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15.3C: Bacterial Eye Diseases - Biology

15.3C: Bacterial Eye Diseases - Biology



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Conjunctivitis is inflammation of the conjunctiva, most commonly due to an infection.

LEARNING OBJECTIVES

Describe the various causes of conjunctivitis and keratitis and its symptoms

Key Points

  • Classification can be either by extent of the inflamed area or by cause (allergic, bacterial, viral, or chemical).
  • Red eye (hyperaemia), irritation (chemosis) and watering (epiphora) of the eyes are symptoms common to all forms of conjunctivitis.
  • Keratitis, a condition in which the eye’s cornea becomes inflamed, is often marked by moderate to intense pain and usually involves impaired eyesight.

Key Terms

  • conjunctivitis: An inflammation of the conjunctiva often due to infection.
  • keratitis: Inflammation of the cornea.

Common Eye Infections

CONJUNCTIVITIS

Conjunctivitis, also called pink eye or Madras eye, is inflammation of the conjunctiva, which consists of the outermost layer of the eye and the inner surface of the eyelids. Conjunctivitis most commonly caused by a viral infection or, less commonly, a bacterial infection, or by an allergic reaction. Classification can be either by extent of the inflamed area or by cause (allergic, bacterial, viral or chemical). Neonatal conjunctivitis is often defined separately due to different organisms.

Symptoms and Diagnosis

An inflamed, red eye (hyperaemia), irritation (chemosis), and watering (epiphora) of the eyes are symptoms common to all forms of conjunctivitis. However, the pupils should be normally reactive and the visual acuity normal. Bacterial conjunctivitis due to common pyogenic (pus-producing) bacteria causes marked grittiness/irritation and a stringy, opaque, greyish or yellowish mucopurulent discharge that may cause the lids to stick together, especially after sleep. Another symptom that could be caused by bacterial conjunctivitis is severe crusting of the infected eye and the surrounding skin.

Contrary to popular belief, discharge is not essential to the diagnosis. Bacteria such as Chlamydia trachomatis or Moraxella can cause a non-exudative but persistent conjunctivitis without much redness. The gritty and/or scratchy feeling is sometimes localized enough for patients to insist they must have a foreign body in the eye. The more acute pyogenic infections can be painful. Like viral conjunctivitis, it usually affects only one eye but may spread easily to the other eye.

Corynebacterium diphtheriae causes membrane formation in conjunctiva of non immunized children. Bacterial conjunctivitis usually resolves without treatment. Antibiotics, eye drops, or ointment may only be needed if no improvement is observed after three days.

Chlamydiaconjunctivitis or trachoma was once the most important cause of blindness worldwide. The infection can be spread from eye to eye by fingers, shared towels or cloths, coughing and sneezing, and by eye-seeking flies. Newborns can also develop chlamydia eye infection through childbirth. Chlamydia can affect infants by causing spontaneous abortion, premature birth, and conjunctivitis, which may lead to blindness and pneumonia. Conjunctivitis due to chlamydia typically occurs one week after birth (compared with chemical causes (within hours) or gonorrhea (2–5 days)).

KERATITIS

Keratitis is a condition in which the eye’s cornea, the front part of the eye, becomes inflamed. The condition is often marked by moderate to intense pain and usually involves impaired eyesight. Superficial keratitis involves the superficial layers (i.e. the epithelium) of the cornea. After healing, this form of keratitis does not generally leave a scar. Deep keratitis involves deeper layers of the cornea (i.e. the epithelium, Bowman’s membrane and often stroma), and the natural course leaves a scar upon healing that impairs vision if it occurs on or near the visual axis. This can be reduced or avoided with the use of topical corticosteroid eyedrops.

Causes and Treatment

Keratitis has multiple causes. Bacterial infection of the cornea can follow from an injury or from result from wearing contact lenses. The bacteria involved are Staphylococcus aureus and, for contact lens wearers, Pseudomonas aeruginosa. Pseudomonas aeruginosa contains enzymes that can digest the cornea. Treatment depends on the cause of the keratitis. Infectious keratitis can progress rapidly, and generally requires urgent antibacterial, antifungal, or antiviral therapy to eliminate the pathogen. Treatment is usually carried out by an ophthalmologist and can involve prescription eye medications, systemic medication, or even intravenous therapy. It is inadvisable to use over-the-counter eye drops as they are typically not helpful in treating infections; using them could also delay crucial correct treatment, increasing the likelihood of sight-threatening complications. In addition, contact lens wearers are typically advised to discontinue contact lens wear and replace contaminated contact lenses and contact lens cases.


Trachoma

Trachoma is a contagious bacterial infection that affects the surface of the eyes. Over time, scar tissue or ulcers can form that lead to blindness. Currently around 1.9 million people worldwide are blind or visually impaired by trachoma, and it remains a public health problem in 44 countries. It spreads when bacteria in the secretions from the eyes of an affected individual extend to others either by person-to-person contact or by eye-seeking flies, particularly the Musca sorbens fly. It occurs most commonly in endemic communities with poor hygiene and lack of access to clean water. It is the leading infectious cause of preventable blindness in the world. Approximately 21 million people in the world have active trachoma. The majority of these are children between 3-6 years of age. The disease is found predominantly in dry, arid lands near the equator, with the largest number of cases in sub-Saharan Africa.

Trachoma Symptom

Vision Loss

Loss of vision can occur suddenly or develop gradually over time. Vision loss may be complete (involving both eyes) or partial, involving only one eye or even certain parts of the visual field. Vision loss is different from blindness that was present at birth, and this article is concerned with causes of vision loss in an individual who previously had normal vision. Vision loss can also be considered as loss of sight that cannot be corrected to a normal level with eyeglasses. The causes of loss of vision are extremely varied and range from conditions affecting the eyes to conditions affecting the visual processing centers in the brain. Impaired vision becomes more common with age. Common causes of vision loss in the elderly include diabetic retinopathy, glaucoma, age-related macular degeneration, and cataracts.

What are the five stages (types) of trachoma?

The World Health Organization created a grading system to classify the five stages of blinding trachoma, based on the clinical signs that are seen as the disease progresses.

  1. Trachomatous inflammation -- follicular (TF): The first sign is the presence of follicles, which are small bumps formed by swollen lymph tissue on the back of the upper eyelid and sometimes extending to the top part of the eye. The presence of five or more follicles greater than 0.5 mm in size on the conjunctiva lining the back of the upper eyelid is considered grade TF.
  2. Trachomatous inflammation -- intense (TI): The next phase is swelling (inflammation) of the conjunctiva that obscures the view of the normal deeper blood vessels of the conjunctiva.
  3. Trachomatous scarring (TS): Bands of scar tissue form within the conjunctiva lining the inside of the upper eyelid.
  4. Trachomatous trichiasis (TT): The bands of scar tissue tighten, causing the lid margins to turn inward (entropion) and the eyelashes to rub against the eye (trichiasis). Over time, this rubbing results in abrasions of the cornea, the clear central covering of the front of the eye.
  5. Corneal opacity: Corneal abrasions can lead to infectious ulcers and ultimately opaque scarring that blocks light from entering the eye, leading to blindness.

QUESTION

What is the cause of trachoma?

The bacteria responsible for trachoma is Chlamydia trachomatis. There are different types of Chlamydia trachomatis. Types A, B, Ba, and C cause blinding trachoma. Other types (D to K) are associated with sexually transmitted chlamydia infection.

Living conditions with poor sanitation, unclean water supply, and lack of regular face washing allow the bacteria to infect and re-infect eyes of individuals living in trachoma-endemic areas.

The active form is most common in young children who spread it to those closest to them such as siblings, playmates, and caregivers. Among adults, women who care for children have a higher incidence of active disease.

What are trachoma symptoms and signs?

The symptoms include irritation of the eyes with tearing, pain, light sensitivity, and vision loss. The signs include the presence of follicles, redness, scarring, and corneal opacity as described in the five stages listed above.

How do doctors diagnose trachoma?

Although there are tests to identify the bacteria, doctors primarily diagnose trachoma by examining the eyes and eyelids of the patient. Health care workers are trained in basic eye health examination techniques and can make the diagnosis by identifying the five stages of blinding trachoma with the aid of a light and simple magnifiers.

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What is the treatment for trachoma? Is it possible to prevent trachoma?

The World Health Organization reported that the number of people at risk for trachoma has fallen from 1.5 billion in 2002 to just over 142 million in 2019.

The WHO Alliance for the Global Elimination of Trachoma by 2020 (GET2020) aims to completely eradicate the disease through implementation of the multifaceted SAFE strategy to prevent and treat trachoma:

  • S = surgery to correct in-turned eyelids and trichiasis
  • A = antibiotics (azithromycin) to treat active infection
  • F = facial cleanliness to reduce human transmission
  • E = environmental improvement (such as access to clean water and hygiene measures to reduce the fly population) to reduce human transmission

The antibiotic treatment for active disease is a onetime use of azithromycin (Zithromax) pills. However, reinfection is common if a person doesn't make improvements in hygiene and access to clean water.

When trachoma has progressed to inward-turning of the lashes, surgery is necessary to correct the lid position.

If significant corneal scarring develops, corneal transplantation surgery is required to restore sight.

Various government agencies and international nongovernmental development organizations (INGDOs), such as the Carter Center Trachoma Control Program, work together to implement the SAFE strategy.

IMAGES

How long does trachoma last?

Some individuals who have trachoma infection of the eyes will have it only once and scarring will not necessarily occur. However, reinfections are common, and over many years, the untreated disease can progress through the five stages to blindness.

What is the prognosis for trachoma?

Community-based implementation of the SAFE strategy improved the prognosis for millions of at-risk individuals. If a doctor diagnoses trachoma and treats it early, before scarring of the eyelids and cornea, the prognosis for preservation of vision is excellent.

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The Differences Between Bacteria and Viruses

Although bacteria and viruses are both too small to be seen without a microscope, they're as different as giraffes and goldfish.

Bacteria are relatively complex, single-celled creatures, many with a rigid wall, and a thin, rubbery membrane surrounding the fluid inside the cell. They can reproduce on their own. Fossilized records show that bacteria have existed for about 3.5 billion years, and bacteria can survive in different environments, including extreme heat and cold, radioactive waste, and the human body.

Most bacteria are harmless, and some actually help by digesting food, destroying disease-causing microbes, fighting cancer cells, and providing essential nutrients. Fewer than 1% of bacteria cause diseases in people.

Viruses are tinier: the largest of them are smaller than the smallest bacteria. All they have is a protein coat and a core of genetic material, either RNA or DNA. Unlike bacteria, viruses can't survive without a host. They can only reproduce by attaching themselves to cells. In most cases, they reprogram the cells to make new viruses until the cells burst and die. In other cases, they turn normal cells into malignant or cancerous cells.

Also unlike bacteria, most viruses do cause disease, and they're quite specific about the cells they attack. For example, certain viruses attack cells in the liver, respiratory system, or blood. In some cases, viruses target bacteria.


Immunoregulatory role of 15-lipoxygenase in the pathogenesis of bacterial keratitis

Although autacoids primarily derived from the cyclooxygenase-2 and 5-lipoxygenase (LOX) pathways are essential mediators of inflammation, endogenous specialized proresolving mediators (SPMs) act as robust agonists of resolution. SPM biosynthesis is initiated by the conversion of arachidonic acid, eicosapentaenoic acid, and docosahexaenoic acid primarily via the 12/15-LOX pathway. Although 12/15-LOX activity is prominent in the cornea, the role of SPM pathway activation during infection remains largely unknown and is the focus of the current study. Pseudomonas keratitis was induced in resistant BALB/c and susceptible C57BL/6 (B6) mice. Biosynthetic pathways for proinflammatory autacoids and SPMs were assessed. Divergent lipid mediator profiles demonstrate the importance of 15-LOX pathways in the pathogenesis of ocular infectious disease. Results indicate that an imbalance of LOX enzymatic pathways contributes to susceptibility observed in B6 mice where deficient activation of SPM circuits, as indicated by reduced 15-hydroxy-eicosatetraenoic acid and 17-hydroxydocosahexaenoic acid levels, prevented transition toward resolution and led to chronic inflammation. In sharp contrast, BALB/c mice demonstrated a well-balanced axis of 5-LOX/12-LOX/15-LOX pathways, resulting in sufficient proresolving bioactive metabolite formation and immune homeostasis. Furthermore, a novel immunoregulatory role for 15-LOX was revealed in inflammatory cells (polymorphonuclear leukocytes and macrophages), which influenced phagocytic activity. These data provide evidence that SPM circuits are essential for host defense during bacterial keratitis.-Carion, T. W., Greenwood, M., Ebrahim, A. S., Jerome, A., Suvas, S., Gronert, K., Berger, E. A. Immunoregulatory role of 15-lipoxygenase in the pathogenesis of bacterial keratitis.

Keywords: inflammation lipid mediators ocular infection resolution.


Lemierre syndrome

Lemierre syndrome is a rare and potentially life-threatening complication of bacterial infections that usually affects previously-healthy adolescents and young adults. It most commonly develops in association with a bacterial throat infection, but it may develop in association with an infection involving the ears, salivary glands (parotitis), sinuses, or teeth or in association with an Epstein-Barr infection. [1] The bacteria typically responsible for infection in Lemierre syndrome is Fusobacterium necrophorum, although a variety of bacteria can be responsible. [1] [2] [3] In people with Lemierre syndrome, the initial infection spreads into tissues and deep spaces within the neck, leading to the formation of an infected blot clot (septic thrombophlebitis), sometimes made up of pus, in the internal jugular vein (the blood vessel that carries blood away from the brain, face, and neck). In addition to worsening symptoms of the initial infection, symptoms at this stage of the disease typically include persistent fever and chills (rigors), as well as pain, tenderness and swelling of the throat and neck. [1] [4] The infected clot then circulates in the blood (septicemia), resulting in the infection also spreading to the lungs (most commonly), skeletal system, and/or other parts of the body such as the spleen, liver, kidney, heart, or brain. [1] [2] [3] This can lead to life-threatening complications such as respiratory distress syndrome due to pulmonary emboli (blood clots in the lung), damage to other affected organs , and/or septic shock (in about 7% of cases). [1]

Lemierre syndrome may be diagnosed based on signs and symptoms, various blood tests, and imaging studies. Because most throat infections in young, healthy people do not cause severe health problems, diagnosis and treatment may be delayed. The main treatment involves intravenous antibiotic therapy over several weeks, but surgery may be necessary when there is abscess formation, respiratory distress, or severe clotting in the chest or brain. [1] [2] [3] The long-term outlook and chance of survival in people with Lemierre syndrome varies depending on how much the syndrome progresses, but even with appropriate treatment, it is fatal in some cases. [1]


Learn More Learn More

These resources provide more information about this condition or associated symptoms. The in-depth resources contain medical and scientific language that may be hard to understand. You may want to review these resources with a medical professional.

Where to Start

  • Genetics Home Reference (GHR) contains information on Spastic paraplegia 15. This website is maintained by the National Library of Medicine.

In-Depth Information

  • The Monarch Initiative brings together data about this condition from humans and other species to help physicians and biomedical researchers. Monarch’s tools are designed to make it easier to compare the signs and symptoms (phenotypes) of different diseases and discover common features. This initiative is a collaboration between several academic institutions across the world and is funded by the National Institutes of Health. Visit the website to explore the biology of this condition.
  • Online Mendelian Inheritance in Man (OMIM) is a catalog of human genes and genetic disorders. Each entry has a summary of related medical articles. It is meant for health care professionals and researchers. OMIM is maintained by Johns Hopkins University School of Medicine.
  • Orphanet is a European reference portal for information on rare diseases and orphan drugs. Access to this database is free of charge.
  • PubMed is a searchable database of medical literature and lists journal articles that discuss Spastic paraplegia 15. Click on the link to view a sample search on this topic.

Bacterial Wilt Disease of Potato Caused by Ralstonia Solanacearum | Plant Diseases

Potato (Solarium tuberosum L.) a poor man’s food, is an important solanaceous vegetable crop. Potato ranks fourth in production, after rice, wheat and maize and provides wholesome food. Potato is grown almost worldwide over 37 countries. Annually about 300 million tones of potatoes are produced and consumed by over one billion people world over.

Potato production has increased most rapidly in the far Eastern countries such as China, India and Indonesia. Potato is a native of Andes in South America. According to Scott (1976), the Inca Indians first cultivated potato in 200 B.C., which they called “papa”.

In 1537, Spanish conquistadors introduced potato in Spain, from where it spread into Italy and then into Central Europe, especially in Germany, Russia and Ireland.

Potato can contribute substantially towards both food and nutritional security in the years to come. It holds a great potential as food for the ever increasing world population per unit time and area as well as its versatility to adapt to a wide range of climate. Potato is a starch rich food (14-16%). which also contains protein (2.8%) and minerals (0.9%).

Potato constituted 18-20 per cent of the total production of the agricultural commodities for utilization as human and animal feed in addition to industrial use. The biological value of potato protein is very high and it contains sufficient quantity of vitamin C and considerable quantities of vitamins of B group.

Potato was introduced from Europe into India by British missionaries in late seventeenth century. The average potato yield in India in 2002-03 was 19.4 t/ha as compared to world average yield of 16.4 t/ha. The total area under potato in 2002- 03 was 1.4 million ha, which accounted for yield of 25.0 million tonnes.

India is the third largest potato producer in the world. According to the International Food Policy Research Institute (IFPRI) and International Potato Centre (CIP), India is likely to have the highest growth rates in production and productivity of potatoes during 1993-2020. India’s potato export has not been exploited to potential (<0.5 % of world export).

In spite of the suitable conditions for the cultivation, of potato, many factors are responsible for its low yield. Fungi, bacteria, viruses, phytoplasma, viroid and nematode are reported to attack and parasitize potato in field during transportation and storage. In India, important diseases of’, potato are reported to cause nearly 30- 40 per cent reduction in yield and this is about 6-10 million tonnes of potato every year.

In addition to foliage blight pathogens, bacteria are among the most potential pathogens, which have been found to cause six diseases in potato crop viz., bacterial wilt or brown rot (Ralstonia solanacearum), soft rot of stem or tubers (Erwinia carolovora, Bacillus sp., Pseudomonas sp.), ring rot (Corynebacierium sepedonicum), common scab (Streptomyces sp.), pink eye (Pseudomonas sp) and leaf spot (Xanthomonas vesicatoria). The ring rot and pink eye do not occur in India.

Bacterial wilt caused by Ralstonia solanacearum (Smith) Yabuuchi is one of the most important and destructive bacterial disease of plants, widely distributed in tropical, subtropical land and some warm temperate regions of the world. It is first bacterial disease recorded in India from Pune, Maharashtra and also first record of its occurrence on potato.

Now the disease has gradually become a problem of increasing importance and the damage caused by it in certain areas seems to be considerable. In India, losses caused by bacterial wilt vary from 20-100 per cent.

The disease may damage the crop due to premature wilting which results in causing yield losses and rotting of tubers both in field and stores. Several non-host crops and weeds can harbour the pathogen in their root systems. The pathogen could also survive in sheltered sites left over in the soil.

Since the pathogen is mainly transmitted through seed tubers, as latent infection in vascular tissues of progeny tubers. There is need to detect latent infection in tubers for disease free seed (tuber) production. Imrnunodiagnostid techniques have been standardized for proper detection of Ralstonia solanacearum in infected plants and soil.

Keeping in view the economic importance of potato crop, detection and diagnosis ofRalstonia solanacearum causing bacterial wilt pathogen by serodiagnosis is discussed here.

Geographical Distribution of Ralstonia Solanacearum:

Bacterial wilt of potato caused by Ralstonia (Pseudomonas) solanacearum (Smith) Yabuuchi is widely distributed in tropical, subtropical and some warm temperate regions of the world. Table 1 shows that Ralstonia solanacearum Race 3, Bio var II has a much greater distribution into both higher latitudes of the globe and greater altitudes in the tropics.

Bacterial wilt is the first bacterial disease recorded in India from Pune, Maharashtra by Cappel (1882) and the first record of occurrence on potato was made by Butler (1903).

Now the disease has gradually become a problem of increasing importance and the damage caused by it in certain areas seems to be considerable. In India, the disease is epidemic in West coast from Trivendrum in Kerala to Khera in Gujarat, in Central Karnataka, Western Maharashtra and Madhya Pradesh, in Eastern plains of Assam, Orrisa, Chhota Nagpur Plateau and Andaman Nicobar Islands (Table 26.2).

Economic Importance:

The major crops affected by Ralstonia solanacearum, belongs to solanaceous vegetables such as summer grown tomato, brinjal in the plains and tomato and potato in hills. Serious incidence of wilt on chillies has also been reported. In India losses caused by bacterial wilt vary from 20-100 per cent.

Verma and Shekhawat (1990) observed the endemic occurrence of bacterial wilt in Mukteswar region of Uttarakhand where potato seed production was taken. They reported that nearly 37 per cent potato produce was lost every year due to brown rot.

In potato, losses reported are upto 13.8- 55 per cent in Kumaon hills, 0.33-40.00 per cent in Maharashtra. 20-25 per cent at Hyderabad and over 75 per cent in some locations of Karnataka. According to Olonya (2002) the potato production and yield losses due to bacterial wilt as high as 100 per cent have been reported in parts of tropical Africa.

Ralstonia solanacearum has been associated with bacterial wilt of potato since it was reported in 1903. With the introduction of molecular technology the generic nominal of the wilt pathogen underwent rapid change from Pseudomonas to Burkhalderia to Ralstonia. Yabuuchi (1992) proposed new genus Burkholderia to accommodate RNA homology group II including Pseudomonas solanacearum with P. cepacia as type species.

Later work based on 16S rRNA genes and polyphasic taxonomy showed dichotomy in genus Burkhoderia and the new genus Ralstonia was proposed with R. picketti as type species.

Ralstonia solanacearum is a gram negative rod measuring approximately 0.5-0.7 x 1.5-2.5 pm. Virulent isolates are mainly non-flagellated, non-motile and are surrounded by extracellular slime. Avirulent isolates are devoid of any extracelluar slime, usually they bear 1-4 polar flagella and are highly motile. Polar fimbrae present with which twitching motility and spreading growth on solid media are associated.

Cells contain inclusion of poly-beta-hydroxybutyrate which are sudanophilic and retractile under phase microscope and commonly show bipolar staining. It is a chemo-organotroph with aerobic respiratory metabolism catalase and kovac’s oxidase positive optimum, temperature for growth varies from 27-37°C depending on the strain.

Diversity in Pathogen:

Intraspecific diversity in Ralstonia solanacearum was evident since early years of 20 th century. Smith (1914) described isolates from Sumatra affecting tobacco as Ralstonia solanacearum var. asiaticum on the basis of acidification of litmus milk containing cream. The strains of Ralstonia solanacearum differ in host range, geographical distribution, pathogenicity, epidemiological relationships, and physiological properties.

It is therefore important to have a classification of strains that is sufficient in information content of’ epidemiology and control of bacterial wilt. For almost the past three decades, a binary system has been in use reflecting two different approaches to differentiation, one placing emphasis on host affinity and establishment of races (Table 4).

The other making use of selected biochemical properties as the basis for separation into biovars.

Isolates collected from different areas of India belonged to Race-1 and 3 and biotype- II, III and IV. The Isolates from cool humid hilly areas belonged to race-3 and biotype- II. However, prevalence of Race-1 in Panchagani hills of Western Ghat, Palni-hills of Tamil Nadu, Kumaon hills of North India have been recorded.

A large number of Ralstonia solanacearum isolates from Indian plains and plateau belong to Race-1 and Biovar-III. Biovar-IV has been recorded only from two locations in Eastern plains, two locations in plateau and in mid-hills of Kumaon. Sunaina (1997) reported an odd type of strain oxidizing only maltose and mannitol from North- Eastern hills.

In contrast to normal white-coloured colonies, this strain produced cream- coloured fluidal colonies on tetrazolium chloride medium. It did not cause disease symptoms in aubergines, Datura streamonium or Capsicum annum but was slightly pathogenic on tomatoes and potatoes respectively, although it did not cause vascular discolouration.

Five potato isolates infecting potato cv. Kufri Jyoti and two isolates infecting tomato cv. Arka Sourabh and groundnut cv. TMV 2 we’re collected from different agro-climatic zones of Karnataka. All these isolates belonged to race-1 and biotype-III on the basis of pathogenicity to various solanaceous and non-solanaceous plants and utilization of carbohydrates.

Detection of Plant Diseases:

Diagnosis of plant diseases is an art as well as a science. The ability > f Ralstonia solanacearum to infect and colonize the potato plant as well as other crops and weed spp., without causing symptoms, has resulted in its widespread dispersal and subsequent establishment in different environments worldwide.

One of the main constraints to developing strategies to efficient management of bacterial wilt has been the lock of rapid and accurate methods to detect the pathogen in large numbers of plant, soil, and water samples on a routine basis.

The authors reviewed diagnostic methods for Ralstonia solanacearum in potatoes under few heads: Simple techniques including syptomatology, Indicator plants, ooze test, culture techniques, biochemical tests, serological techniques and methods involving detection of pathogen specific DNA.

The pathogen affects both above and underground parts of the crop. The first symptom in the potato plant is partial wilting of the upper leaves. These become pale green and even yellow. A slight yellowing may be observed on the lower leaves.

Plant affected by brown rot pathogen frequently show wilting of only one branch with a leaf wilt, and later a progressive wilting, stunting and death of the whole plant.

Smith (1997) reported that initially, leaves wilt during the day but recover during the night time. Leaves may develop a bronze cast and petioles may develop epinasty. In advanced stage, the lower stem will have a streaked brown appearance.

According to Hingorani (1956) the characteristic symptoms of the disease include wilting, stunting and yellowing of the foliage followed by collapse of the affected plants (Fig. 26.1).

Diseased plants show dark narrow stripes beneath the epidermis of the stem, which correspond to the affected vascular bundles. In cross section of a stem, these bundles show brown colouring and in advanced stage white ooze forms on the cut surface within a few minutes.

The infected plant roots at advanced stage turn dark and decay. Symptoms on tubers are very important and diagnostic for this disease. Infected tuber eyes show grayish brown discolouration at advanced stages.

Tubers from the diseased plants show a brown discolouration (ring) in vascular tissue (Fig. 26.2) and blacking of eye buds in a severely decayed potato. In Simla, Meghalaya and Darjeling hills, lenticel infection of potato tubers was also observed occasionally.

It has been reported that less virulent forms of some Indian isolates cause no wilting in potato plants but when inoculated to tomato plants produce swelling around inoculated site giving bottle-shaped appearance. Petioles of such plants become swollen and show epinasty and roots remain stunted. Sometimes cracks are noticed around inoculated portions. Some variants may also cause scorching/burning in the leaves.

The yellowing of lower leaves and stunting of plants are not observed in India. Although vascular browning has been reported to be a characteristic symptoms of the disease but strains of Ralstonia solanacearum that do not produce vascular browning in potato tubers have also been recorded in. Portugal, Kenya and Australia.

Since the use of the hypersensitive reaction (dark brown necrotic lesions) technique in tobacco leaves, there has been a number of attempts made to detect Ralstonia solanacearum.

Potato shoots cut from healthy tubers or surface-sterilized tomato seeds and tomato seedlings of susceptible cultivars also have been used as planting materials for indicator plants which showed symptoms within 4 weeks under controlled conditions when inoculated or planted in the soil sick with pathogen. Ravnika (1999) used tomato as well as brinjal as indicator plants.

Ooze test from wilt suspected stem/root or tuber in clear water from the vascular ring is a simple field test to confirm whether a diseased sample has bacterial wilt or not (Fig. 26.3). Shiny white exudates in the eyes of severely infected tubers can be observed with naked eye.

Cut surface of, infected tubers, when slightly pressed exudes milky white droplets from the vascular bundles. Latently infected tubers stored or grown in pots of sterilized soil above 25°C for 4-6 weeks can encourage bacterial wilt symptom development from infected tubers.

Culturing Technique:

Kelman (1954) developed a tetrazolium medium which allows to identify colonies of Ralstonia solanacearum among those of other bacteria by their typical fluidal, smooth, white appearance with red internal whirling patterns.

Several recipes for selective media have been developed that rely on the specific resistance of Ralstonia solanacearum to different antibiotics.

Biochemical Test:

Suslow 1982 suggested the gram reaction can be predicted by determining solubility of the bacterial ooze in 3 per cent aqueous KOH solution (KOH test) and a milky thread upon lifting the toothpick indicates the presence of the gram-negative pathogen.

Kovac (1956) determined oxidase test by smearing young bacterial culture on strip of filter paper soaked with 1% solution of tetramethyl-p-phenyldiamine resulting purple colour. This test can be performed directly on diseased tubers.

Shekhawat (2000) reported change of media colour containing urea to violet when incubated for an hour at 35-37°C with bacteria (Urease test).

Lelliot and Stead (1987) and Venkatesh (2000) observed fluorescent bright orange colour under fluorescent microscope when poly-3-hydrobutyrate (PHV) granules, an intracellular inclusions produced by Ralstonia solanacearum has been stained with 1% aqueous solution of Nile blue A.

Venkatesh (2000) observed pink discoloration at the vascular region in the potato slices having latent infection when dipped in 1 per cent tetrazolium chloride (TZC) solution (Fig. 26.4).

Cultural and Physiological Test:

He (1983) Schaad (2001) and Williamson (2002) observed the cultural and physiological test of Ralstonia solanacearum on different media and reported that bacteria was gram negative, oxidase and catalase positive, non-fluorescent on King’s B medium and produced cream coloured colonies on yeast dextrose calcium carbonate medium (YDC).

The correct diagnosis is a prerequisite of effective disease management. The more rapidly and accurately the causal organism is identified, the sooner proper control can be instituted.

Biochemical and physiological tests which are routinely used to identity plant pathogenic bacteria are not entirely satisfactory. Serological techniques now offer sensitive and easily used alternative methods for detecting Ralstonia solanacearum in plant samples (Fig. 26.5).

Perez (1962) developed antisera against polysaccharide-containing bacterial extracts were used successfully to identify P. solanacearum isolates but did not differentiate strains from different host. Morton (1966) prepared race specific antisera against Races 1, 2 and 3 of Ralstonia solanacearum and reported that Race 2 and 3 were more closely related.

Digat and Cambra (1976) described cell surface antigens in four categories: exopolysaccharide (EPS), cell wall structural (somatic) components (“O” antigens), extra cellular glycoprotein, and flagella components (“H” antigens). Glycoproteins tend to be strain specific whereas EPS and somatic antigens are common to all strains of Ralstonia solanacearum.

Chakrabarti (1993) standardized a protocol of alkaline phosphatase based DAS- ELISA to detect Ralstonia solanacearum either from infected stems or tubers using antiserum produced against formalin killed bacteria (Race 1).

Further, Chakrabarti (1995) produced antisera against formalinised whole cell, glycoprotein and lipopolysaccharide (LPS) fractions of the bacterium. In slide agglutination test, no race specificity was observed. The antiserum against whole cells proves effective for ELISA of low concentration of pathogen from infected plants.

Robinson (1993) developed strains specific monoclonal antibody against Ralstonia solanacearum to detect it and reported that the indirect ELISA system can detect as few as 10 4 cfu/ml in pure or mixed bacterial suspensions or plant extracts.

Elphinstone and Standford (1998) detected the latent infection of the potato tubers using all methods including culture on semi-selective medium, ELISA, indirect immunofluorescent-antibody staining (IFAS) of fixed cells, immunofluorescent colony staining (IFAS), detection of specific DNA sequences following amplification by the PCR and bioassay in tomato seedlings.

ELISA and PCR were improved by pre-enrichment of samples in semi-selective broth prior to testing.

Griep (1998) developed recombinant single chain antibodies (ScFvs) against the lipopolysaccharide of Ralstonia solanacearum (Biovar 2, Race 3) were successfully selected, by phage display from a large combinatorial antibody library.

The selected antibodies had improved characteristics when compared with the polyclonal antiserum that was used for diagnosis of brown rot of potato in the Netherlands. The isolates monoclonal ScFvs reacts in broth ELISA immunofluorescence cell staining with all Race 3 strains tested but with only some strains belonging to other races.

Several methods were compared for the detection of Ralstonia solanacearum in tubers, including indirect ELISA and sensitivity of each method was determined in artificially inoculated potato extracts. Reliability of ELISA PCR was improved by incubating samples in semi-selective broth prior to testing.

Priou (1999) developed post-enrichment NCM-ELISA (enzyme linked immunosorbent assay on nitrocellulose membrane using enriched sample) was as sensitive as the double-antibody sandwich (DAS-ELISA), but was much easier and quicker.

Wolf (1999) described a comparative test of an immunofluorescence cell-staining (IF) and ELISA methods based on both polyclonal and recombinant monoclonal antibodies for the detection of Ralstonia soanacearum in potato tuber extracts.

No differences in detection levels were found in sensitivity of the assays based on polyclonal or monoclonal antibodies nor between water and potato tubers extracts as diluents.

Kumar (2002) have evaluated the suitability of NCM-ELISA kit, developed at CIP, Lima, Peru, for detecting bacterial wilt pathogen in ginger. The result indicated that the antibodies were sensitive enough to detect Ralstonia solanacearum from ginger, chilli, chromolaena and tomato.

The sensitivity of the kit was determined to be 42 cell/ml of ginger extract. Caruso (2002) developed a sensitive and specific routine detection of Ralstonia solanacearum in symptomless potato tubers was achieved by efficient enrichment followed by a reliable DAS-Indirect ELISA based as the specific monoclonal antibody 8B- IVIA.

This monoclonal antibody reacted with 168 typical Ralstonia solanacearum strains and did not recognize 174 other pathogenic or unidentified bacteria isolated from potato. Analysis of 233 commercial potato lots by this method provided results that coincided with the results of conventional methods.

In India, losses caused by bacterial wilt vary from 20-100 per cent. Since pathogen is mainly transmitted through seed tubers, as latent infection in vascular tissues of progeny tubers which may be detrimental factor for epidemic occurrence of bacterial wilt in disease free regions.

There are several tests including biochemical and physiological tests routinely used to detect bacterial infection which are not entirely satisfactory. Therefore to produce disease free breeder/certified seed tubers, it urgently needed to detect latent infection in seed tubers using antibody for serodiagnosis.


Treatment Treatment

Stenotrophomonas maltophilia (S. maltophilia) bacteria are resistant to many antibiotics , so treatment options may be limited. As of 2018, treatment usually begins with trimethoprim-sulfamethoxazole (also called co-trimoxazole, or TMP-SMX), but this may vary due to the antibiotic resistance of the particular strain causing the infection and/or new antibiotics being developed. Potential alternatives for people unable to tolerate TMP-SMX include a class of antibiotics called fluoroquinolones, in particular, levofloxacin. Minocycline and tigecycline have also been shown to be effective in small retrospective studies. Combination therapy (using more than one antibiotic) may be necessary in life-threatening cases. However, data regarding the benefit of combination therapy are currently limited, so its role remains uncertain. [2] [3]

The duration of therapy often depends on the site of infection. [1] [2] A longer duration of therapy may be necessary for people with a weakened immune system . [2] Consultation with an infectious disease specialist is important to develop an individualized treatment plan. [1] [2]

More detailed information about medications used to treat S. maltophilia infection is available from Medscape Reference.


Dysentery

Bacillary dysentery is an intestinal inflammation caused by bacteria in the genus Shigella. Similar to cholera, it is spread by contaminated food and water. Dysentery is also spread by individuals who do not wash their hands after using the toilet. Dysentery symptoms can range from mild to severe. Severe symptoms include bloody diarrhea, high fever, and pain. Like cholera, dysentery is typically treated by hydration. It can also be treated with antibiotics based on severity. The best way to prevent the spread of Shigella is to wash and dry your hands properly before handling food and avoid drinking local water in areas where there may be a high risk of getting dysentery.


Find a Specialist Find a Specialist

If you need medical advice, you can look for doctors or other healthcare professionals who have experience with this disease. You may find these specialists through advocacy organizations, clinical trials, or articles published in medical journals. You may also want to contact a university or tertiary medical center in your area, because these centers tend to see more complex cases and have the latest technology and treatments.

If you can’t find a specialist in your local area, try contacting national or international specialists. They may be able to refer you to someone they know through conferences or research efforts. Some specialists may be willing to consult with you or your local doctors over the phone or by email if you can't travel to them for care.

You can find more tips in our guide, How to Find a Disease Specialist. We also encourage you to explore the rest of this page to find resources that can help you find specialists.