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Recrudescence

Recrudescence refers to a new outbreak or renewal of an activity, condition, or phenomenon after a period of abatement, inactivity, or remission.^[1] The term originates from the Latin recrudescere, meaning "to become raw again," evoking the image of a wound reopening, and first appeared in English around 1707 to describe both literal physical revivals and figurative resurgences.^[2] In medical contexts, recrudescence commonly denotes the reemergence of disease symptoms following partial recovery or treatment, distinct from relapse (which often involves reactivation from dormant or latent forms) or reinfection (new exposure to the pathogen).^[3] For instance, in malaria, it describes the reactivation of Plasmodium parasites due to incomplete eradication by antimalarial drugs, a critical factor in assessing treatment efficacy as per World Health Organization guidelines.^[4] Similarly, post-stroke recrudescence involves the transient recurrence of resolved neurological deficits triggered by stressors like infection or fatigue, without new brain lesions.^[5] Beyond medicine, the concept applies to social or political phenomena, such as the recrudescence of violence in conflict zones after ceasefires.^[1] This multifaceted term underscores patterns of intermittency in both biological and societal systems, highlighting the challenges of achieving lasting suppression.

Definition and Terminology

Definition

Recrudescence derives from the Latin verb recrudescere, meaning "to become raw again," originally evoking the reopening of a wound or sore, which later extended metaphorically to the revival of any dormant condition.^[2] In general usage, recrudescence refers to the reappearance or renewal of an activity, process, or state after a period of inactivity, remission, or apparent suppression, often carrying connotations of something undesirable resurfacing.^[1] In medical contexts, recrudescence specifically denotes the return of disease symptoms or pathological activity following partial suppression or a temporary remission, where the causative agent has not been fully eradicated, leading to a resurgence without external re-exposure.^[6] This contrasts with relapse, which typically involves reactivation from dormant or latent pathogen forms, and reinfection, which requires new exposure to the pathogen.^[7] The term entered English in the mid-17th century, with its earliest documented use in 1665 (per Oxford English Dictionary), primarily in medical writings to describe the recurrence of illnesses or symptoms after abatement.^[1] While broader applications include the recrudescence of social conflicts or violence after quiescence, its foundational and most precise employment remains in medicine, underscoring the reactivation of latent or subdued pathological processes.^[2] Recrudescence refers to the reappearance of symptoms or detectable pathogens from an existing infection due to incomplete or inadequate treatment, allowing the original pathogen population to regrow without involving new exposure or latent stages.^[7] In contrast, relapse typically involves the reactivation of dormant or persistent pathogen forms, such as hypnozoites in Plasmodium vivax malaria or latent reservoirs in other infections, indicating incomplete eradication of the pathogen's lifecycle but distinct from failures in active treatment phases.^[8] Reinfection, meanwhile, arises from a new external source of the pathogen after the initial infection has been fully cleared, often through vector transmission, direct contact, or environmental exposure.^[7] The key distinction lies in the mechanism and absence of external factors in recrudescence: it specifically stems from subtherapeutic drug levels or insufficient therapy duration, leading to the resurgence of the same infecting strain without latency or re-exposure, whereas relapse implies a dormant phase and reinfection requires pathogen reintroduction.^[8] For instance, in malaria, recrudescence might occur weeks after treatment if blood-stage parasites persist due to drug resistance, differing from relapse driven by liver-stage hypnozoites months later.^[9] This differentiation is crucial for epidemiological tracking and therapeutic adjustments, as misclassification can overestimate drug efficacy or transmission rates.^[8] These contexts highlight recrudescence's tie to therapeutic shortcomings, contrasting with relapse's reliance on host-pathogen dormancy or reinfection's external etiology.^[7]

Term	Cause	Timing	Examples
Recrudescence	Incomplete therapy or subtherapeutic drug levels allowing regrowth of active pathogens	Weeks to months after treatment	Drug-resistant Plasmodium falciparum resurgence in malaria; bacterial regrowth in inadequately treated foci^[9]^[7]
Relapse	Reactivation of dormant or latent forms (e.g., hypnozoites, viral reservoirs)	Months to years after clearance	Hypnozoite-driven Plasmodium vivax recurrence^[8]
Reinfection	New exposure to the pathogen after full clearance	Variable, post-recovery	Re-bite by infected mosquito in malaria-endemic areas^[7]^[8]

Recrudescence in Human Infectious Diseases

Malaria

Recrudescence in malaria represents the resurgence of Plasmodium parasites from an initial infection due to inadequate antimalarial treatment, permitting surviving asexual blood-stage parasites to multiply and cause renewed parasitemia. This mechanism primarily affects blood-stage forms and contrasts with relapse in species like Plasmodium vivax and P. ovale, where dormant hypnozoites in the liver activate independently of treatment efficacy. In P. falciparum, the predominant species in Africa, recrudescence arises solely from incomplete blood-stage clearance, while in P. vivax it can occur alongside potential relapse but is specifically tied to treatment failure of blood stages.^[10]^[9]^[8] Clinically, recrudescence manifests 2–4 weeks after treatment, typically within the 28-day monitoring period of therapeutic efficacy studies, with detectable parasitemia returning in the absence of new mosquito bites. Symptoms mirror the primary infection, including recurrent fever cycles, chills, sweats, headache, and worsening anemia, though severity may escalate in cases of high parasitemia or delayed diagnosis. Key risk factors encompass sub-optimal drug dosing, poor adherence, and emerging parasite resistance, notably historical chloroquine-resistant strains that facilitated higher recrudescence in the 1990s.^[11]^[12]^[13] Diagnosis relies on molecular techniques such as polymerase chain reaction (PCR) genotyping to confirm the persistence of the same parasite strain, distinguishing recrudescence from reinfection or relapse. The World Health Organization recommends PCR-based analysis of multiple neutral genetic markers, employing algorithms like the 3/3 match-counting method, where a recurrent infection is classified as recrudescence if at least three markers match the pre-treatment sample. This approach is essential in high-transmission settings to accurately assess drug efficacy.^[14] Prevention centers on administering full-dose artemisinin-based combination therapies (ACTs), such as artemether-lumefantrine or artesunate-amodiaquine, which synergistically clear parasites and minimize survival risks compared to monotherapies. Historically, before widespread ACT adoption in the early 2000s, recrudescence rates with chloroquine in sub-Saharan Africa often exceeded 20% and reached up to 50% or more in resistant areas during the 1990s. Globally, recrudescence accounts for 10–20% of treatment failures in endemic regions like sub-Saharan Africa, sustaining parasite reservoirs, complicating control efforts, and contributing to ongoing morbidity and transmission.^[15]^[16]^[17]

Melioidosis

Melioidosis is caused by Burkholderia pseudomallei, a gram-negative, soil-dwelling bacterium endemic to tropical regions, particularly Southeast Asia and northern Australia.^[18] This facultative intracellular pathogen is typically acquired through percutaneous inoculation, inhalation, or ingestion from contaminated environmental sources, such as soil and surface water in endemic areas.^[19] In Thailand, where the disease is highly prevalent, annual cases are estimated at 4,000–5,000, with occupational exposure prominent among rice farmers due to frequent contact with wet soil during planting seasons.^[20] Diabetes mellitus is a major risk factor, affecting 23–60% of patients, alongside other conditions like chronic renal disease that predispose individuals to infection.^[21] The mechanism of recrudescence in melioidosis involves intracellular persistence of B. pseudomallei within host macrophages following the initial acute infection, allowing the bacterium to evade immune clearance and establish latency.^[22] This latent state can persist for months to decades, with reactivation often triggered by immunosuppression, such as from diabetes or renal impairment, or by incomplete antibiotic therapy that fails to eradicate persistent bacteria.^[23] Similar to latency in tuberculosis, B. pseudomallei survives intracellularly, leading to relapse rather than reinfection in most recurrent cases, as confirmed by molecular typing showing persistence of the original strain.^[24] Clinically, melioidosis manifests in acute septicemic forms, characterized by rapid bacteremia and multi-organ involvement, or chronic localized forms with abscess formation; recrudescence typically presents as chronic abscesses in sites like the lungs, liver, spleen, or prostate.^[25] Diagnosis of recrudescence relies primarily on culture isolation of B. pseudomallei from blood, pus, or tissue samples, as serologic tests like indirect hemagglutination are less reliable for confirming active or recurrent disease due to cross-reactivity and poor specificity.^[26] Molecular methods, such as multilocus sequence typing, are essential to distinguish relapse from reinfection by verifying strain identity.^[27] Treatment poses significant challenges due to the bacterium's intrinsic resistance and ability to form biofilms, necessitating a prolonged regimen: an intensive phase of intravenous ceftazidime (or meropenem) for at least 10–14 days, followed by an eradication phase of oral trimethoprim-sulfamethoxazole for 3–6 months.^[28] Incomplete therapy, particularly less than 6 months total duration, results in recrudescence rates of 10–30%, often within 1–2 years, underscoring the need for adherence to prevent relapse.^[18] Latent periods can extend up to 20–30 years or longer in rare cases, as evidenced by reactivation in veterans exposed decades prior.^[29]

Tuberculosis

Tuberculosis (TB), caused by the bacterium Mycobacterium tuberculosis, establishes latency through the formation of granulomas in the host's tissues, where dormant bacilli can persist for years or decades without causing active disease. Recrudescence in TB refers to the reactivation of these latent bacilli, leading to active infection, primarily in the lungs but also in extrapulmonary sites such as the lymph nodes, pleura, or bones; this process is often triggered by waning cell-mediated immunity, such as in aging individuals, or by poor adherence to incomplete treatment regimens that fail to eradicate all persistent bacteria. Key risk factors for TB recrudescence include HIV co-infection, which elevates the risk 20- to 30-fold by impairing granuloma maintenance, as well as diabetes mellitus and tobacco smoking, which compromise immune surveillance and alveolar macrophage function.^[30] Globally, TB affected an estimated 10.8 million people in 2023 (95% uncertainty interval: 10.1–11.7 million), with a substantial proportion of cases—estimated at 25–50% globally, varying by region and transmission setting—attributable to recrudescence from latent infections rather than recent transmission, underscoring its role as a major public health challenge in high-burden regions. Clinically, recrudescent TB often manifests as cavitary lung disease with symptoms including chronic cough, weight loss, night sweats, and hemoptysis due to tissue destruction by reactivated bacilli; in severe cases, particularly among immunocompromised patients, it can progress to miliary TB, characterized by widespread dissemination and millet-seed-like lesions on imaging. Diagnosis relies on microbiological confirmation via sputum acid-fast bacilli smear microscopy for initial detection, followed by nucleic acid amplification tests like the GeneXpert MTB/RIF assay, which identifies M. tuberculosis and detects rifampin resistance in under two hours; strain confirmation for recrudescence versus reinfection uses IS6110-based restriction fragment length polymorphism genotyping or whole-genome sequencing. Standard treatment for recrudescent TB follows a 6-month regimen of four first-line drugs—isoniazid, rifampin, pyrazinamide, and ethambutol—for the initial phase, followed by isoniazid and rifampin for continuation; however, treatment interruptions increase the likelihood of recrudescence and the emergence of multidrug-resistant TB (MDR-TB), necessitating longer, more complex therapies. Historically, before the advent of antibiotics in the mid-20th century, recrudescence was a common outcome following primary infection, with sanatorium-based rest providing limited prevention; today, the World Health Organization endorses preventive therapy for latent TB, such as the 3HP regimen (3 months of weekly isoniazid plus rifapentine), which reduces reactivation risk by up to 90% in adherent patients. This intracellular persistence in macrophages shares mechanistic similarities with recrudescence in melioidosis.

Herpesvirus Infections

Herpesvirus infections, particularly those caused by human alphaherpesviruses such as herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) and varicella-zoster virus (VZV), exemplify recrudescence through lifelong latent persistence in sensory neurons followed by periodic reactivation. HSV-1 primarily causes oral herpes, manifesting as recurrent cold sores or labial lesions, while HSV-2 is associated with genital herpes, leading to vesicular outbreaks in the anogenital region. VZV, responsible for childhood chickenpox (varicella), establishes latency after primary infection and reactivates later in life as herpes zoster, commonly known as shingles, characterized by a unilateral dermatomal rash. These viruses integrate into the host genome in neuronal cells, evading immune detection during latency, and recrudescence occurs when environmental or physiological cues disrupt this dormancy, resulting in viral replication and symptomatic disease.^[31] The mechanism of recrudescence in these herpesviruses involves establishment of latency in sensory ganglia—trigeminal ganglia for HSV-1, sacral ganglia for HSV-2, and dorsal root or cranial nerve ganglia for VZV—where the viral genome persists as an episome without lytic replication. During latency, viral gene expression is minimal, limited to non-coding RNAs like the latency-associated transcript (LAT) in HSV, which promotes neuronal survival and suppresses apoptosis. Reactivation is initiated by stimuli that trigger expression of immediate-early (IE) genes, such as ICP0 and ICP4 in HSV, leading to full lytic cycle resumption, virion production, and anterograde transport along axons to epithelial sites. Common triggers include ultraviolet (UV) light exposure, which impairs local immunity and directly activates viral promoters; psychological or physical stress, elevating glucocorticoids that suppress T-cell responses; and immunosuppression, such as from aging, HIV, or chemotherapy, reducing cell-mediated immunity essential for controlling latency. This process underscores the viruses' adaptation for lifelong persistence, with recrudescence episodes often milder than primary infection due to partial immune memory.^[32]^[33]^[34] For HSV infections, recrudescence manifests as recurrent lesions, with oral HSV-1 affecting up to 40-50% of seropositive individuals with symptomatic episodes over their lifetime, though subclinical shedding occurs frequently. Initial genital HSV-2 recurrences average 4-6 per year, decreasing to 1-2 annually after the first year as immune adaptation strengthens, with episodes typically lasting 5-10 days and involving painful vesicles, ulcers, and flu-like symptoms. Prodromal tingling or itching often precedes outbreaks, and while most resolve without scarring, frequent recrudescence can lead to psychological distress and increased HIV transmission risk due to mucosal disruption. In contrast, VZV recrudescence as herpes zoster presents as a painful, vesicular rash confined to one or two adjacent dermatomes, often with prodromal pain, and affects approximately 1 million people annually in the United States, with incidence rising sharply after age 60 to 8-11 cases per 1,000 person-years. Complications include postherpetic neuralgia (PHN) in 10-20% of cases, defined as persistent neuropathic pain lasting over three months, which is more severe and prolonged in older adults due to nerve damage. Nearly all adults have prior VZV exposure from childhood varicella, conferring latent infection with a lifetime zoster risk of about 30%, exacerbated by waning immunity.^[35]^[36]^[37] Diagnosis of herpesvirus recrudescence relies on clinical presentation but is confirmed through laboratory methods, including polymerase chain reaction (PCR) assays on lesion swabs or fluid, which detect viral DNA with high sensitivity and specificity, distinguishing HSV from VZV. The Tzanck smear, a rapid bedside test, reveals multinucleated giant cells in 60-80% of active lesions but lacks viral type specificity and is less sensitive than PCR. Serology for IgG antibodies indicates past exposure but not active recrudescence, while IgM is unreliable for recurrences. Antiviral therapies like acyclovir, valacyclovir, or famciclovir shorten outbreak duration by 1-2 days and suppress recurrences by 70-80% when used prophylactically, though they do not eradicate latent virus. For VZV, the recombinant zoster vaccine (Shingrix) prevents recrudescence with over 90% efficacy in adults over 50, reducing both zoster incidence and PHN risk by eliciting robust T-cell responses against latent virus. Globally, HSV-2 seroprevalence stands at approximately 13% among adults aged 15-49, with higher rates in Africa, while VZV infection is nearly universal in unvaccinated populations by adolescence.^[38]^[39]^[40]

Recrudescence in Non-Infectious Human Conditions

Post-Stroke Recrudescence

Post-stroke recrudescence (PSR) in neurology refers to the transient reemergence or worsening of previously resolved focal neurological deficits from an earlier stroke, such as hemiparesis or aphasia, typically lasting from hours to a few days.^[41]^[5] This phenomenon occurs in the absence of a new cerebrovascular event and is triggered by physiological stressors, distinguishing it from recurrent stroke.^[42] The condition has been described in the medical literature, with reports noting the reappearance of stroke symptoms under stress, though it remained underrecognized for decades.^[43] Recent reviews, including those from 2023, have emphasized its non-vascular etiology and the need for greater awareness among clinicians to avoid misdiagnosis as recurrent ischemia.^[41]^[5] PSR affects approximately 2-10% of stroke survivors, particularly those presenting with transient neurological symptoms that mimic acute stroke, and is often underrecognized in rehabilitation settings where patients may experience subtle recurrences.^[5]^[41] Common triggers include systemic infections (such as urinary tract infections), metabolic imbalances (e.g., hyponatremia or hyperglycemia), hypotension, surgery, insomnia, and emotional stress, with studies identifying metabolic derangements and infections as the most frequent precipitants, accounting for over 70% of identified triggers in one cohort.^[43]^[44]^[41] The underlying pathophysiology involves a reduction in cerebral reserve following the initial stroke, where brain regions with prior damage become vulnerable to unmasking of deficits through systemic factors like inflammation, cerebral edema, or altered neuronal excitability induced by the stressor.^[43]^[41] Unlike ischemic recurrence, PSR does not involve new vascular occlusion, as evidenced by neuroimaging showing no acute infarcts on MRI or CT.^[45]^[5] Clinically, PSR manifests as mild to moderate worsening of prior symptoms, which are typically self-limiting and resolve within 24-48 hours once the trigger is addressed, though episodes can last up to several days.^[46]^[43] Differentiation from transient ischemic attack (TIA) relies on history of prior stroke deficits, absence of new lesions on diffusion-weighted MRI, and identification of a systemic trigger, preventing unnecessary thrombolysis or anticoagulation.^[41]^[44] Management focuses on promptly identifying and treating the underlying trigger, such as administering antibiotics for infections or correcting electrolyte imbalances (e.g., intravenous fluids for hyponatremia), alongside supportive care like hydration and rest.^[5]^[42] Prognosis is generally favorable, with full resolution of symptoms in most cases and no associated increase in mortality or long-term disability beyond the initial stroke.^[41]^[44] Supporting evidence from cohort studies indicates that metabolic triggers predominate in rehabilitation contexts, with infection-related cases showing higher incidence compared to TIA mimics, underscoring PSR's distinct profile from vascular events.^[43]^[44] A 2023 systematic review highlighted its frequency in up to 10% of suspected stroke presentations, advocating for routine screening of stressors in post-stroke patients to improve outcomes.^[5]

Psychiatric Symptom Recrudescence

Psychiatric symptom recrudescence refers to the re-emergence of previously remitted symptoms in disorders such as schizophrenia and bipolar disorder, often manifesting as the return of hallucinations and delusions in schizophrenia or recurrent depressive episodes in bipolar disorder following a period of remission.^[47] In schizophrenia, these episodes can involve acute psychotic breaks, while in bipolar disorder, they typically present as mood instability leading to severe depression or mania. This phenomenon disrupts functional recovery and underscores the chronic, relapsing nature of these conditions.^[48] Mechanisms underlying recrudescence include neurochemical imbalances, such as surges in dopamine activity that exacerbate psychotic symptoms, and stress-induced elevations in cortisol levels that amplify vulnerability through hypothalamic-pituitary-adrenal axis dysregulation.^[49] In some cases, recrudescence links to underlying autoimmunity, as seen in anti-NMDA receptor encephalitis, where autoantibodies target glutamate receptors, precipitating psychotic relapses with symptoms like paranoia and hallucinations.^[50] These processes highlight how environmental stressors and biological vulnerabilities interact to trigger symptom return. Key risk factors for recrudescence include medication discontinuation, which carries approximately a 50% relapse risk within one year for schizophrenia, alongside trauma and non-adherence.^[47] Even among adherent patients in remission, prevalence reaches 20-30% in first-episode psychosis cases.^[51] Clinically, recrudescence often presents as acute worsening, potentially requiring hospitalization, with assessment tools like the Positive and Negative Syndrome Scale (PANSS) used to quantify symptom severity in schizophrenia.^[52] Management focuses on reinstating antipsychotics, such as risperidone, combined with psychotherapy to address triggers, while early intervention strategies can shorten episode duration and improve outcomes.^[53] Longitudinal studies indicate that up to 80% of first-episode psychosis patients experience recrudescence within five years without maintenance therapy, emphasizing the need for sustained treatment.^[48] Stress triggers in psychiatric recrudescence parallel those in post-stroke contexts, involving cortisol-mediated pathways.^[49]

Recrudescence in Veterinary Medicine

Bovine Viral Diarrhea

Bovine viral diarrhea virus (BVDV), a positive-sense single-stranded RNA virus in the genus Pestivirus of the family Flaviviridae, causes both acute and persistent infections in cattle, with subtypes BVDV-1 and BVDV-2 being the primary agents responsible for disease worldwide.^[54] Persistent infection (PI) arises specifically from in utero exposure during early gestation (approximately days 40-125), where the developing fetal immune system fails to recognize the noncytopathic (NCP) biotype of the virus as foreign, resulting in immune tolerance and lifelong viremia without eliciting a neutralizing antibody response.^[55] PI animals shed the virus continuously through bodily secretions and excretions, serving as the main reservoir for herd transmission, and this persistent shedding resembles mechanisms seen in herpesvirus infections but involves continuous systemic replication rather than latency.^[56] In PI cattle, stressors such as transportation, calving, or concurrent infections can exacerbate clinical signs or increase virus shedding, leading to severe diarrhea, respiratory distress, and increased susceptibility to secondary pathogens due to BVDV-induced immunosuppression. During these episodes, transmission risk within the herd can increase, potentially precipitating outbreaks of acute disease in naive animals.^[54] A particularly devastating outcome in PI animals is the development of mucosal disease, a fatal condition triggered by superinfection with a cytopathic (CP) biotype of BVDV, characterized by erosive oral lesions, profuse diarrhea, and widespread epithelial necrosis, often culminating in death within weeks.^[57] Diagnosis of PI relies on detecting viral antigen via enzyme-linked immunosorbent assay (ELISA) on ear notch skin samples, which is highly sensitive for identifying carriers as early as birth, while reverse transcription polymerase chain reaction (RT-PCR) enables subtyping and genotyping to distinguish BVDV-1 from BVDV-2.^[55] Epidemiologically, BVDV is ubiquitous, with seroprevalence varying widely by region (often 50–90% in high-income countries), reflecting widespread exposure and the virus's role in substantial economic burdens estimated at $25 to $100 annually per affected cow due to reduced productivity, reproductive losses, and treatment costs.^[58]^[59] Control strategies center on identifying and culling PI animals to eliminate the infection source, complemented by vaccination with modified live virus (MLV) vaccines that induce protective immunity against acute disease, though they do not prevent PI establishment in exposed fetuses.^[60] In the European Union, compulsory eradication programs implemented since the 2010s—such as those in Germany, the Netherlands, and Scandinavia—have achieved over 90% reductions in PI incidence through systematic testing, biosecurity, and movement restrictions, demonstrating the feasibility of regional elimination.^[61]^[62]

Bovine Herpesvirus 1 Infection

Bovine herpesvirus 1 (BHV-1), a member of the Alphaherpesvirinae subfamily in the genus Varicellovirus, is the causative agent of infectious bovine rhinotracheitis (IBR), as well as genital and systemic diseases in cattle.^[63] Following acute primary infection, which typically enters via mucosal surfaces and spreads to sensory neurons, BHV-1 establishes lifelong latency primarily in the trigeminal ganglia, with occasional persistence in lymphoid tissues like the pharyngeal tonsils.^[64] During latency, viral gene expression is restricted, with the latency-related gene (LR gene) playing a central role in suppressing lytic replication and evading host immunity.^[65] This latent state allows carrier animals to remain asymptomatic while serving as reservoirs for transmission. Recrudescence occurs when latent BHV-1 reactivates, often triggered by stressors such as transportation, overcrowding, or administration of corticosteroids like dexamethasone, which disrupt latency maintenance through pathways involving the glucocorticoid receptor and Wnt/β-catenin signaling.^[64] Reactivation leads to anterograde transport of the virus along axons back to mucosal sites, resulting in shedding primarily through nasal or ocular secretions, typically without overt clinical signs in previously infected animals.^[66] In contrast, primary infections manifest with respiratory symptoms including high fever, mucopurulent nasal discharge, conjunctivitis, rhinitis, and dyspnea, alongside potential genital lesions or abortions in pregnant cattle; recrudescence contributes to subclinical spread and exacerbates bovine respiratory disease complex (BRD) by predisposing animals to secondary bacterial infections.^[67] Virus shedding during recrudescence typically lasts 3–10 days, facilitating herd-level transmission even in vaccinated populations.^[65] Diagnosis of BHV-1 infection and recrudescence relies on viral isolation from nasal or ocular swabs during shedding episodes, detection of antibodies via glycoprotein B (gB)-specific ELISA, and molecular confirmation of latent virus in ganglia using PCR or in situ hybridization.^[67] Epidemiologically, BHV-1 is distributed worldwide in cattle populations, with seroprevalence in the United States ranging from 20–40% and carrier rates of 30–50% in affected herds, enabling persistent circulation despite control efforts.^[65] Modified-live and inactivated vaccines reduce clinical disease severity and shedding during primary infection but fail to prevent latency establishment or reactivation, necessitating complementary strategies like quarantine, biosecurity, and serological surveillance for eradication programs.^[63] Recrudescence-driven transmission imposes significant economic burdens, including reduced milk production, treatment costs, and losses from BRD, estimated at billions annually in the cattle industry.^[67] This neuronal latency-reactivation cycle mirrors mechanisms in human alphaherpesvirus infections.^[64]

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