Parinaud Oculoglandular Syndrome

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Parinaud Oculoglandular Syndrome

Disease Entity

Parinaud oculoglandular syndrome is a conjunctival disease characterized by a unilateral granulomatous follicular conjunctivitis associated with ipsilateral regional lymphadenopathy. There are many vectors that transmit organisms that cause oculoglandular syndrome, of which, Cat Scratch Disease is the most common cause. Prognosis in most cases is excellent. [1]

Diagnostic testing and treatment should be dictated by patient history, clinical findings, and symptoms.


Most common

Cat-Scratch Disease

Bartonella henselae

More common


Francisella tularensis


Sporothrix schenckii

Less common


Mycobacterium tuberculosis


Coccidioides immitis


Treponema pallidum


Herpes Simplex

Herpes virus



Haemophilus ducreyi


Pasteurella multocida

Yersinia sp.

Yersinia enterocolitica

Yersinia pseudotuberculosis

Hansen’s disease

Mycobacterium leprae


Listeria monocytogenes


Mumps virus

Infectious mononucleosis

Epstein-Barr virus


Blastomyces dermatitidis

Mediterranean fever

Rickettsia conorii


Smallpox vaccine

Lymphogranuloma Venereum (LGV)

Chlamydia trachomatis-LGV subtype


Paracoccidioides brasiliensis


Burkholderia mallei

General Pathology

Cat-Scratch Disease

Image of a patient with Parinaud oculoglandular syndrome.10 (© 2018 American Academy of Ophthalmology)

Cat-scratch disease (CSD) is a zoonosis caused by the bacterium Bartonella henselae, a small fastidious gram-negative bacillus that may enter the eye through facial scratches or the conjunctiva. [1]Parinaud oculoglandular syndrome occurs in 5-7% of patients with CSD.[2] [3] Immature domestic cats are the most frequently implicated vector with other sources including dogs, cat fleas, and sandflies.[4][5]


Tularemia is a zoonotic disease caused by the bacterium Francisella tularensis, a pleomorphic aerobic gram- negative coccobacillus. A wide range of animals serve as reservoirs (rabbits, squirrels, game bird, muskrats, hamsters, prairie dogs, sheep, beavers, cats, tick, flea, and mosquito). F. tularensis can be aerosolized and can be found in soil and water.[6]


Sporotrichosis is a rare mycosis caused by Sporothrix schenckii, a dimorphic fungus existing in mycelial and yeast phase. Infection rates are higher in tropical and subtropical areas such as Brazil and Peru,[7] where Sporothrix schenckii is endemic. It is commonly found in plant organic matter such as leaves, wood, soil, and water. [8] Sporothrix schenckii has also been recovered from animal fur, feces, and oral cavities (i.e. cats, horse, dogs, rabbits, and rats).[9]


Cat-Scratch Disease

The incubation period is typically anywhere from 3 days to 3 weeks. B. henselae is frequently transmitted through hand-to-eye contact, or from contamination of an open wound.[2] Aerosolized cat flea feces is another proposed mechanism. Unlike other manifestations of CSD, the oculoglandular form rarely manifests after a scratch.[10] A higher number of cases are reported among children and veterinary workers. To evaluate for potential exposure, clinicians should assess for recent contact with cats, dogs, human body lice, sandflies, or fleas. [5] It is important to note that although a history of cat contact is often present, a cat bite or scratch may not be apparent.[1]


Tularemia has an incubation period of approximately 2 to 5 days, and rarely up to 3 weeks. Infected individuals are typically meat-handlers, campers, or hunters who have had recent contact with animals or contaminated particles. The mechanism of ocular involvement is hand-to-eye contact, or splash from contaminated animal body fluids or water.[11] History should include recent travel, outdoor activities, game ingestion, handling of animal carcasses, and tick exposure.


Sporotrichosis can be transmitted through traumatic inoculation of the skin with organic matter,[12] infected respiratory secretions,[7] and hand-to-eye contact with infected animal fluids.[13] Occupations or activities that have been associated with infection include plant or soil handling and contact with sick or healthy animals (i.e. gardener, miners, hunters, farmers, veterinarians, etc).

Physical examination

Cat-Scratch Disease

Ocular signs of Cat-Scratch disease range from scant to copious serous and/or mucoid discharge, mild periorbital edema, conjunctival ulceration overlying a granuloma, and/or conjunctival nodules. Rarely, peripheral corneal ulceration may occur.[1] A papule may appear at the site of inoculation. Patients typically develop tender lymphadenopathy (pre- or post-auricular, submandibular, or cervical lymph nodes). [3][14][15] Less common manifestations are low grade fever, pain, and suppurative lymphadenopathy. It can take several weeks for the granuloma to resolve, and several months for the regional lymphadenopathy to clear.[11]


Oculoglandular syndrome is a rare presentation of Tularemia (2-14%). Signs of ocular involvement include mucopurulent discharge, conjunctival chemosis, corneal epithelial defects, ulceration, nodules, and periorbital edema. Less common ocular signs are dacryocystitis and corneal ulcer. Patients develop headaches, anorexia, high fever, sore throat, and painful lymphadenopathy (preauricular, submandibular, cervical, parotid, or axillary). [10][16]


In Sporotrichosis oculoglandular syndrome, conjunctival granuloma and/or ulcer, eyelid ulcer, and purulent discharge are some common ocular findings.[7][8] Commonly associated signs include non-tender preauricular and submandibular lymphadenopathy. Less commonly, patients experience painful lymphadenopathy, dacryocystitis,[7] or fever.[13]


Cat-Scratch Disease

Cat-scratch disease is diagnosed with serology, culture,[17] or polymerase chain reaction (PCR).[18] In practice, serology is the most often used modality. Titers of immunoglobulin M (IgM) greater or equal to 1:20, immunoglobulin G (IgG) greater or equal to 1:256, or a fourfold increase in serum IgG titers between acute and convalescent phase are indicative of active infection.[3] If CSD is tested later in the disease course, IgM titers are typically low and IgG titers are high. Therefore, IgG titers of 1:512 are indicative of recent infection. Cultures are difficult to obtain and require long incubation periods. In the past, B. henselae was diagnosed using the Hanger-Rose test on lymph node aspirates.[19] For biopsies, Warthin- Starry, Steiner silver stain, or Brown- Hopp stain can be used to show the presence of gram- negative bacilli. [1]


Tularemia is diagnosed with culture, serology, PCR, or direct fluorescent antibody assay. Potential specimens are lymph node aspirates, conjunctival nodule biopsy, conjunctival swab or serum. In practice, serology is the most often used modality. Serologic titers greater than 1:128 indicate prior or current infection. Because it takes 2 weeks for titers to increase, the first samples should be obtained early, followed by repeat samples at day 14 and weeks 3 to 4. A fourfold increase in F. tularensis antibodies confirms an active infection. Titers greater than 1:160 at 2 to 3 weeks after onset of symptoms onset indicate an active infection.[10] For cultures, the organism needs a cysteine-enriched media to grow—such as modified Thayer-Martin media or chocolate agar (GCII agar with 1% haemoglobin and 1% IsoVitaleX).[20]


Sporotrichosis is typically diagnosed with culture (Sabouraud 2%). If a conjunctival nodule is present, it can be biopsied and sent for histopathology (Gomori-Methenamine-Silver (GMS), Periodic Acid-Schiff (PAS) stains), or electron microscopy (EM).[12]


Cat-Scratch Disease

The role of antibiotic therapy in CSD has not been established in a controlled study. As CSD is generally self-limited, treatment is usually supportive. Broad-spectrum ophthalmic drops are used to prevent secondary infections.[19] Systemic antibiotics are recommended for moderate to severe disease, which more commonly involve immunocompromised patients. A wide variety of antibiotics and antibiotic combinations have been utilized to treat CSD including doxycycline, azithromycin, trimethoprim/sulfamethoxazole DS, ciprofloxacin, and rifampin. The duration of treatment varies depending on the patient’s clinical course, and should be individualized.[3][15]


For severe disease, first line agents are streptomycin or gentamicin for 7 to 14 days. For less severe disease, the recommended treatment is oral or intravenous doxycycline or ciprofloxacin for 14-21 days.[5] Topical treatment options include ciprofloxacin ophthalmic drops, or tobramycin ophthalmic drops or ointment. [11] With therapy, ocular symptoms improve in approximately 1 week, and overall recovery may be seen in 2 to 3 months.[10][21]


There are no controlled studies to evaluate the effectiveness of antifungal agents for the treatment of sporotrichosis. Currently, Sporotrichosis oculoglandular syndrome is treated with oral itraconazole, potassium iodide, or fluconazole. Topical fluconazole ophthalmic drops have also been utilized with success. Nonetheless, sporotrichosis typically responds well to treatment. Duration and treatment are usually weeks to months, and symptoms resolve in 1 to 4 months. [9] [12][13]


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