Bacillary Dysentery

Definition

Bacillary dysentery is an acute invasive enteric infection caused by bacteria belonging to the genus Shigella. It is clinically manifested by diarrhea that is frequently bloody. In addition, it is an infection disease that causes intestinal inflammation that leads to the formation of micro-ulcers and inflammatory exudates, and causes inflammatory cells (polymorphonuclear leukocytes, PMNs) and blood to appear in the stool which can range from minor to severe and can be life-threatening to the patient

The infection is also called shigellosis, bloody flux and Marlow Syndrome.

Morphological Description

The causative agent, Shigella, is a small, gram-negative, straight rod, non-motile, non-lactose fermenting, facultative and anaerobic and coliform bacillus. Moreover, it possesses a capsule non-spore forming rod-shaped bacterium closely related to Eschericia coli and Salmonella. In addition, the rod-shaped bacterium contains K antigen and O antigen wherein the K antigen is not useful in serologic typing, but can interfere with O antigen determination. In addition, it belongs to the family Enterobacteriacae. There are for Shigella species, all of which causes bacillary dysentery: Shigella dysenteriae, Shigella flexneri, Shigella boydii and Shigella sonnei (also known as Groups A, B, C, D respectively)

Mode of Transmission

The bacterium is spread by direct contact with an infected person. Transmission by fecal-oral route occurs via fecally contaminated water and hand-to-hand contact.

Signs and Symptoms

Bacillary dysentery signs and symptoms include diarrhea with or without the release of blood, tenesmus, and mild to very high fever, rectal pain, abdominal cramps and nausea and vomiting. These acute bacillary symptoms may last for a week or even for months. However, chronic bacillary dysentery may even cause some severe and fatal diseases such as hemolytic uremic syndrome. Chronic bacillary dysentery in children especially in malnourished children may unfortunately lead to the influx of bacteria into the bloodstream. Other symptoms may be intermittent and may include recurring low fevers, abdominal cramps, increased gas, and milder and firmer diarrhea. One may feel weak and anemic, or lose weight over a prolonged period (emaciation).

Diagnostics and Laboratory Tests

The different diagnostic and laboratory tests in determination of the infection are the following:

1.       Examination of the stool sample.

2.       Confirmatory tests

3.       Serological identification for the presence of Shigella.

4.       Sensitivity tests

Furthermore, there are series of specific tests to determine the presence of the bacterium.

1.       Specimens from fresh stool, mucus flecks and rectal swab for culture

2.       Culture.

Serotype	Mannitol	Lactose	Glucose	ONPG	Tartrate Utilization
A	-	-	+	V	+
B	+	-	+	-	-
C	+	-	+	V	-
D	+	-/+	+	+	+

*v – variable 10-89%  of strains are positive

·         EMB/ MacConkey – positive visible result of colorless colonies

·         SSA – colorless colonies without black center

·         HEA – green colonies without black center

·         TSI – acid butt, alkaline slant, no gas and H₂S

·         MR – positive result

·         Citrate test, ODC test, ADH test, Deaminase and Urease test – negative result

·         Sucrose, salicin and adonitol and dulcitol – negative result

·         D-mannose – positive visible result in CHO fermentation

Period of Communicability

The infection is communicable for 1-7 days with an average of 4 days as long as the infected person excretes Shigella in stool.

Incubation Period

            1-4 days but may be as long as 8 days.

Prognosis

The disease is self-limiting, has mild infections usually subside within 10 days. Severe infections, however, may persist for 2-6 weeks. Most cases of the infection subside within 10 days with correct treatment. Most individuals will achieve a full recovery within 2-4 weeks after beginning proper treatment. If the disease is left untreated, the prognosis varies with the immune status of the individual and the severity of the disease. The person can be a carrier of the infection for up to four weeks but usually less.

Prevention and Treatment

Antibiotics usually used in treating Shigellosis are the following:

1.                   Fluoroquinones (DOC)

2.                   TMP – SMX (trimethorpin-sulfamethoxazole)

3.                   Azithromycin

Some supportive measures can prevent the disease, such as proper hand-washing, drinking safe water, breastfeeding infants and safe handling and processing of food.

Cholera El Tor

I.      Definition

An acute bacterial enteric disease of the GIT characterized by profuse diarrhea, vomiting, massive loss of fluid and electrolyte and could result to hypovolemic shock, acidosis and death. The intestinal infection is caused by the bacterium Vibrio cholera serogroups 01 and 0139 in the family Vibrionaceae. Serogroup 01 V. cholerae is subdivided into three serotypes based on specific antigens in the O antigen: Ogawa, Inaba and Hikojima.

Cholera has been a devastating disease for centuries. It is estimated to have 3-5million cholera cases and 100,000-120,000 death caused by cholera in the world annually. Cases mostly occur in Asia and Africa where it has been endemic. The infection is also called as Asiatic Cholera and Epidemic Cholera.

II.     Morphological Description

     Vibrio cholerae/ Vibrio coma – “comma” shaped gram-negative bacteria with a single, polar flagellum. Vibrios are facultative anaerobes that ferment and grow on ordinary or selective media containing bile at 37˚C (22-40˚C). They possess unique O and H antigens and membrane receptor antigens that provide some basis for classifying members of the family. There are two major biotypes, called classic and El tor.

III.   Pathogenesis

  

1.Fluid loss is attributed to the enterotoxin elaborated by the organism as they lie within the lining of the cells of the intestines

2.The toxin stimulates adenylate cyclase, which results in the conversion of ATP to cAMP

3.The mucosal cell is stimulated to increase secretion of chloride, with water and HCO₃ loss.

4.The toxin acts upon the intact epithelium on the vasculator of the bowel, thus, resulting in outpouring of intestinal fluids.

5.Fluid loss of 5-10% of the body wt. resulting in dehydration and metabolic acidosis.

6.If the treatment is delayed, acute renal failure and hypokalemia become secondary problems.

7.Death can occur from hypovolemic shock, metabolic acidosis, and uremia resulting from acute tubular necrosis.

IV.     Mode of Transmission

·         Ingestion of contaminated food, milk or water

·         Vibrio associated with certain plankton, chitinous shelled animals and vegetation is also crucial for its long term survival

·         Raw fish

·         Flies, soiled hands and utensils also serve to transmit infection

·         Contaminated food at room temperature supports the growth of the bacterium

V.      Signs and Symptoms

     After an incubation period of a few hours-days, symptoms begin abruptly with nausea vomiting, followed by a profuse painless diarrhea that is described as “rice-water” stool in nature called secretory diarrhea or rice-watery diarrhea. The intestinal contents are lost very quickly, leaving only secreted fluids. Fluid losses or nearly 1 liter per hour have been reported in severe cases. The diarrhea causes loss of blood volume, acidosis from HCO₃ loss, and potassium depletion, which manifest in muscle cramps, severe thirst, flaccid skin, sunken eyes and in young children, coma and convulsions. In case of cholera gravis, there is a rapid loss of body fluids of 6 liters per hour containing 10⁷ vibrios/mL and has sunken eyes. Secondary circulatory consequences can include hypotension, tachycardia, cyanosis, and collapse from shock within 18-24 hrs. If cholera is left untreated, death can occur in less than 48 hrs, and the mortality rate approaches 55%.

VI.     Diagnosis

      V. cholerae can be readily isolated and identified in the laboratory from stool samples. Direct dark-field microscopic observation reveals the bacterium in groups of similar to “schools of fish” and its serotype is determined by immobilization with Inaba or Ogawa specific anti-serum. Best selective medium is TCBS(Thiosulfate-citrate-bile salts-sucrose agar) on which the organisms grow as a typical opaque yellow colonies.

"schools of fish"

VII.   Period of Communicability

    

      People are infectious during the stool positive stage for a few days after recovery. By the end of the first week, 70% of patients are non-infectious. While at the end of third week, 98% are non-infectious. Carrier state may persist for months and chronic biliary infection with intermittent shedding of organisms may last for years.

VIII. Incubation Period

      Two hours to five days after the ingestion of the bacteria with an average of 2-3 days.

IX.     Prognosis

      The infection manifests a 50-60% mortality rate for untreated cholera. While if properly treated, no patient should die of cholera, but if treatment is delayed or is given too slowly, case fatality rates exceed at 5%

X.      Prevention and Treatment

     Effective prevention is contingent upon proper sewage treatment and water purification. Detecting and treating carriers with mild or asymptomatic cholera are serious goals, but they are difficult to accomplish because of inadequate medical provisions in those countries where cholera is endemic. Control measures include sterilization of water and pasteurization of milk. Seafoods must be thoroughly cooked and vegetables and fruits should be washed before consumption. Washing of hands is the fundamental way of preventing the infection.

     Vaccines are available which contains a sterile suspension of killed Vibrio cholerae of the Inaba and Ogawa strains in NSS or suitable diluents. It contains 8 billion v. cholera per mL and preserved by addition of 0.5% phenol. But it only protects for only 6 months or less. E For infants, passive immunity is feasible through ingestion of breast milk. ORS solution should be considered as the first treatment if the patient is vomiting for rapid replacement of fluids to correct dehydration. Drug of choice is doxycycline for sensitive strains. Other clinically effective antibiotics include tetracycline, cotrimoxazole, chloramphenicol, flurazolidone, erythromycin, azithromycin and ciprofloxacin.

Typhoid Fever

I.      Definition

Typhoid fever is so named because it bears a superficial resemblance to typhus, a rickettsial disease. It is an acute illness caused by the typhi variant of Salmonella enteric that may lead to septicemia by its invasiveness. It is transmitted through the ingestion of food and drink contaminated by the feces or urine of infected people. It may also be transmitted directly by handling patients, using a contaminated toilet and neglecting hygiene. The infection is also known as “Enteric Fever”

II.    Morphologic Description

Salmonella are motile; they ferment glucose, but never lactose or sucrose, with acid and sometimes gas; and most of them produce hydrogen sulfide but not urease. Here are some of its characteristics:

·         Gram-negative

·         Non-spore forming

·         Facultative

·         Rod-shaped

·         Peritrichous flagella

·         Capsulated

·         Anaerobic

These gram-negative enteric bacteria are named and designated according to the following antigens:

·         H (flagellar) antigen – a protein that helps the organism to evade the immune system. It is used to agglutinate the organism

·         O (somatic, cell wall) antigen – a lipopolysaccaride that elicits inflammatory responses. It is also used to agglutinate the organism

III.  Pathogenesis

1. When ingested, the salmonella transverses the acid barrier of the stomach that may cause the decrease of stomach acidity or intestinal integrity which increases the susceptibility of the infection.

2. The bacteria then penetrates the mucous layer of the gut and transverse the intestinal layer through phagocytic microfold (M) cells that reside within the Peyer’s patches (ulcers). Here, it will form ruffles in normally nonphagocytic epithelial cells. These ruffles reach out and enclose adherent bacteria within large vesicles by a process reffered as BME (bacterial-mediated endocytosis). The salmonella will encode a type III secretion system that inject virulence proteins in the epithelial cells. These proteins disrupt the normal brush border and force the cell membrane ruffles, which engulf the bacilli and create vesicles. These vesicles carry the bacteria across the cytoplasm and are presented to macrophages.

3. The bacterium infiltrates the mesenteric lymph nodes and the phagocytes of the liver and spleen.

4. When the bacteria are shed into the bloodstream, fever and symptomatic stage is manifested.

5. If left untreated, serious medical complications may develop. The bacteria may infect the organs of the reticuloendothelial system, thoracic duct where macrophages are killed.

6. Reinfection of the small intestine may occur due to the flow of the bile.

IV.    Signs and Symptoms

First week	Second week	Third week
Fever (39.4-40˚C)	Continuing high fever	Delirious
Headache	Diarrhea (pea-soup stool) or severe constipation	Motionless and exhausted (typhoid state)
Weakness & Fatigue	Weight loss	Life-threatening complication may develop
Abdominal pain	Rose spots (2-4mm)	Leucopenia & anemia
Diarrhea	Extremely distended abdomen
Rash

In some people, the small intestine develops areas of ulceration that are vulnerable to hemorrhage, perforation, and peritonitis. Its presence in the circulatory system may lead to nodules or abscesses in the liver or urinary tract. Here are some complications that may develop by this infection if left untreated:

·         Intestinal perforation – most fatal complication; common during 3^rd week

·         Intestinal hemorrhage – indicated by rare abdominal pain, rise in pulse rate, sudden fall in temperature, sweating and hypotenstion

·         Encephalopathy – agitation to delirium and coma; may cause liver failure

V.      Diagnosis

The typhoid fever requires the isolation of S. typhi or S. paratyphi in a blood, stool and bone marrow samples. Positive results for the microorganism are tabulated below:

Culture Media	Positive Result
HEA (Hektoen Enteric Aagar)	Blue green w/ black center
SS (Salmonella Shigella Agar)	Colorless w/ a black center
MacConkey Agar	Yellow to colorless
EMB	Colorless

For typhoid bacilli in the bile duct or gall bladder, best specimen for the patient is bone marrow culture.

VI.    Period of Communicability

Infected persons are communicable as long as organisms are excreted in the feces or urine, typically beginning during the first week after onset and continuing through convalescence and for a variable period.

VII.  Incubation Period

Ø  Usual range: 8-14 days

Ø  Parathyroid fever: 1-10 days

Ø  Convalescent carrier: 6 months

Ø  Persistent carrier: positive stool culture for a year

Ø  Chronic carrier: positive stool culture for a year

VIII.     Prognosis

The prognosis depends on several factors:

Ø  The dose and the virulence of the salmonella

Ø  The general resistance and health of the population involved

Ø  The time and stage of the disease at which treatment is started

Ø  The effectiveness of treatment

Typhoid fever mortality rates vary between 10% and 32%. Relapses involving acute illness occur in 5-20% of the illness’ cases. Some 1-5% of patients carrying the disease apparently become chronic carriers. And complications occur in 10-15% of patients, particularly those who have been ill for more than two weeks.

IX.    Prevention and Treatment

   Prevention is based on ensuring access to safe water and by promoting safe food handling practices. Health education is paramount to raise public awareness and induce behavior change particularly in hygiene. 

   Specific treatment for the infection includes chloramphenicol, ampicillin or trimethoprim w/ sulfamethoxazole, an alternative for chloramphenicol. While for non-specific treatment, acetaminophen or paracetamol and hydrotherapeutic measures will be prescribed for febrile patients. 

   In cases of epidemic, introduction of vaccine is recommended. (e.g. Typhim Vi) However, vaccination doesn’t provide absolute immunity. It may develop the disease if the patient receives a large dose of the virulent bacilli. Immunization is indicated in foreign travel where typhoid fever is endemic, epidemic, and in areas exposed to a known typhoid occurrences.

Amoebic Dysentery

I. Definition

   Amoebic Dysentery also called as Amoebiasis, Protozoal Dysentery, Entamoebiasis or Amoebiasis Protozoal Infection. It is an infection of the intestine that may involve the colon, soft tissues, lungs or liver. Dysentery is an inflammatory disorder of the intestine, and more of the colon that results in severe diarrhea containing blood, mucus and pus in the stool. The frequency of stool passages is 10-30 times per day. This infection is caused by Entamoeba hystolytica. The disease can be acquired by ingestion of food or water or by sexual contact: orogenital, oroanal, proctogenital

   Entamoeba hystolytica is a parasitic protozoan of humans which is under the classification of Sarcodina of the Protozoans. These species are in vitro at 37˚C. They are widely distributed in aquatic habitats and are packed with food vacuoles with host cells & bacteria. More protozoa are recognized by a motile feeding stage called the trophozoite that requires ample food and moisture to remain active. A large number of species are also capable of entering into a dormant, resting stage called a cyst when conditions in the environment become unfavorable for growth and feeding.

II. Morphological Description

   Entamoeba hystolytica has three stages in its life cycle:

1.     The trophozoite

2.     The precyst

3.     The cyst

   1. The trophozoite - 0.1-0.6mm in size

                      - contains RBC in its inclusion; feeding

                        stage 

                      - invasive stage; has an irregular

                        finger-like shape(pseudopodium)

                      - move by extending a pseudopodium pulling

                        the rest of the body forward (called

                        the amoeboid movement)

                      - fixative: PVA (polyvinyl alcohol)

   2. The precyst - immature; forms a wall during encystment -

                    the trophozoite cell rounds up into a sphere,

                    and its ectoplasm secretes a tough, thick

                    cuticle around the cell membrane.

                  - cyst wall is composed of chitin which

                    provides resistance to environmental factors

                  - has Chromatoidal bars - short, rod-shaped

                    structures w/ rounded ends

   3. The cyst - mature; 0.1 - 0.2mm in size

               - infective stage (upon excretion with the feces)

               - cyst maturation involves 2 rounds of nuclear

                 replication w/o cell division and cysts with 1-4

                 nuclei are found in the feces

               - Fixative: formalin

              

   Pathogenecity of E. hystolytica:

      A cyst secretes 4 trophozoites. There, the trophozoites attach by fine pseudopods , multiply, actively move about and feed. The severity of infection depends on the strain of the parasite, inoculum size, diet, and host resistance.

      The secretion of lytic enzymes by the amoeba seems to induce apoptosis of host cells. This means that the host is contributing to the process by destroying its own tissues on cells from the protozoans. It invasiveness is also a clear contributor to its pathogenicity.

   E. hystolytica actions: 

      1. Amoeba secretes enzyme     

      2. Dissolves tissues

      3. Penetrate deeper mucosa

      4. Causes erosive ulcerations (dysentery = bloody, mucus-

         filled stools)

   Parasite proteins:

• Eh-lectin - responsible for the lysis within minutes of adhering to them in the presence of extracellular calcium. It is involved in resistance to complement mediated lysis.
• Amebapore - to lyse ingested bacteria
• Proteases - enzymes that degrade other proteins

III. Signs & Symptoms

   Clinical amoebiasis exist in intestinal and extraintestinal forms. The initial targets of intestinal amoebiasis are the cecum, appendix, colon, and rectum. The amoeba secretes enzymes that dissolve tissues and it actively penetrates deeper layers of the mucosa, leaving erosive ulcerations. This phase is marked by dysentery, abdominal pain, fever, diarrhea, and weight loss. The most life-threatening manifestations of intestinal infection are hemorrhage, perforation, appendicitis, and tumorlike growths called amoebomas. Lesions in the mucosa of the colon have a characteristic flask-like shape.

   Extraintestinal infection occurs when amoebas invade the viscera of the peritoneal cavity. The most common site of invasion is the liver. Here, abscesses containing necrotic tissue and trophozoites develop and cause amoebic hepatitis. Another rarer complication is pulmonary amoebiasis. Other than infrequent targets of infection are the spleen, adrenals, kidney, skin, and brain.

IV. Diagnostic/Lab Tests

• Microscopic stool for examination - For cyst or trophozoites characteristics
• ELISA tests of stool - For E. histolytica antigens
• Sigmoidoscopy
• Serological testing - For presence of antibodies to the pathogen (+)

V. Period of Communicability

   The microorganism is communicable for the entire duration of the illness.

VI. Incubation Period

 > severe infections = 3 days.

 > subacute and chronic forms = lasts for several months.

 > average cases = 3 to 4 weeks.

 > Extraintestinal amoebiasis/hepatic abscesses = years

     Asymptomatic carrier excrete 15M cysts/day while chronic carriers excrete them seldom.

VII. Prognosis

   With proper treatment, most individuals recover fully withing 2-4 weeks after beginning of treatment. Without treatment, however, mortality can be high and serious medical complication can develop such as liver, lung or brain infection (extraintestinal infections). Because medication cannot keep you from getting infected again, repeat episodes of amoebiasis may occur if you continue to travel or live in areas where amoebas are present. 

VII. Epidemiology

   E. hystolytica is harbored by chronic carrier whose intestines favor the encystment stage of the life cycle. Cyst formation cannot occur in active dysentery because the feces are so rapidly flushed from the body; but after recuperation, cysts are continuously shed in feces. The amoeba is thought to be carried by one-tenth of the world's population, and it kills up to 100,000 people a year. Occurrence is highest in tropical regions such as Africa, Asia and Latin America. Although the prevalence of the disease is lower in the United States, as many as 10 million people could harbor the agent.

VIII. Prevention

   Purification of water by means of chlorination, however may not be enough, so boiling and introduction of iodine is require. Cyst forms can be destroyed by boiling water, dessication, direct sunlight, heat or by adding 200ppm of iodine. The best way of preventing the disease is by washing your hands.

IX. Treatment

   No vaccine yet exists for the amoeba. Effective treatment usually involves the use of drugs such as iodoquinol, which acts in the feces, and metronidazole (DOC) or chloroquine, which works in the tissues. The principle behind for metronidazole is it binds to protozoal DNA to cause loss of helican structure and strand breakage, it also inhibits nucleic acid synthesis and causes cell death. The most common drug used is Flagyl. Dehydrometine is used to control symptoms but it will not cure the disease. Lost fluid and elecrolytes are replaced by oral or intravenous therapy this includes ORS, NSS and Dextrose.