Acute hemorrhagic conjunctivitis

Author: Paul W. Wright, Marlyn P. Langford
Date: Jan, 1992

Acute hemorrhagic conjunctivitis is a highly contagious enteroviral eye infection. It seems to have suddenly appeared in Ghana, West Africa, in 1969. Because this illness emerged at the time of the Apollo 11 moon landing, it was nicknamed "Apollo 11" disease. In West Africa, the disease is still referred to as "Apollo." From 1969 to 1972, the disease spread as a pandemic from Ghana across tropical and subtropical western and central Africa to the Middle East, Asia and a few cities in Europe.

After several other epidemics, occurring mostly in Asia and Africa, a second pandemic of the disease began in India and spread through Asia to Africa and then to the Western Hemisphere. From 1980 to 1982, over 2 million cases of acute hemorrhagic conjunctivitis occurred in the Caribbean, the northern part of South America, Central America and southern Florida. [1] Small clusters of cases were also reported in North California, Minnesota, California, New York and Ontario, Canada.

Clinical Picture

Typically, acute hemorrhagic conjunctivitis begins suddenly, with ocular redness, epiphora (excessive tearing), lid swelling, photophobia and pain developing in one eye over a period of six to 12 hours. [2] The other eye is affected within 24 hours of onset in 80 percent of cases. Pain is frequently the initial and most notable symptom and is described as a burning, itching, foreign-body sensation or as frank ocular pain.

The most alarming sign of infection is subconjunctival hemorrhage. It may present as petechiae or frank blotches of hemorrhage, usually located beneath the superior bulbar conjunctiva (Figure 1). Punctate epithelial keratitis (corneal epithelial inflammation identified by punctate corneal staining with fluorescein) may be observed in most cases of acute hemorrhagic conjunctivitis and is thought to be the cause of the foreign-body sensation.

Additional symptoms may include blurred vision, malaise, myalgias, fever, headache, depression and upper respiratory tract symptoms. Common physical findings include serous, seromucoid or purulent discharge, lid edema with pseudoptosis (swelling of the upper lid, which appears to be drooping), and chemotic (edematous) and hyperemic conjunctivae. Preauricular lymphadenopathy may be present, and nodes may be tender on palpation.

Symptoms usually develop after an incubation period of 24 to 28 hours, persist for three to five days and gradually resolve over seven to 10 days. However, sequelae such as subconjunctival hemorrhage, lymphadenopathy and hyperemia may persist for two to three weeks.

The most serious ophtalmologic sequela has been secondary bacterial infection, which occurs in 1 to 2 percent of cases. [2] In addition, the use of steroids for acute hemorrhagic conjunctivitis has been associated with worsening of the condition, delayed recovery, and severe and permanent ocular problems. In Honduras and Miami, cases of blindness have been reported in persons who acquired bacterial superinfections after they attempted to treat their eyes with urine.

Neurologic sequelae, which have been reported only in cases caused by infection with enterovirus 70, occur in approximately one in 10,000 cases and result in significant morbidity. Neurologic symptoms have been observed in both children and adults. The neurologic manifestations vary from a transient, mild cranial nerve palsy to painful lumbosacral radiculomyelitis with temporary or permanent flaccid paralysis.

Neurologic symptoms usually develop 10 to 20 days after the onset of conjunctivitis but may occur as early as seven days or as late as three months after acute hemorrhagic conjunctivitis. Approximately one-third of patients sustain permanent neurologic impairment, most commonly facial or lower limb paralysis. Other cranial nerve involvement, including primary optic atrophy, may also occur.

While the pathogenesis of the neurologic sequelae remains unclear, the connection with enterovirus 70 is well established. Although the virus has not been isolated from cerebrospinal fluid, elevated and rising neutralizing antibody titers to enterovirus 70 have been found in both the serum and the cerebospinal fluid of patients with neurologic disease. The role of enterovirus 70 in producing neurologic symptoms is further supported by the observation of paralytic disease in monkeys who were injected intrathecally and intracranially with the virus. [3]


Enterovirus 70 and coxsakievirus A24 are picornaviruses. They are antigenically distinct members of the enterovirus group and are more closely related to the acid-stable polioviruses than the acidlabile rhinoviruses. Both polioviruses and rhinoviruses are members of this family.


The eye symptoms are caused by replication of the virus in the epithelial cells of the palpebral (lid) and bulbar (globe) conjunctiva and cornea (Figure 2). The virus destroys the cell. Erosion of the dead epithelial and corneal cells results in defects (small pits, one to several cells deep) in the surface of the conjunctiva and cornea. [4] Usually, virus replication peaks about 24 hours after infection, then declines rapidly.

The decline in viral replication coincides with the occurrence of symptoms and natural host defenses (interferon, antibody, inflammation, etc.) [5] The clinical symptoms appear as the virus-infected cells of the conjunctiva and cornea erode and the inflammatory response begins. The severity of disease is highly variable and may be related to the number of cells infected and the extent of inflammation in the ocular tissues.


Since the first known outbreak of acute hemorrhagic conjunctivitis in 1969, millions of people have been affected. The geographic distribution of past epidemics indicates that the condition tends to spread rapidly through densely populated areas in tropical climates (between 40[degrees] latitude in the Northern Hemisphere and 15[degrees] in the Southern Hemisphere).

Epidemics are explosive in nature, have a rapid course and may occur at any time during the year. The disease has a short incubation period (one to two days). When an individual becomes infected, other members in the household will probably become infected within a short period. Infection rates of 70 to 100 percent have been reported in household members, and up to 15 percent of the population may be affected during an epidemic. [6] During the Florida epidemic, interestingly, the high rate of spread among familites was related not to the number of persons per family dwelling, but to the number of family members sharing a common bath facility.

Most people are susceptible to the infection, and reinfection has been observed during some epidemics. The incidence of asymptomatic cases is usually low (less than 10 percent). Acute hemorrhagic conjunctivitis has been reported to affect individuals


of all ages. However, the disease may be less severe in children than in adults. No predilection exists for sex or race.


The diagnosis is suggested by the acute onset of severely painful conjunctivitis in one eye (with progression to the other eye), accompanied by extensive subconjunctival hemorrhage. When a patient presents with these symptoms during an epidemic, the diagnosis can be made with great certainty.

Laboratory confirmation is accomplished by the isolation of enterovirus 70 or coxsackievirus A24 on cell culture systems from freshly collected conjunctival swabs. A fourfold increase between acute and convalescent titers or convalescent titers of 1:16 or greater enterovirus 70 or coxsackievirus A24 is suggestive of infection.


The differential diagnosis of acute conjunctivitis with subconjunctival hemorrhage includes ocular trauma (contact, toxic or irritative), other viral infections (usually adenovirus), bacterial conjunctivitis and, rarely, allergic conjunctivitis. Table 1 compares features of acute hemorrhagic conjunctivities with those of other conjunctival syndromes.

Adenorival conjunctivitis, most commonly due to types 3, 7, 8, 11 and 19, occasionally presents as acute conjunctivitis with subconjunctival hemorrhage and thus can be focused with acute hemorrhagic conjuctivitis. In particular, epidemic keratoconjunctivitis, a type of adenorival conjunctivitis, exhibits a similar clinical triad of conjunctivitis, keratitis and epidemic occurrence.

Characteristics that distinguish acute hemorrhagic conjunctivitis from other viral conjunctival syndromes are listed in Table 2.


Only supportive therapy is currently available for acute hemorrhagic conjunctivitis. Secondary bacterial infections should be treated with appropriate antibiotics. Topical corticosteroids should be avoided because of their potential adverse side effects. Treatment with human leukocyte interferon ophthalmic drops has been studied but does not appear to affect the clinical course or spread of the disease. [7] Artificial tears and topical decongestants have not been shown to be more beneficial than simple cold compresses. [8]

Prevention is an important consideration in dealing with this infection. The human leukocyte interferon study [7] and other studies [9] demonstrate that patient education can markedly curtail transmission of the infection. During the 1981 epidemic in Florida, public health measures limited the spread of this illness. Such measures included increased surveillance with early disease recognition, education concerning hygienic prevention (especially hand washing) and exclusion of infected patients from school, the workplace and certain health facilities. Patients should not return to work or school until 14 days after the onset of symptoms.

Physicians and other health care providers should review examination procedures that might result in transfer of the virus. Special care should be taken with any patient with acute conjunctivitis. The simplest and most effective steps to prevent cross infection are sterilization of instruments and rigorous hand washing before each examination.

Education about acute hemorrhagic conjunctivitis will enable the primary care physician to recognize and treat this illness, either as an isolated case or during an epidemic. Future epidemics are possible in the United States because most people in the Western Hemisphere are probably susceptible to enterovirus 70. [10] While development of a vaccine had been discussed, it has yet to be accomplished. [11] Such a vaccine would be extremely beneficial if it could safely prevent or attenuate this severely painful and contagious conjunctivitis.


[1] Patricia PA. Clinical experience with acute hemorrhagic conjunctivitis in the United States. In: Uchida Y, Ishii K, Miyamura K, Yamazaki S, eds. Acute hemorrhagic conjunctivitis: etiology, epidemiology, and clinical manifestations. New York: Karger Press, 1989:49-56.

[2] Uchica Y. Clinical features of acute hemorrhagic conjunctivitis due to enterovirus 70. In: Uchida Y, Ishii K, Miyamura K, Yamazaki S, eds. Acute hemorrhagic conjunctivitis: etiology, epidemiology, and clinical manifestations. New York: Karger Press, 1989:213-24.

[3] Kono R, Sasagawa A, Kodama H, et al. Neurovirulence of acute-haemorrhagic-conjunctivitis virus in monkeys. Lancet 1973;1(7794):61-3.

[4] Langford MP, Yin-Murphy M, Barber JC, Heard HK, Stanton GJ. Conjunctivitis in rabbits caused by enterovirus type 70 (EV70). Invest Ophthalmol Vis Sci 1986;27:915-20.

[5] Langford MP, Stanton GJ, Barber JC, Baron S. Early-appearing antiviral activity in human tears during a case of picornavirus epidemic conjunctivitis. J Infect Dis 1979;139:653-8.

[6] Patricia PA, Onorato IM, Sklar VE, et al. Acute hemorrhagic conjunctivitis. Investation of a large-scale community outbreak in Dade County, Florida. JAMA 1983;249:1283-9.

[7] Stansfield SK, de la Pena W, Koenig S, et al. Human leukocyte interferon in the treatment and prophylaxis of acute hemorrhagic conjunctivitis. J Infect Dis 1984;149:822-3.

[8] Sklar VE, Patriarca PA, Onorato IM, et al. Clinical findings and results of treatment in an outbreak of acute hemorrhagic conjunctivitis in southern Florida. Am J Ophthalmol 1983;95:45-54.

[9] Malison MD, Gunn RA, Hatch MH, Bernard KW, White MC. Acute hemorrhagic conjunctivitis, Key West, Florida. An assessment of risk factors for introduction of illness into households and secondary spread during the 1981 epidemic. Am J Epidemiol 1984;120:717-26.

[10] Hierholzer JC, Hilliard KA, Esposito JJ. Serosurvey for "acute hemorrhagic conjunctivitis" virus (Enterovirus 70) antibodies in the Southeastern United States, with review of the literature and some epidemiologic implications. Am J Epidemiol 1975;102:533-44.

[11] Wadia NH, Wadia PN, Katrak SM, Misra VP. Neurological manifestations of acute hemorrhagic conjunctivitis [Letter]. Lancet 1981;2:(8245):528-9.

The Authors

PAUL. W. WRIGHT, M.D. is associate professor of family practice at the University of Texas Health Center at Tyler. A graduate of the University of Kentucky College of Medicine, Lexington, he completed a family practice residency at John Peter Smith Hospital, Forth Worth, Tex.

GLENN H. STRAUSS, M.D. is clinical assistant professor in the Department of Ophthalmology at the University of Texas Medical Branch at Galveston, where he also received his medical degree. Strauss is also in private practice in Tyler, Tex.

MARLYN P. LANGFORD, M.S., PH.D. is associate professor in the Department of Ophthalmology at the Louisiana State University Medical Center in Shreveport. He graduated from the University of Texas Medical Branch at Galveston, where he also completed a post-doctoral fellowship in infection and immunity.

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