Rate (ESR), and C-Reactive Protein (CRP): To evaluate organ function and inflammatory markers.
Hepatitis A, B, and C Serologies: If LFTs are abnormal, to rule out viral hepatitis.
Blood Cultures (x3): Collected from different sites, several hours apart, and before initiating antibiotic therapy, to maximize pathogen detection.
HIV Antibody Assay and HIV Viral Load: For patients with identified high-risk factors for HIV infection.
Urinalysis with Microscopic Examination and Urine Culture: To assess for urinary tract infection.
Chest X-ray (CXR): To screen for pulmonary pathology.

Table 11.2

Initial evaluation for FUO

Epidemiology: Table 11.1 provides a detailed breakdown of FUO etiologies.

Table 11.1

Etiologies of FUO [1]

11.2.3. General Principles in the Treatment of FUO (Table 11.2)

When managing FUO, it is crucial to reassure patients that it is a recognized medical entity requiring thorough investigation, thereby mitigating patient anxiety. Empirical therapy with antimicrobials or glucocorticoids is generally not recommended for stable FUO patients as it can obscure the underlying diagnosis and impede diagnostic progress [29]. This is due to several factors:

Antimicrobial therapy can reduce the diagnostic yield of investigations like cultures.
Empirical treatment for one infection can mask or complicate the diagnosis of another (e.g., rifampicin for tuberculosis may suppress staphylococcal osteomyelitis or hinder the detection of fastidious organisms causing endocarditis).
The optimal duration of a therapeutic trial remains undefined in FUO.
Initiating glucocorticoids before excluding infection can lead to severe, life-threatening infectious complications.

However, there are specific exceptions where empirical treatment in FUO patients is warranted:

Septic or Hemodynamically Unstable Patients: In these critical cases, immediate empirical antimicrobial therapy is essential.
Immunocompromised or Neutropenic Patients: Due to their heightened risk of severe infections, empirical treatment is often necessary.
Suspected Giant Cell Arteritis: Corticosteroids should be initiated promptly to mitigate the risk of visual loss, pending biopsy results.

Figure 11.1 presents a suggested algorithm for approaching patients with FUO, guiding clinicians through a logical diagnostic pathway.

Fig. 11.1

Suggested algorithm to approach patient with FUO

11.2.4. Tips in FUO

Navigating the complexities of FUO diagnosis requires a strategic mindset. Key considerations include:

Prioritize considering atypical presentations of common diseases over rare conditions.
In rheumatology, consider rheumatological etiologies more frequently than malignancies.
In patients over 40 years of age, the likelihood of infection exceeds malignancy and rheumatological causes.
Rheumatological diseases typically manifest in a stable clinical condition.
Empirical treatment is generally discouraged unless specific indications are present.
If empirical treatment is unavoidable, avoid quinolones due to the risk of inducing tuberculosis resistance.
Chills, rigors, and night sweats are more indicative of infection than rheumatological disease.
Many undiagnosed FUO cases are attributable to viral infections that are not routinely investigated.
Viral infections can induce high fevers (up to 40–41 °C) and persist for up to 3 weeks, with an average duration of 9 days.

11.3. Fever and Rheumatology

11.3.1. Introduction

Managing fever in patients with rheumatic diseases is particularly challenging due to the broad differential diagnosis, encompassing infection, underlying disease activity, and medication side effects. Fever attributed to active rheumatic disease is prevalent in over 50% of SLE patients [30], whereas it is a less common manifestation of rheumatoid arthritis (RA) disease activity. Diagnosing and treating infections in this patient population is often complicated by several factors:

The clinical presentations of infections and rheumatic disease flares can be indistinguishable, creating diagnostic ambiguity [52–55].
Typical signs and symptoms of infection may be attenuated or absent due to concurrent immunosuppressive therapies [56–58].
The anti-inflammatory and antipyretic effects of glucocorticoids can mask the usual systemic and localized signs of infection.
The immunosuppressive effects of both the disease and its treatment expand the spectrum of potential pathogens, complicating empirical treatment strategies.

In patients with rheumatoid arthritis, infections frequently involve bones, joints, skin, soft tissues, and the respiratory tract [33]. Respiratory tract infections are the most common in patients with chronic inflammatory rheumatic or autoimmune diseases without arthritis. It is paramount to diligently exclude infection before attributing fever to the underlying rheumatological disease in immunosuppressed patients. Figure 11.2 provides a suggested algorithm for evaluating patients with rheumatic disorders presenting with fever, aiding in the differential diagnosis process.

Fig. 11.2

Suggested algorithm to approach a patient with rheumatic disorder presenting with fever

Risk factors for infection in rheumatic disease patients include:

Active rheumatic disease state.
Long-standing disease-related damage.
Neutropenia.
Lymphopenia.
Hypocomplementemia.
Renal involvement.
Neuropsychiatric manifestations.
Use of glucocorticoids and other immunosuppressive medications.
Arthrocentesis procedures [23].

Key points to consider when evaluating fever in this patient group:

Respiratory viral infections are the most common cause of fever in rheumatological patients, mirroring the general population.
No single clinical or laboratory finding definitively distinguishes between infection, disease activity, or drug-induced fever. Differential diagnosis relies on integrating clinical and laboratory findings with sound clinical judgment.
Determining the cause of fever crucially depends on understanding the patient’s baseline disease activity and current immunosuppressive therapy regimen.
Both the underlying rheumatic disease and its treatment influence white blood cell counts in febrile immunosuppressed patients:
- Glucocorticoid therapy can induce neutrophilic leukocytosis.
- Cytotoxic drugs can impair the body’s ability to mount a neutrophilic leukocytosis in response to infection.
- Neutrophilic leukocytosis can be a manifestation of certain rheumatic diseases, such as active granulomatosis with polyangiitis [101].
Recent meta-analysis suggests procalcitonin as a valuable diagnostic marker for bacterial infection in autoimmune disease patients:
- Procalcitonin demonstrates higher diagnostic value than CRP for detecting bacterial sepsis in autoimmune disease patients, exhibiting greater specificity but lower sensitivity [32].
- Procalcitonin testing alone is not recommended as a definitive rule-out tool for bacterial infection [32].

11.4. Fever in Rheumatology Patient

11.4.1. History

A meticulous and thorough history is paramount in evaluating fever in rheumatology patients, including:

Medication History: Detailed information on immunosuppressive medications (type and duration) is essential. Suspect new infections, especially if other signs of active rheumatic disease are improving.
Symptom Onset:
- Acute onset (few days) suggests infection.
- Subacute onset (days to weeks) may indicate disease activity or opportunistic infection.
Fever Pattern:
- Episodic fever patterns may be seen in both disease activity and infection.
- Sustained fever patterns can be associated with drug fever or central nervous system (CNS) involvement.
Shaking Chills: Significantly more common in patients with proven infections (68% vs. 27% in non-infectious fever).
Contact with Children: Raises suspicion for viral infections.
Recent Travel and Tuberculosis Exposure: Important for epidemiological risk assessment.
Vaccination History: Essential to assess preventative measures and potential vaccine-related reactions.

11.4.2. Physical Examination (Table 11.3)

A complete physical examination should be performed, including:

Oral Mucosal Candidiasis: Suggests significant immunodeficiency and increased risk of opportunistic infections like Pneumocystis pneumonia (PCP) [36].
Erythematous Necrotic Cutaneous Lesions: Raise suspicion for Gram-negative sepsis, particularly Pseudomonas aeruginosa.
Cutaneous Vesicular Rash: Indicates possible varicella-zoster virus infection.
Pulmonary Infiltrates with Cutaneous Lesions: May suggest disseminated histoplasmosis, Cryptococcus, or nocardiosis (Table 11.4).
Pulmonary Infiltrates with Focal Neurologic Deficits: Consider disseminated infection with mycobacteria, fungi (Cryptococcus neoformans, Aspergillus spp.), or Nocardia spp. (Table 11.5).
Detailed Neurological Examination: Should be performed and repeated frequently to monitor patient progress and detect subtle changes.
Ophthalmologic Examination: Careful examination for papilledema, signs of retinal and choroid infection (e.g., cryptococcosis, toxoplasmosis), and proptosis (suggesting orbital infection or cavernous sinus involvement).
Parotid Gland Enlargement: Suggestive of mumps.

Table 11.3

Possible pathogens by the predominant immune system defect caused by pharmacological agent used in the treatment of rheumatic disease [37]

Table 11.4

Causes of CXR abnormalities in patient with rheumatic disease^a

Table 11.5

Infections in rheumatological patient and most common causes [34]

[39–57, 59–99].

11.5. Rheumatologic Manifestation of Infectious Diseases

11.5.1. Introduction

Rheumatologic manifestations of infectious diseases are well-documented and relatively common, forming a crucial aspect of differential diagnosis in patients presenting with arthritis and fever. This section will review the most prevalent infectious diseases associated with rheumatologic symptoms, offering an overview of each infectious agent and its related manifestations.

11.5.1.1. Hepatitis B Virus Arthritis [104]

Evidence indicates a strong association between hepatitis B virus (HBV) infection and four distinct rheumatologic syndromes. The clinical and laboratory features of each syndrome are detailed below, aiding in the differential diagnosis of arthritis and fever.

11.5.1.2. Acute Hepatitis B and Arthritis

Acute hepatitis B infection can present with an abrupt onset of symptoms, including low-grade fever and symmetrical polyarthritis. This arthritis may exhibit an additive or migratory pattern, accompanied by morning stiffness and systemic constitutional symptoms. The knees and small joints of the hands are most frequently affected, although any peripheral joint can be involved with arthralgia or frank arthritis. Symptoms can persist from several days to months, highlighting the importance of considering HBV in the differential diagnosis of acute arthritis and fever.

11.5.1.3. Chronic Active Hepatitis B

Chronic active hepatitis B infection is linked to joint discomfort and occasional rash. Joint abnormalities typically manifest as fleeting arthralgias (Table 11.6), which can contribute to the diagnostic complexity of arthritis and fever in patients with chronic HBV.

Table 11.6

Rheumatic manifestations of hepatitis B virus

11.5.1.4. Polyarteritis Nodosa

The prevalence of Hepatitis B surface antigen (HBsAg) in polyarteritis nodosa varies based on diagnostic criteria and HBsAg detection sensitivity. Clinically, patients may exhibit multisystem involvement, affecting the skin, muscles, nervous system, lungs, and joints (polyarthritis), alongside liver disease. The association with HBV underscores the need to consider viral hepatitis in the differential diagnosis of polyarteritis nodosa presenting with fever and arthritis.

11.5.1.5. Essential Mixed Cryoglobulinemia

Essential mixed cryoglobulinemia, linked to HBV, presents with clinical features including non-thrombocytopenic purpura upon cold exposure, diffuse arthralgia, generalized weakness, and hepatosplenomegaly. Neuropathy and gangrene are less common but possible manifestations. Cryoglobulinemia should be considered in the differential diagnosis of patients with arthritis, fever, and these characteristic features.

11.5.2. Hepatitis C Virus Arthritis

Hepatitis C virus (HCV) is associated with a spectrum of rheumatologic manifestations affecting joints, muscles, and connective tissue. These manifestations arise from the body’s immune response to HCV antigens, leading to immune complex formation and deposition in various tissues, triggering inflammatory reactions and organ damage. Many HCV-infected individuals are asymptomatic, emphasizing the importance of screening for HCV in patients newly diagnosed with arthritis or cryoglobulinemia. Furthermore, certain HCV treatments, such as interferon, can exacerbate pre-existing rheumatologic conditions.

Arthritis is reported in 2–20% of HCV patients [107, 108]. The arthritis typically presents as an evanescent rheumatoid-like syndrome in two-thirds of cases and an oligoarthritis pattern in the remaining cases. Rheumatologic symptoms include joint pain, muscle pain, and fatigue (often the most prominent complaint), with less frequent joint swelling and vasculitis.

Cryoglobulinemia in HCV infection occurs when cryoglobulins (abnormal immunoglobulins) precipitate at cold temperatures, potentially affecting blood vessels, particularly in cold weather, leading to Raynaud’s phenomenon [105, 106]. HCV diagnosis is confirmed by detecting HCV Immunoglobulins or viral RNA. HCV-related arthritis and cryoglobulinemia are vital considerations in the differential diagnosis of arthritis and fever, especially in patients with risk factors for HCV infection.

11.5.3. Parvovirus B19 Arthropathy

Parvovirus B19, the causative agent of fifth disease (erythema infectiosum or “slapped cheeks”), can manifest with rash, arthritis/arthralgia, laboratory abnormalities, and mimic other connective tissue diseases, including systemic lupus erythematosus (SLE) in both children and adults (Table 11.7) [109, 110].

Table 11.7

Rheumatic manifestations of Parvovirus B19 infection

Arthritis/arthralgia may coincide with or follow the characteristic skin eruption. Rheumatologic symptoms can persist for weeks or, rarely, months before resolving, although recurrences have been reported [111, 112].

Diagnosis of acute parvovirus B19 infection is established by detecting IgM antibodies, while IgG antibodies indicate prior exposure. Acute phase reactants (ESR and CRP) may be elevated. Leukocyte counts are typically normal, but rheumatoid factor and antinuclear antibodies can be present transiently during the acute phase. Parvovirus B19 arthropathy should be included in the differential diagnosis of acute onset polyarthritis with or without fever, particularly in the context of rash or potential SLE mimicry.

11.5.4. Dengue Virus

Dengue virus infection, a mosquito-borne illness, can present with fever, severe myalgia, arthralgia, and rash. Laboratory investigations may reveal leucopenia, thrombocytopenia, and elevated liver enzymes. A small proportion of patients develop severe, potentially lethal forms: dengue hemorrhagic fever and dengue shock syndrome [115]. Dengue should be considered in the differential diagnosis of fever and polyarthralgia, especially in individuals with travel history to endemic regions.

11.5.5. Septic Arthritis

Septic arthritis, a bacterial infection of a joint, is generally treatable, but significant morbidity and mortality remain, especially in patients with underlying rheumatoid arthritis, prosthetic joints, elderly individuals, and those with multiple comorbidities. The incidence of septic arthritis is approximately 10 cases per 100,000 patient-years in the general European population [116]. In rheumatoid arthritis patients, the incidence is notably higher.

(Based on prospective British Society for Rheumatology Biologics Register)

1.8 cases per 1,000 patient-years in 3,673 patients on non-biologic disease-modifying antirheumatic drugs (DMARDs).
4.2 cases per 1,000 patient-years in 11,881 patients receiving anti-tumor necrosis factor (anti-TNF) therapy.

Septic arthritis typically presents as monoarthritis, but polyarticular involvement occurs in up to 20% of cases [116]. The knee is most commonly affected (approximately 50%), followed by the hip, shoulder, and elbow [120]. In intravenous drug users, axial skeletal joints are frequently involved, often with Staphylococcus aureus.

Common causative agents in adults include [116]:

Staphylococcus aureus (most frequent), followed by Streptococcus species.
Neisseria gonorrhoeae (considered separately as disseminated gonococcal infection).
Gram-negative bacteria, and Haemophilus species, more common in older patients.

In IV drug users, septic arthritis is often caused by methicillin-resistant Staphylococcus aureus (MRSA), mixed infections, fungal infections, or unusual organisms [116]. Patients may present with 1–2 weeks of joint pain, tenderness, warmth, redness, restricted motion, loss of function, and fever. Risk factors for joint infection include joint prosthesis, intra-articular injections, and joint trauma [119]. Fever is present in approximately one-third of patients [116]. Large joints of the legs (hips and knees) are typical sites of infection [116–118].

Septic arthritis diagnosis is based on clinical signs (hot, red, tender, swollen, restricted joint) and any of the following:

Pathogenic organism detected in synovial fluid by culture and Gram stain.
Pathogenic organism isolated from blood or another site.
Turbid synovial fluid in patients with recent antibiotic treatment.
Synovial white blood cell (WBC) count exceeding 30,000 cells/µL.
Leukocytosis in peripheral blood.

Septic arthritis represents a critical differential diagnosis in any patient presenting with acute monoarthritis or polyarthritis and fever, particularly in the presence of risk factors. Prompt diagnosis and treatment are essential to minimize joint damage and systemic complications.

11.5.6. Poncet’s Disease (Reactive Arthritis Associated with Tuberculosis) [121]

Poncet’s disease (PD), or tuberculous rheumatism, is a form of reactive arthritis linked to tuberculosis (TB). It is a sterile reactive arthritis that can develop during any stage of active TB infection. A retrospective case series study identified seven cases of Poncet’s disease:

Extrapulmonary TB was the most common presentation, involving multiple sites.
Six of seven patients developed arthritis after initiating anti-TB drugs.
One patient developed polyarthritis after completing anti-TB medication.
Asymmetrical polyarthritis was the most frequent pattern of joint involvement.

Arthritis resolution was achieved with symptomatic treatment and continued anti-TB therapy. PD can manifest variably during active TB infection. Clinicians should be aware of this rare complication of a common disease to avoid diagnostic delays and ensure appropriate treatment initiation. Poncet’s disease should be considered in the differential diagnosis of polyarthritis and fever in patients with known or suspected tuberculosis.

11.6. Vaccination in Adult Patient with Autoimmune Inflammatory Rheumatic Diseases (AIIRD)

11.6.1. Introduction

Vaccination is a cornerstone of infectious disease prevention. As previously discussed, patients with autoimmune inflammatory rheumatic diseases (AIIRD) are at increased risk of infection, particularly respiratory infections, compared to the general population [122, 123]. However, vaccinating immunocompromised patients with AIIRD presents unique challenges concerning both vaccine efficacy and safety. Vaccine efficacy may be reduced in AIIRD patients, and there is a potential risk of AIIRD flares following vaccination. Two primary concerns in vaccine administration to this population are the expected immune response and the potential for exacerbating the underlying disease.

11.6.2. General Rules

Inactivated vaccines are generally safe for administration to individuals with AIIRD, regardless of whether they are killed whole organisms or recombinant, subunit, toxoid, polysaccharide, or polysaccharide protein-conjugate vaccines. Live viral and bacterial vaccines should be avoided whenever possible in immunosuppressed AIIRD patients due to the risk of severe infection in immunocompromised hosts (Table 11.8). Table 11.9 provides vaccination recommendations for adult patients with AIIRD, guiding clinicians in appropriate vaccination strategies for this vulnerable population. Vaccination is a critical preventive measure to reduce the risk of infection, a key component in the differential diagnosis and management of fever in arthritis patients.

Table 11.8

Vaccinations by type

Table 11.9

Vaccination recommendation in AIIRD * [124]

Acknowledgments

The Authors would like to thank Abdullah Sakkat, MD, for his contributions to this chapter in the previous edition.

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