Salmonellosis, Shigellosis and Escherichia Coli |Pathogens

The below mentioned article provides a study-note on the Salmonellosis, Shigellosis and Escherichia Coli.

Family Enterobacteriacae include many inter­related bacteria; few are saprophytic and found in soil and water; some of which are common inhabit­ants of intestine of men and animals, while others are the causative agents of salmonellosis (typhoid and paratyphoid enteric fever); shigellosis (bacillary dysentery); gastroenteritis in children or infantile diarrhoea and urinary tract infection (Escherichia coli and Proteus).

All of which are Gram-negative rods, either motile with peritrichous flagella or non-motile. They are non-sporing and grow on ordinary me­dia; all ferment glucose rapidly with or without gas production and reduce nitrates to nitrites.

The family can be divided into the following genera:

Salmonella:

It is now well established that the genus Salmo­nella comprises more than 1,000 serotypes which are mainly parasites of animals (S. typhi and its cousin, the three paratyphoid bacilli are essentially parasites of man). Bacterial food poisoning is more commonly caused by ingestion of foods contaminated with any of the numerous serotypes of the genus Salmonella: S. typhimurium, S. Dublin, S. Heidelberg, S. Enteritidis, S. Newport, S. Infantis, S. Thompson. These serotypes cause primarily septicaemic disease in animals (natu­ral host), but they cause food poisoning in man (un­natural host).

Symptoms are vomiting, abdominal pain and diarrhea. The severity of diarrhoea varies from the very slight, i.e., passage of one or two loose stools which may be disregarded by the patient, to a violent diarrhoea. The carcass or animal products, e.g., cooked meat, eggs or milk of naturally infected domestic animals are the commonest sources of food poison­ing infection. Flesh may be infected when an ill, sep­ticaemic animal is slaughtered. More commonly uninfected meat or carcass may be infected in the abattoir by a human case or carrier.

Control measures. In an endeavour to reduce the incidence of food poisoning, two basic principles must be followed:

1. Raw food stuffs which are partially contami­nated must never have contact, either di­rect or indirect, with cooked meat;

2. If a foodstuff is contaminated with salmonellae, it should be treated or held under temperature conditions which pre­vent the organisms growing, i.e., either under refrigeration or at sufficiently high, temperature and then consumed imme­diately.

Enteric Fever:

Enteric fever includes both Typhoid and Paraty­phoid which are clinically similar. The word “Typhoid” is derived from “Typhoid Mary”— a cook in a restau­rant in England was a carrier of S. typhi and transmit­ted to the community. Typhoid is caused by S. typhi and paratyphoid by S. paratyphi.

A significant endemic level of infection with S. typhi persists in the warm climate. S. paratyphi A is frequently endemic in Eastern Europe, America and India; S. paratyphi C as a cause of paratyphoid fever in Eastern Europe and Asia.

Morphologically, members of the genus Salmo­nella cannot be distinguished from each other and from other members of the family. Enter obacteriacae. They are motile, non-capsulated. On differential or selective media, MacConkey, Desoxycholate citrate agar (DCA) media, the colo­nies are pale coloured, i.e., they are non-lactose fermenters, similar to Shigella.

Pathogenesis and Disease in Man:

Natural in­fection in the enteric fever is mostly by ingestion of contaminated water or foods. S. typhi penetrates the mucous membrane of the small intestine and sub-mucosa where they are phagocytosed by polymorphs and multiply in them, kill and escape.

The organisms pass via the lymphatic’s to the mesenteric lymph nodes. After a period of multiplication, they invade the blood stream via the thoracic duct; the blood cul­ture is positive; Staphylococcal slide conglutination test appears to be rapid and simple to diagnose Ty­phoid fever in the first week when culture facilities are lacking.

Latex agglutination test for rapid diagnosis of Typhoid fever is more useful and sensitive to patients with prior history of antibiotic therapy; the liver, gall bladder, spleen, kidney and bone marrow become infected during the primary bacteriaemic phase in the first 7-10 days of incubation period.

After multi­plication in these organs, bacilli pass into the blood causing secondary bacteriaemia. During this second­ary phase, pyrexia and other clinical signs develop – Widal test (serological test) or slide Salmonella ag­glutination test is positive in the second week of the infection.

In second and fourth week, S. typhi may appear in the urine (bacteriuria) and stools; some­times it may be present in the stool from first to fourth week; from the gall bladder, a further invasion of the intestine takes place as a result Peyer’s patches and lymphoid follicles are involved.

They become inflammed and infiltration with mononuclear cells fol­lowed by necrosis, sloughing and formation of typical “typhoid ulcer” with hemorrhage. In severe complicated cases, there is perforation through a necrotic Peyer’s patch leading to peritonitis.

Fever and illness continue for 3-4 weeks. Temperature shows a step ladder rise over the first week of the illness, remains at 39.5 to 40°C for 7-10 days and then falls by lysis during the third and fourth week. The symptoms are headache, body pain, loss of appetite.

The bowels may be constipated or loose, abdomi­nal bloating and discomfort may occur. Dry cough and nose bleeding are occasional features. It is im­portant to exclude malaria, tuberculosis and other generalized illness which mimic typhoid. If untreated, the fever rises unabated, and the patient becomes dehydrated. Either delirium or stupor may supervene and the patient may go into coma.

In very few cases, bleeding into the gut or perforation of the gut may occur, giving rise to pain, a fall in blood pressure and shock. Otherwise, slowly abate and the fever comes down in a month. Severe weakness during the pe­riod of convalesce and temporary loss of hair are feared sequelae. A pregnant woman affected by ty­phoid may abort in third and fourth month.

Epidemiology:

Typhoid remains a disease that is several hundred times more common in India; than in the developed world. It is not notifiable disease in India. It is estimated that during the rainy season, ty­phoid outbreaks are common.

The reasons for its wide prevalence in India are lack of proper sanitation and effective sewage dis­posal, faecal pollution of soil and drinking water and improper personal hygiene as well as food and kitchen hygiene. Typhoid can be contracted from two types of persons — a patient suffering from the disease and from a carrier who is healthy but harbours the bacte­ria in his body.

S. typhi is usually excreted in the faeces. Faecal contamination of food, milk, drinking water or our own hands help the bacteria to enter the intestine and spread into the body. Flies too are potent disease spreading agents as the bacteria survive in them throughout their life time of 20 days.

In water, S. typhi can live for more than couple of days, whilst in moist soil it can live up to 2 months. Thus vegetables grown in such soil, if improperly cooked and eaten, can lead to typhoid. Milk is another medium in which the bac­teria can multiply without altering its taste and appearance. Typhoid bacilli are easily killed by heat, dry­ing, boiling, chlorination and other disinfectants; it however resists the freezing, so ice-cream is a dan­gerous source of the spread of typhoid.

Treatment:

Antibiotics are the corner-stone of typhoid treatment. Chloramphenicol introduced four decades ago still remains the drug of choice though bacterial resistance to it is being reported to now-a- days. The fever takes two to four days to come down, but the drug should be taken for at least two weeks.

Because of a rare risk of suppression of blood forma­tion associated with the use of chloramphenicol, some physician prefers ampicillin, amoxycillin or cotrimoxazole (Septran or Bactrim); these drugs how­ever take a longer time to bring down the fever.

S. typhi resistant to these drugs are sensitive to latest newer antibiotics (floxacin, norfloxacin or ciprofloxacin). Corticosteroids are not advisable ex­cept in severe illness with high fever and altered con­sciousness. Furazolidine is also effective against chlo­ramphenicol resistant S. typhi.

A few patients have a relapse of typhoid espe­cially if they use the drug irregularly. Treatment of a relapse is as for the first attack. On the other hand, a few persons, who have recovered from the illness, continue to excrete the bacteria. Such carriers must be detected. Some carriers need removal of the gall bladder which may be harbouring S. typhi. Carriers (as cooks, waiters etc.) must not be allowed to come into contact with food and observe routine measures of hygiene and sanitation.

Prophylaxis:

1. Personal hygiene;

2. Proper cooking methods;

3. Disinfection or boiling of drinking water;

4. Avoiding eating out during the rainy sea­son and at the time of epidemics.

Immunity:

One attack of typhoid gives fairly last­ing immunity. Heat killed TAB (S.typhi, S.paratyphi A and S. Paratyphi B) Vaccine given in two doses, gives a seventy five per cent protection against typhoid for three years, after which a booster dose may be given. Another live vaccine which claims 100 per cent pro­tection is under trial.

“Porin” isolated from the outer membrane of S.typhi at Madurai Kamaraj University, Immunology department, India (Chennai) is a protein with immense potential in the prevention and diagnosis of typhoid, which is under experimentation. The oral live attenuated typhoid vaccine S. typhi Ty21a provides a relatively effective, safe and more expeditions alternative to the traditional parenterally administrated killed S. typhi ‘vaccine.

Shigellosis:

Bacillary dysentery. Dysentery or bloody flux, known clinically since biblical time, is characterised by the frequent passage of stools mixed with blood and mucus, pus and caused by the genus shigella. It is also prevalent in many countries with temperate cli­mate.

The genus Shigella (Dysentery bacilli) is one of the several genera in the large family enterobacteriacae. The shigellae are Gram-negative bacilli very similar to other enterobacteria; but they are non-motile and non-capsulate. On Mac Conkey or Desoxychocolate citrate agar (DCA), they are lac­tose non-fermenters; hence they form “Pale” colo­nies similar to the genus Salmonella.

They can be dif­ferentiated from Salmonella, since Salmonella are motile, produce gas and acid in sugar solution,Triple Sugar Iron (TSI) agar. There are four species of Shig­ella: Sh. dysenteriae, Sh. flexneri, Sh. boydii, Sh. sonnei.

The first species, Sh. dysenteriae, was discov­ered and described by a Japanese physician, Shiga; similar type, later discovered in Europe, was called as Sh. ambiguae or Schmitz bacillus. Another type was discovered by American physician, Flexner, in 1906 and named as Flexner dysentery bacillus or Sh. flexneri. Still another type common in United States first discovered by Duval and described by Sonne is now called as Sonne dysentery bacillus (Sh. sonnei). Later on British worker, Boyd, first discovered Sh. sonnei.

Resistance:

Dysentery bacilli live in the exter­nal environment for a period of 5-10 days (in soil, food stuffs, water, on objects, plates and dishes). Di­rect sunlight and a 1 percent phenol solution destroy the organisms in 10 minutes. The bacilli are easily killed by treatment with chloramine and calcium chlo­ride solutions. Sh. dysenteriae are most sensitive to physical and chemical factors to which Sh. sonnei are relatively resistant. Dysentery bacilli may acquire resistance to drugs (sulphonamides, antibiotics) and to ionising radiations. Dependal, Amicline plus are drugs of choice for treatment.

Transmission:

Dysentery bacilli are transmitted by the faecal-oral route as typhoid, that is by faeces, fingers, flies, milk, foods by other objects contami­nated with the faeces of a patient or carrier. Water-borne epidemics of bacillary dysentery are less com­mon than those of typhoid. Shigella species are not commonly found in animals.

Pathogenesis and disease in man. People suf­fering from acute and chronic dysentery as well as carriers are source of infection. Infection takes place through the mouth by ingestion of contaminated food stuffs and water, by contaminated hands, house flies and other objects.

Dysentery bacilli are confined to the intestinal mucosa and sub-mucosal layer where they multiply and do not invade the blood. The in­fected epithelial cells are killed and lamina propria and sub-mucosa develop an inflammatory reaction with capillary thrombosis. Patches of necrotic epithe­lium are sloughed and ulcers form. There is polymor­phonuclear cell infiltration.

Sh. dysenteriae is usually associated with a se­vere abdominal pain, tenesmus, pyrexia, prostration and, sometimes, convulsions, the stools loose their usual faecal character, are small and frequent and are composed mainly of fresh stool, pus and mucus. The illness associated with Sh. sonnei is mild and con­fined to the passage of few loose stools with abdomi­nal discomfort. The illness due to Sh. Flexneri and Sh. Boydii is more severe than the Sonne dysentery. Death due to bacillary dysentery is uncommon.

Laboratory Diagnosis:

Diagnosis of bacillary dys­entery in the laboratory is similar to that of typhoid, except the blood culture, since dysentery bacilli do not invade the blood stream. Repeated stool exami­nation is necessary. Since Shigella are fragile, the re­sponsible nurse should have knowledge that stool specimens should be transported in glycerosaline transport medium.

Control of the disease is ensured by a complex of general and specific measures:

1. Hospitalization of patients or their isola­tion at home with observance of the re­quired regimes.

2. Thorough disinfection of sources of dis­ease.

3. Adequate treatment of patients with highly effective antibiotics and use of chemotherapy.

4. Babies should be kept away from the pa­tient of bacillary dysentery.

5. A person caring for a child with summer diarrhea should not cook the food for other children or adults.

6. The diapers of infants suffering from diar­rhoea should be disinfected at once by placing in a bucket of full of 2 per cent saponated cresol or other good disinfect­ant.

7. Old linen should be burnt. The public health nurses connected with baby wel­fare clinics visit the homes and teach the mothers correct methods of preparing the baby’s food and the general care of the child.

Escherichia:

Escherichia coli:

Gastroenteritis; urinary tract in­fection.

E. colias a pathogen is associated with two main clinical syndromes:

(1) Acute gastroenteritis in in­fants under two years of age and rarely in adults with lowered resistance;

(2) Infection of urinary tract, par­ticularly in married women but also in girls and in elderly man with prostate enlargement. E. coli may be the causal organism of appendicular abscess, peri­tonitis, cholecystitis, wound infection etc.

Description:

E. coli is Gram-negative, motile, non-sporing bacillus, morphologically identical to sal­monella and on ordinary media their colonies are very similar. On MacConkey medium, E. coli yields rose pink colonies since they ferment lactose in the me­dium. But they grow poorly on DCA or Salmonella Shigella (SS) medium.They can be differentiated from other enterobacteriacae by biochemical test, IMV_(i)C – Indole and MR are positive and VP and citrate are negative.

Resistance:

E. coli survives in the external envi­ronment for months. It is more resistant to physical and chemical factors of the external environment than typhoid and dysentery bacilli. It is killed com­paratively rapidly by all methods and preparations used for disinfection. At 55°C the organism perishes in one hour and at 60°C in 15 minutes.

E. coli is sensitive to brilliant green. Gastroenteritis is caused by E.coli. The enteropathogenic strains of E. coli seem to belong to a limited number of Oserotypes. The most common and widely distributed serotypes are 0 26; 0 55; 0 111; 0 127; 128. Outbreaks of acute gastroenteritis occur in infants, nurseries, and pediatric units under 18 years of age. More widespread outbreaks may occur in the general community.

The pathophysiology of infantile gastroenteritis associated with enteropathogenic E. coli is character­ised by massive fluid loss from the gut, causing acute dehydration, acidosis and hypovolaemic shock. The pathogenesis of infantile gastroenteritis seems to be related to the production of an enterotoxin similar in action to the cholera enterotoxin.

Four groups of E. coli responsible for diarrhoea in infants, children and adults are: Enteropathogenic E. coli (EPEC); Enterotoxigenic E. coli (ETEC); Enteroinvasive E. coli (EIEC); Enterohaemorrhagic E. coli (EHEC).

EPEC is responsible for infantile diarrhoea. The pathogenic mechanism of EPEC has only recently been developed. They adhere to the intestinal mu­cosa, cause the loss of microvilli and prevent entry of bacteria into the mucosa. It also produces a shigella- like toxin.

ETEC:

Its enterotoxin is now known to produce diarrhoea in children, traveller’s diarrhoea in adults and sometimes cholera infantum similar to cholera. ETEC also possesses colonisation factors (pili, K anti­gen) to enhance its virulence.

EIEC does not produce enterotoxin, but invades the intestinal mucosa like dysentery bacilli. It causes kerato conjunctivitis on instillation in to the eyes of guinea pig (Sereney test) which is a diagnostic method for EIEC. Another diagnostic method is its invasion of HeLa cells in tissue culture. It has an antigenic relationship with shigella. EHEC has been very recently identified and is found to cause colitis with marked haemorrhage and absence of fever, produces verotoxin (cytotoxin) which affects the vero cells in tissue culture.

Urinary tract infection:

Predisposing factors of urinary tract infection are the urinary retention and stasis in pregnancy and in elderly males. E. coli is the most common coliform species present in the urine of pregnant woman with signifi­cant bacteriuria. Serotypes 01,02,04,06 and 075 are most commonly involved in urinary tract infection.

Transmission:

Outbreaks of gastroenteritis oc­cur most commonly in institutions and affect either new born babies in a maternity nursery or infants up to 18 months of age in pediatric wards or other insti­tutions. The infection occurs much more frequently in artificially fed babies than in wholly breastfed babies. This may be due to the milk feed; and feeding bottles are the most likely vehicles of infection from a case or carrier. Infantile enteritis may occur during or shortly after weaning.

Control measure:

Since outbreaks of gastroen­teritis may result in high fatality rate in maternity nurs­eries and institutions caring for young children, every precaution should be taken to prevent the introduc­tion of infection, particularly by infants coming from other institutions. This may require some system of preliminary quarantine and bacteriological screening of new admission. If the infection becomes estab­lished, drastic measures should be taken for its con­trol, including closure of a ward, nursery or institu­tion.

Generally, the prevention of infantile gastroen­teritis demands that bottle milk feeds served to in­fants must be sterilised in hospital that is best ef­fected by terminal heat sterilisation or the fully pre­pared, sterilised feed in the feeding bottle. In the house, the mother should be encouraged to use do­mestic pressure cookers for the same purpose.

The most effective preventive measure is breast feeding. Nurse should make every effort to encourage moth­ers to appreciate that breast feeding is best for the babies. In case of acute infantile diarrhoea, mothers should follow Oral Rehydration Therapy (ORT) rec­ommended by World Health Organisation (WHO).

Klebsiellan:

It is widely distributed in nature occurring both as commensals in intestine and saprophyte in soil and water. It is non-motile, capsulated rod, grows on ordinary media. In MacConkey’s agar medium, its colo­nies are large, dome-shaped, mucoid and pink. It is indole and methyl red negative and Voges Proskarer and citrate positive. It causes urinary, pyogenic infections (abscess, meningitis), diarrhoea, pneumonia characterised by massive mucoid inflammatory exudate, and nosoco­mial infection.