Shigella spp.

Babylon University
College of Medicine
Dept.Of Microbiology
Proph.Dr.Ilham AL-Saedi Assis.Prof.Dr.Maysa Salih
Shigella spp.
• Gram – negative , non – motile rods
• Non lactose fermenters
• Not a member of normal colonic flora
Classification: 4 groups on the basis of :
• Different somatic (O) antigens & Fermentation of glucose & mannitol
1. Group a-S. Dysenteriae – 10 serotypes:
2. (Type I – shiga bacillus)- causes severe dysentery
3. Group b – S. flexneri
4. Group c – S. boydii
5. Group d – S .sonei
• Transmission :
• from person to person by four fs fingers , flies , food , and faces.
- Causes shigellosis (dysentery)
- Only a human disease
- Disease of GIT – invasion of distal ileum and colon
• Pathogenesis of Shigella:
• Very low infective dose (LD50) ,Ingestion of as few as 100 bacilli can cause disease as bacteria, are not easily killed by stomach acid.
Shigella is taken up by M cells in the Large intestine by endocytosis Bacteria are quickly released from endosomes and leaving Shigella free in the cytoplasm. The bacteria multiply &enter the inferior and lateral aspects of the epithelial cells. Actin filaments quickly form a tail and Push the bacteria in to next cell where they multiply, Macrophages that up Shigella are killed and release organism. Infected cells die and slough off. Acute inflammatory response occurs with bleeding and abscess formation.

- Organisms induce their own endocytosis by epithelial cells- particularly m – cells.
- Within 15 min they escape phagocytic vacuole – enter cytoplasm and replicate interacellularly.
- Organisms may reach lamina propria and evoke inflammatory response.
- Some strains of S. Dysenteriae produce Shiga toxin like EHEC –contributes to severity of disease.
- The toxin has a strong association with hemolytic uremic syndrome. In this RBCs break up in tiny blood vessels resulting in anemia and kidney failure.

• Clinical features of shigellosis:
- Commonly called bacillary dysentery
- Incubation period : 3-4 days
- Initially abdominal cramps followed by diarrhea (watery at first) and later on dysentery (contains blood, pus and mucous) – small volume of bloody mucoid stools.
- S .Dysenteriae - most severe , S. Sonei – mild fever
- Disease is self – limiting within few days.
• Lab identification
- Specimen: stool
- Microscopy
- Methylene blue staining to see PMNLs: if present (Invasive organisms like Shigella, Campylobacter rather than: toxin producing organisms like V. cholera, E. coli, C. perfringens).
- Culture on: MacConkey or Salmonella – Shigella agar (SS ager) non- lactose fermenting colonies identified by :
- Motility (non –motile)
- TSI –butt – acidic, slant- alkaline; no H2S Serological grouping: a-d subtypes.
-

• Treatment
- Rehydration
- Antibiotics – Ciprofloxacin is drug of choices – Ampicillin
• Immunity
- Short lived ; preparation of oral live attenuated vaccine is on the way to stimulate mucosal IgA
• Prevention
- Sanitary precautions
- Good personal hygiene(hand washing)
====================================================
Salmonella spp.
- Comprises of over 2,400 serotypes
- Parasite of intestine of poultry and animals (cattle)
- S. typhi and paratyphi – humen are the only hosts
• Antigenic structure
- Somatic (O)antigen
- Flagellar (H)antigen
- Virulence (Vi) antigen – by S. typhi and S. paratyphi
• Classification
- A. Ewing s classification three spaesies :
1. S. typhi (one serotype )
2. S. choleraesuis (one serotyhe )
3. S. enteritidis (>2,400 serotypes )
- B. Kaunfman –classification
Each serotype given a species name (>2,400 species e.g. S. Dublin,
S. tamale ect.).
• Important members are:
- S. typhi
- S. parathyphi A,B,C
- S. typhimurium
- S. choleraesuis
-
• Diseases caused by Salmonella
1. Gastorenteritis: S. typhimuriun
2. Entermia fever: S. typhi (typhoid fever), S. paratyphi A, B, C (paratyphoid fevers).
3. Bacteremia: mostly S. cholerasuis, S. typhi.
• Transmission:
- Animal food stuffs
- Poultry – (eggs infected transovarially )
- Contaminated water and vegetables
- Ingestion of raw milk has been associated with outbreak
- Seasonal variation – peak in summer – full
• Diseases caused by salmonella
- Gastroenteritis (entercolitis )
- Most common cause is S. typhimuriun but other also be the cause
- Infective dose: 10,000 bacilli or more
- Incubation period: 24-48 hours.
• Pathogenesis:
- After ingestion bacilli are internalized by induced endocytosis in the epithelial cells of ileum & colon penetrate to lamina propria inflammation and poor absorption.
- PMNL response limits infection to gut
- Bacteremia is infrequent
• Clinical features:
- Nausea & vomiting
- Abdominal cramps & diarrhea.

• Pathogenesis of Typhoid Fever:
- Salmonella are taken up by M cells in the small intestine by endocytosis.
- Bacteria multiply within endosomes and Kill M cells. Bacteria are taken up by Macrophages in Peyer s patches.
- The bacteria multiply inside cells leading To death of macrophages Are carried via Lymphatic to macrophages in mesenteric L , spleen , bone marrow where they multiply cuse bacteremia
- Symptoms of the disease problem due to endotoxins
• Virulence factor
- Invasion
- Survival & multiplication in macrophages of R.E.S.
- Vi antigen – protects o antigen – prevents phagocytosis
- Endotoxins
• Clinical features of enteric fever:
First week
- Gradual increase in fever – step – ladder pattern
• Generalized aches &pains
• Anorexia &constipation
• Relative bradycardia
Second week
- High – grade fever
- Abdominal pain &diarrhea , weakness
- Enlarged spleen , rose spots on abdomen
Third week
- If no complications – recovery starts.
- Complications of enteric fever:
- Intestinal perforation in terminal ileum
- Abscess formation
- Pneumonia
- Myocarditis , damaged heart valves
- Thrombophlebitis
- Carrier state (30%)
Typhoid Mary
- Mary Mallon was cook in a family for 3 years , and 1901 she developed typhoid fever About the same time 2 members in the house developed typhoid fever 1902 , in a new place & soon 7 member of the house were sick 1904 in a new place : four servants were attacked 1906 in another family : 6 of the 11 member of this family were attacked with typhoid At this time , the cook was first suspected 1907 she entered a home in NEW YORK city and2 months after her arrival 2 cases developed one of , which proved fatal. During these 5 years typhoid Mary is known to have been the cause of 26 cases of typhoid fever she was virtually imprisoned by the New York department of health in a hospital from March 19, 1907. Cultures taken every few days showed bacilli now and then for 3 years. Sometimes the stools contained enormous numbers of typhoid bacilli and again for days none could be found Typhoid Mart then escaped form observation until 1914. In October of that year she was engaged as cook in the Sloane hospital for women in New York. In January and February of 1915 an outbreak of typhoid occurred principally among the doctors, nurses and helper of the institution, involving 25 cases. The cook was suspected but she left the premises on a few hours leave, and did not return or leave her address. She was however; located by the health department under an assumed name and an investigation established her identity as the famous Typhoid Mary. A subsequent study of her career showed that she had infected still other individuals beyond those already mentioned, and that she may have given rise to the well- known waterborne outbreak of typhoid in Ithaca , New York , in 1903 , involving over 1300 cases . The fact is that a person by the name of Mary Mallow had been employed as a cook in the vicinity of the place where the first case appeared, and from which contamination of the water supply occurred .
-
Yersinia Pestis
- Member of family enterobacteriaceae
- Causative agent of PLAGUE (black death )
- Between 1346 -1350 million out of 105 million population of Europe died of plague
- In 1894 , Yersinia isolated the bacteria in China
-
• Mode of transmission:
? Transmission via fleas: The primary reservoir for Y. pestis is rodents (230 species, but especially rats globally, and prairie dogs and squirrels in the U.S.). Transmission among rodents and other wild animals occurs via flea bites. Many infections in humans and domestic animals (accidental hosts in terms of the life cycle of the organism) are ALSO contracted through the bite of an infected flea. Yersinia pestis express a phospholipase enzyme that allows the bacteria to avoid killing and survive in the midget of fleas. Subsequently, the blood meal in the flea s foregut clots, providing a focus for replication of the organism, and the ensuing blockage of the foregut causes regurgitation of the organisms the next time the flea tries to feed.
? Transmission by ingestion of infected animals: Ingestion of infected rodents is a common method of transmission to domestic cats, and can also be a route of infection for humans.
? Transmission through contact with body fluids from infected animals: Humans can contract Y. pestis directly through contact with blood, pus or aerosols from infected animals.
For this reason, veterinarians and wildlife personnel are at risk for zoonotic transmission. Cats are the domestic animal of most concern for zoonotic spread to veterinarians. Since 1977, 23 human cases of plague (including 5 fatal cases) have been linked to direct exposure to Y. pestis-infected cats. Six of the cases were in DVMs or their staff.

• Clinical features of plague
? Bubonic Plague
- Painful swellings,enlargement of (LN) in groin &axillae
- Fever &malaise
- Without treatment 50- 70 %deaths (due to Gram – negative septic shoch )
? Pneumonic Plague
- Fever &malaise
- Tightness in chest
- Mucoid bloody sputum
- Death within 2-3 days
• Lab identification
- Specimens: sputum , aspirate from LN
- Direct Gram – smear – G-ve bacilli with bipolar staining
- Culture : Non – lactose fermenter on MacConkey agar
• Treatment
- Streptomycin – drug of choice
• Prevention
- Urban plague : Rat control , Public health measures &Isolation of patient.
Sylvatic Plague: Difficult to control