Encyclopedia of Ayurvedic Medicinal Plants

Spirochaetes - Syphilis

Syphilis is a specific infectious disease caused by Treponema pallidum. It is

either acquired by intimate body contact, usually coitus, or through the placenta of a syphilitic mother in the case of the congenital disease. The tissue reaction to the organism is by perivascular infiltration and obliterative endarteritis, phlebitis and lymphangitis. A gumma is the characteristic lesion consisting of a necrotic central area surrounded by giant and epithelioid cells

with a peripheral mantle of small lymphocytes and plasma cells.

Acquired syphilis. There are three stages. The primary external lesion is the

chancre usually appearing 2-4 weeks after contact, which sloughs centrally to give a punched-out appearance. Examination of the slough may reveal the

treponema on dark ground illumination. After the chancre has been present

for two or more weeks, mucous membrane ulcers or skin rashes appear and

the serological tests become positive, constituting the secondary stage. This

stage may be complicated by conjunctivitis with a marked papillary reaction, scleritis and later a severe granulomatous iridocyclitis, choroiditis and optic

neuritis. If basilar meningitis occurs it may lead to papilloedema, optic atrophy or cranial nerve palsies. The tertiary stage occurs ten or more years after the chancre in the form of tabes dorsalis or general paralysis of the insane (GPI). There are few organisms found but gumma formation is destructive and may occur almost anywhere including the lids and uveal tract. In the CNS degenerative changes may occur in the posterior columns of the spinal cord with ataxia and loss of vibration and muscie and joint sense. Deep reflexes are lost and posterior root 'lightning pains' may occur. Argyil- Robertson pupils which are small, irregular and react briskly to accommodation and convergence but poorly or not at all to light, are diagnostic of tabes. The lesion is considered to be in the posterior part of the midbrain. Primary optic atrophy  is the next most common sign of tabes

causing peripheral field restriction which proceeds to tubular vision and finally loss of sight. Serological tests on blood and cerebrospinal fluid may be positive in tabes but not as invariably as in general paralysis, which is a slowly progressive organic psychosis due to continued inflammatory reaction in the CNS, In the advanced state there is pyramidal tract involvement giving a positive Babinski sign or exaggerated deep reflexes as well as slurred speech and tremors. Ocular involvement in tertiary syphilis usually occurs in those who have had inadequate therapy. The absorbed fluorescent treponemal antibody test (FTA-ABS) is specific. Active infection can be distinguished by the presence of IgM antibodies, when penicillin therapy is highly effective.

Congenital syphilis. In congenital syphilis the foetus is infected in utero.

Infants may also suffer the acquired disease due to infection after birth, and

the condition then follows the usual adult course. Symptoms of congenital

syphilis may be present at birth with a fatal bullous eruption but they usually appear after about four weeks as a papillo-macular rash with a snuffly nose

and fissures around the mouth. There is a failure to thrive and later Hutchinson's triad of notched incisor teeth, nerve deafness and interstitial keratitis may be found. Saddle bridge of the nose due to collapse of the nasal

septum, splenomegaly, periostitis of the (sabre) tibiae and exostosis of the

cranial bones (hot cross bun head) are also characteristic signs.

HIV/AIDS

Epidemiology. In 1981 the first cases of acquired immunodeficiency syndrome (AIDS) were reported. By 1994 the millionth case was reported to the World Health Organisation (WHO) and the pandemic is now affecting all continents. Case definitions and laboratory facilities for diagnosis vary

between countries. Africa bears the biggest burden of infection, however the

numbers in Asia are rising fast.The three principal modes of transmission of the virus are:

1. heterosexual or homosexual intercourse 2. transfusion of infected blood or

injections with infected needles (drug related) 3. mother and infant transmission in utero or by breast feeding.

The WHO global estimate of HIV/AIDS sufferers at the beginning of 2000

was 34.3 million distributed . A survey by the Joint

United Nations Programme on HIV/AIDS (Unaids) at the beginning of 2000

estimated the death toll from HIV/AIDS related diseases during 1999 to be

2.6 million. Of these 95% are in the developing world, 70% of whom are in

sub-Saharan Africa, and most of these will die during the next ten years to

join the 13.7 million Africans who have already died from the epidemic.

Unaids also reports that HIV infections have doubled in the last two years in

the former Soviet Union mainly due to the use of infected syringes for drug

taking. Half of all people infected by HIV were less than 25 years old and

tragically they typically died by the age of 35. The report emphasised that the disease remains fatal and that the decline in deaths due to anti-retroviral therapy is tapering off.

       There are many systemic infective patterns which may occur with the

acquired immunodeficiency syndrome. Use of the drug AZT (zidovudine)

lengthens survival in patients with AIDS.

Cytomegalovirus (CMV) is a widespread virus disease resulting in large cells with inclusion bodies which are found in secretions or tissues. Pregnant

women may show a raised antibody titre and about 2% of newborn excrete

the virus but few show signs of the disease. In those who do, many tissues

may be involved causing jaundice, splenomegaly, haemolytic anaemia and

encephalitis with its sequelae. It is one cause of intracranial calcification. The eyes may be affected by choroidoretinitis varying from a single focus to

severe disorganisation. An acute retinal vasculitis may occur in patients with

AIDS and adults following organ transplants involving immuno-suppressive

treatment. Anti-viral treatment is partially effective as described in the therapy of AIDS but there is a serious risk of retinal detachment.

Tuberculosis

Tuberculosis in man is caused by human and bovine strains of the tubercle bacillus. Primary infection in children is characterised by the local formation of tuberculous follicles and a similar but greater reaction in the draining lymph nodes. Depending on the degree of immunity and hypersensitivity acquired as a result of the primary episode, re-infection may lead in the immune non-allergic patient to a fibrotic reaction. Re-infection in the hypersensitive patient leads to varying degrees of caseation which may present as a circumscribed tuberculoma when immunity is good or, when it is poor, as diffuse tuberculous granulation tissue with some caseation. In the non-allergic patient a bacillaemia may lead to acute miliary tuberculosis when immunity is low or to chronic miliary tuberculosis if it is high.

Primary disease. The conjunctiva and its preauricular nodes may be the site

of a primary tuberculous complex (pi94) presumably caused by droplet infection. This may spread locally into the eye or by the blood stream into the lungs. It is one cause of Parinaud's Oculo-Glandular Syndrome which

embraces a group of conditions which are characterised by a unilateral necrotic conjunctival lesion with preauricular adenitis. The syndrome also includes lymphogranuloma venereum, chancre, tularaemia and 'cat scratch fever'. Phlyctenulosis. Primary ocular tuberculosis is rare but tuberculoprotein from primary infection in the lung or elsewhere may be a frequent cause of allergic phlyctenular disease in countries where tuberculosis is common. This is a condition mainly affecting the conjunctiva in children (p205). Symptoms may be slight or there may be a complicating mucopurulent conjunctivitis. When the cornea is involved, photophobia and lacrimation are often intense. The phlyctenule is a small pinkish-white elevation often situated near the corneoscleral junction with an associated leash of conjunctival vessels. If the cornea is affected, nodules appear in the superficial layers followed by connective tissue formation and deep and superficial vascularisation. Eventually in the absence of treatment, corneal scarring may be severe. The phlyctenule consists of an exudation of polymorphonuclear and mononuclear leucocytes into the deeper layers of the conjunctiva. Untreated, it may resolve but more often it sloughs and heals by granulation. The tubercle bacillus is not found in the phlycten which is a Type IV hypersensitivity reaction and is readily controlled by local steroid applications with antibiotics as necessary. Phlyctenular disease may indicate active pulmonary tuberculosis but increasingly in the UK it results from allergy to other organisms.

Miliary disease. The eye is commonly affected in miliary tuberculosis by direct haematogenous infection. Characteristic tubercles are seen in the choroid and sometimes in the iris. The choroidal lesions appear first as indefinite white patches under a zone of slight vitreous haze, later becoming more defined and slightly pigmented

Adult tuberculosis. Ocular tuberculosis is seldom seen in patients with active post-primary tuberculosis but those affected are often healthy individuals with apparently inactive lesions. It is presumably due to an occasional bacillaemia. It is usually difficult to establish the tuberculous nature of uveitis. It has been shown that ocular tuberculosis with a high local sensitivity to tuberculo- protein is compatible with a low skin sensitivity. However, a high skin sensitivity in conjunction with clinical features and after exclusion of other known aetiological factors is some evidence in favour of the tuberculous nature of an eye lesion. A non-specific uveitis is usual but a granulomatous response may result in nodules in the iris, ciliary body and choroid.Retinal tuberculosis is usually caused by direct extension from choroidal tubercles but may take the form of retinal periphlebitis. Optic neuritis may occur. The sclera may develop a chronic, dusky red, brawny congestion which can be seen beneath the bulbar conjunctiva anteriorly and

which heals eventually as a white scar (p494). When Tenon's capsule is involved there may be proptosis or immobility of the eye with oedema of the

lids. There is always some underlying uveitis. Episcleritis is a more superficial condition, being an allergic reaction to a variety of allergens of which tuberculo-protein may be one (Plate 25.15 p493). The cornea may be affected by extension from the sclera or as a sectorial patch of interstitial keratitis, vascularised by both superficial and deep vessels. It is also frequently unilateral and leaves heavy scarring. In contrast, syphilitic interstitial keratitis is almost always bilateral, involves all parts of the cornea and scarring is often less dense. The treatment of ocular tuberculosis is prolonged and normally involves isoniazid, rifampicin and pyrazinamide for 2 months followed by isoniazid and rifampicin for 4 months. Ethambutol or streptomycin is included in the initial regime until sensitivity results are available. If there is no improvement in the condition after 1 month of therapy the diagnosis must be questioned. In uveitis suspected of tuberculous origin and under treatment, atropine drops and the careful use of steroids locally may reduce the inflammatory response.

Leprosy (Hansen's disease)

Mycobacterium leprae was discovered as the cause of leprosy in 1873 by

Hansen. The optimum temperature for growth of this slowly dividing organism is below 37°C hence the heaviest infiltrations are in the cooler areas of the body. Humans are the only natural host and the immune response to infection is extremely variable. There are two polar forms of leprosy; tuberculoid, in which cell mediated immunity (CMI) is high, and lepromatous, in which CMI is low. Intermediate forms have been recognised between these extremes which are unstable and may change with time. The disease primarily affects the skin, peripheral nerves and anterior ocular structures.

Treatment. Because ocular leprosy is a significant threat to vision, early diagnosis and treatment is critical. Diagnosis beyond clinical detection, still often relies on skin scrapings or biopsies. A simple, reproducible screening test is required along the lines of the protein-glycolipid-1-antigen ELISA.

Polymerase chain reaction methods are also being developed. Dapsone used

to be the only therapy required for this disease lOmg/kilo body weight per

week over 2 or 3 years or longer but resistance to this drug means that multidrug therapy is now preferred involving dapsone, rifampicin, and clofazimine lOOmg on alternate days. Therapy may need to be taken for up to 2 years but episodes of ocular inflammation may recur. Many of the allergic effects can be alleviated by the judicious use of corticosteroids.

Posterior Uveitis Due to Toxoplasmosis

Definition: Focal chorioretinal inflammation caused by infection.

Epidemiology. This clinical syndrome is encountered frequently.

Pathogenesis. The pathogen, Toxoplasma gondii, is transmitted by ingestion of tissue cysts in raw or undercooked meat or by oocysts from cat feces. In congenital toxoplasmosis, the child acquires the pathogen through transplacental transmission.

Symptoms and diagnostic considerations. As a general rule, a negative complement fixation test does not exclude Toxoplasma infection where classic clinical symptoms are present. Both forms of the disorder present with characteristic

grayish white chorioretinal focal lesions surrounded by vitreous infiltration

and associated vasculitis.In congenital toxoplasmosis

the affected children have a macular scar that significantly

impairs visual acuity. This often leads to secondary strabismus. Intracerebral

involvement can also result in hydrocephalus and intracranial calcifications.

In the acquired form, visual acuity is impaired only where the macula is involved. This is rarely the case.

Differential diagnosis. Chorioretinitis with tuberculosis, sarcoidosis, borreliosis (Lyme disease), or syphilis should be excluded by serologic studies.

Treatment. The treatment of choice consists of a combination of pyrimethamine, sulfonamide, folinic acid, and steroids in their respective standard doses.