Bacterial Diseases Pathology Notes

Bacterial Diseases

In order to gain an upper hand in the human host, bacteria must resist early engulfment by neutrophils. They survive and damage the host in a variety of ways such as by generation of toxins (for example, Gas-forming anaerobes), by forming a slippery capsule that resists attachment to macrophages.

• For example, Pneumococci, By inhibition of fusion of phagocytic vacuoles with lysosomes (for example, Tubercle bacilli) etc.
• Provides an abbreviated classification of bacterial diseases and their etiologic agents. A few common and important examples amongst these are discussed below.

Read And Learn More Infectious Diseases

Plague

Plague has been a great killer since the 14th century (black death) and is known to have wiped out populations of cities. World over, presently about 1000 to 3000 cases are reported annually.

Plague regularly occurs in Madagascar and Brazil. However, it is not a serious health problem in modern Europe, Australia and US. In India after about 50 years quiescent period, an outbreak occurred in Surat in Gujarat state in 1994.

Etiopathogenesis:

Plague is caused by Yersinia (Pasteurella) pestis which is a small Gram-negative coccobacillus that grows rapidly on most culture media. Direct identification of the organism in tissues is possible by fluorescence antisera methods.

• Plague is a zoonotic disease spreads by rodents, primarily by rats, both wild and domestic Others are squirrels and rabbits.
• Humans are incidental hosts other than rodents. Infection to humans occurs by rat-flea or by inhalation.
• After the organisms enter the bloodstream, they reach the draining lymph nodes where, instead of being phagocytosed by phagocytic cells, they proliferate rapidly giving rise to tender lymphadenopathy.

This occurs within 24-48 hours of infection and is accompanied by:

• Chills
• Fever
• Myalgia
• Nausea
• Vomiting and
• Marked prostration

If untreated, death occurs from disseminated intravascular coagulation (DIC) within 1 to 2 days with development of widespread petechiae and ecchymoses leading to gangrene, and hence the name black death.

In other cases, death results from multi-organ failure due to profound toxaemia. The patient and his fluids are highly infectious and can be transmitted by arthropods as well as person-to-person contact, giving rise to secondary cases.

Virulence of the organism Y. pestis is attributed to the elaboration of plague toxins: pesticide and lipopolysaccharide endotoxin.

Morphologic Features:

Following forms of plague are recognised:

1. Bubonic plague, the most common
2. Septicaemic plague
3. Typhoidal plague
4. Pneumonic plague

These are:

1. Bubonic Plague: This form is characterised by rapid appearance of tender, fluctuant and enlarged regional lymph nodes, several centimeters in diameter, and may have discharging sinuses on the skin.
   • Microscopically: The features are as under:
     • Effaced architecture of lymph nodes due to necrosis in and around the affected nodes.
     • Multiple necrotising granulomas.
     • Characteristic mononuclear inflammatory response.
     • Masses of proliferating bacilli in sinusoids of lymph nodes.
     • Cellulitis in the vicinity.
2. Septicaemic Plague: This is a form of progressive, fulminant bacterial infection associated with profound septicaemia in the absence of apparent regional lymphadenitis.
3. Typhoidal Plague:  This form of plague is not associated with regional lymphadenopathy.
   • The lesions in typhoidal plague are as follows:
     • Necrotic foci in visceral lymphoid tissue.
     • Necrotic areas in parenchymal visceral organs.
     • GI manifestations with diarrhoea and pain abdomen.
4. Pneumonic Plague: This is the most dreaded form of plague that occurs by inhalation of bacilli from air-borne particles of carcasses of animals or from affected patient’s cough.
   • It is characterised by the occurrence of bronchopneumonia, with the following conspicuous microscopic features:
     • Necrosis of alveolar walls.
     • Intense hyperaemia and haemorrhages.
     • Numerous bacilli in the alveolar lumina.
     • Characteristic mononuclear inflammatory response with very scanty neutrophils.

Diseases Caused by bacteria , spirochetes and mycobacteria:

Prognosis:

If plague is treated early, the death rate is low (1-15%). However, if it is allowed to evolve into septicaemic plague, the death rate is high (40%). But pneumonic plague has the worst prognosis and is always fatal with a 100% death rate.

Anthrax

Anthrax is a bacterial disease of antiquity that spreads from animals to humans. The disease is widely prevalent in cattle and sheep but human infection is rare. However, much of knowledge on human anthrax has been gained owing to fear of use of these bacteria for military purposes by rogue countries or for bio-terrorism (page 265).

In India, anthrax in animals is endemic in most states due to the large unprotected and uncontrolled livestock population.

Etiopathogenesis:

The causative organism, Bacillus anthracis, is a gram-positive, aerobic bacillus, 4.5 µm long. It is a spore-forming bacillus and the spores so formed outside the body are quite resistant.

The disease occurs as an exogenous infection by contact with soil or animal products contaminated with spores.

Depending upon the portal of entry, three types of human anthrax is known to occur:

1. Cutaneous form: B by direct contact with skin and is most common.
2. Pulmonary form:  By inhalation, also called as “wool sorter’s disease” and is most fatal.
3. Gastrointestinal form:  By ingestion and is rare.

The mechanism of infection includes spread of bacilli from the portal of entry to the regional lymph nodes through lymphatics where the bacteria proliferate. There is delayed accumulation of polymorphs and macrophages. Macrophages also play a role in expression of bacterial toxicity; bacterial toxin is quite lethal to macrophages.

Morphologic Features:

The characteristic lesions of anthrax are haemorrhage, oedema and necrosis at the portal of entry.

1. Cutaneous anthrax: Cutaneous anthrax is the most common and occurs in two forms:
   • One type is characterised by necrotic lesions due to vascular thrombosis, or haemorrhage.
   •  Acellular necrosis, while the other form begins as a pimple at the point of entry of the organism into the abraded exposed skin, more often in the region of hands and the head and neck.
   • The initial lesion develops into a vesicle or blister containing clear serous or blood-stained fluid swarming with anthrax bacilli which can be identified readily by smear examination.
   • The bursting of the blister is followed by extensive oedema and black tissue necrosis resulting in the formation of severe ‘malignant pustule’.
   • Regional lymph nodes are invariably involved along with profound septicaemia.
2. Pulmonary anthrax (wool-sorters’ disease): Pulmonary anthrax occurs from inhalation of spores.
   • B. anthracis in infectious aerosols and results in the rapid development of malignant pustule in the bronchus.
   • This is followed by the development of primary extensive necrotising pneumonia and haemorrhagic mediastinitis which is invariably fatal.
3. Intestinal anthrax: Intestinal anthrax is rare in human beings and is quite similar to that seen in cattle.
   • Septicaemia and death often result in this type too.
   • The lesions consist of mucosal oedema, Small necrotic ulcers, massive fluid loss and haemorrhagic mesenteric lymphadenitis.

Besides, anthrax septicaemia results in the spread of infection to all other organs.

Laboratory Diagnosis: 

Anthrax can be diagnosed by a few simple techniques:

• Smear examination: Gram-stained smear shows rod-shaped, spore-forming, gram-positive bacilli. Endospores are detectable by the presence of unstained defects or holes within the cell.
• Culture: Anthrax bacteria grow on sheep blood agar as flat colonies with an irregular margin (medusa head). Anthrax-contaminated work surfaces, materials and equipment must be decontaminated with 5% hypochlorite or 5% phenol.

Whooping Cough (Pertussis)

Whooping cough is a highly communicable acute bacterial disease of childhood caused by Bordetella pertussis. The use of DPT vaccine has reduced the prevalence of whooping cough in different populations.

The causative organism, B. pertussis, has a strong tropism for the brush border of the bronchial epithelium.

The organisms proliferate here and stimulate the bronchial epithelium to produce abundant tenacious mucus:

• Within 7-10 days after exposure, the catarrhal stage begins which is the most infectious stage.
• There is low-grade fever, rhinorrhoea, conjunctivitis and excess tear production. Paroxysms of cough occur with characteristic ‘whoop’.
• The condition is self-limiting but may cause death due to asphyxia in infants. B. pertussis produces a heat-labile toxin, a heatstable endotoxin, and
• A lymphocytosis-producing factor called histamine-sensitising factor.

Microscopically:

• The lesions in the respiratory tract consist of necrotic bronchial epithelium covered by thick mucopurulent exudate. In severe cases, there is mucosal erosion and hyperaemia.
• The peripheral blood shows marked lymphocytosis up to 90% and enlargement of lymphoid follicles in the bronchial mucosa and peribronchial lymph nodes.

Donovanosis

Donovanosis also called granuloma inguinale is a sexually-transmitted disease affecting the genitalia, inguinal and perianal regions caused by Calymmatobacterium donovani.

• The disease is common in tropical and subtropical countries such as New Guinea, Southern Africa, Australia and India. The organism inhabits the intestinal tract.
• The infection is transmitted through vaginal or anal intercourse and by autoinoculation. The incubation period varies from 2 to 4 weeks.
• Initially, the lesion is in the form of a papule, a subcutaneous nodule or an ulcer.
• Within a few weeks, it develops into a raised, soft, painless, reddish ulcer with exuberant granulation tissue.
• Genitalia are involved in 90% of cases and inguinal and anal region in 10%. Regional lymphadenopathy generally does not occur.
• Microscopically, the margin of the ulcer shows epithelial hyperplasia. The ulcer bed shows neutrophilic abscesses.
• The dermis and subcutaneous tissues are infiltrated by numerous histiocytes containing many bacteria called Donovan bodies, lymphocytes, plasma cells and neutrophils.
• These organisms are best demonstrated by silver impregnation techniques.

Lymphogranuloma Venereum

Lymphogranuloma venereum (LGV) is a sexually-transmitted disease caused by Chlamydia trachomatis and is characterised by mucocutaneous lesions and regional lymphadenopathy.

• Chlamydia is no more considered a filterable viruses as was previously thought but is instead intracellular gram-negative bacteria.’
• LGV is worldwide in distribution but its prevalence rate is high in tropics and subtropics in Africa, South-East Asia and India.
• The condition begins as a painless, herpes-like lesion on the cervix, vagina, or penis.
• The organisms are carried via lymphatics to regional lymph nodes. The involved lymph nodes are tender, fluctuant and may ulcerate and drain pus.

Microscopically:

• The lymph nodes have characteristic stellate-shaped abscesses surrounded by a zone of epithelioid cells (granuloma).
• Healing stage of the acute lesion takes place by fibrosis and permanent destruction of the lymphoid structure.

Cat-Scratch Disease

Another condition related to LGV, cat-scratch disease, is caused by Bartonella henselae, an organism linked to rickettsiae but unlike rickettsiae this organism can be grown in culture.

The condition occurs more commonly in children (under 18 years of age). There is regional nodal enlargement which appears about 2 weeks after cat-scratch, and sometimes after thorn injury.

The lymphadenopathy is self-limited and regresses in 2-4 months.

Microscopically:

The changes in lymph node are characteristics:

1. Initially, there is the formation of non-caseating sarcoid-like granulomas.
2. Subsequently, there are neutrophilic abscesses surrounded by palisaded histiocytes and fibroblasts, an appearance simulating LGV discussed above.
3. The organism is extracellular and can be identified by silver stains.

Staphylococcal Infections

Staphylococci are gram-positive cocci which are present everywhere—in the skin, umbilicus, nasal vestibule, stool etc. Three species are pathogenic to human beings: Staph. aureus, Staph.epidermidis and Staph. saprophyticus.

Most staphylococcal infections are caused by Staph. aureus. Staphylococcal infections are among the commonest antibiotic-resistant hospital-acquired infection in surgical wounds.

A wide variety of suppurative diseases are caused by Staph. aureus which includes the following in given below.

1.  Infections of the skin: 
   • • Staphylococcal infections of the skin are quite common.
     • The infection begins from the lodgement of cocci in the hair root due to poor hygiene and results in obstruction of sweat or sebaceous gland duct. This is termed folliculitis.
     • Involvement of adjacent follicles results in larger lesions called furuncle. Further spread of infection horizontally under the skin and subcutaneous tissue causes carbuncle or cellulitis.
     • Styes are staphylococcal infections of the sebaceous glands of Zeis, the glands of Moll and eyelash follicles.
     • Impetigo is yet another staphylococcal skin infection common in school children in which there are multiple pustular lesions on face forming honey-yellow crusts.
     • Breast abscess may occur following delivery when staphylococci are transmitted from infant having neonatal sepsis or due to stasis of milk.
2. Infections of burns and surgical wounds: These are quite common due to contamination from the patient’s own nasal secretions or from hospital staff. Elderly, malnourished, obese patients and neonates have increased susceptibility.
3. Infections of the upper and lower respiratory tract: Small children under 2 years of age get staphylococcal infections of the respiratory tract commonly. These include pharyngitis, bronchopneumonia, staphylococcal pneumonia and its complications.
4. Bacterial arthritis:  Septic arthritis in the elderly is caused by Staph. aureus.
5. Infection of bone (Osteomyelitis):  Young boys having a history of trauma or infection may develop acute staphylococcal osteomyelitis.
6. Bacterial endocarditis: Acute and subacute bacterial endocarditis are complications of infection with Staph. aureus and Staph. epidermidis.
7. Bacterial meningitis:  Surgical procedures on the central nervous system may lead to staphylococcal meningitis.
8. Septicaemia Staphylococcal:  Septicaemia may occur in patients with lowered resistance or in patients having underlying staphylococcal infections. Patients present with features of bacteraemia such as shaking chills and fever.
9. Toxic shock syndrome:  Toxic shock syndrome is a serious complication of staphylococcal infection characterised by fever, hypotension and exfoliative skin rash. The condition affected young menstruating women who used tampons of some brands which when kept inside the vagina caused absorption of staphylococcal toxins from the vagina.

Streptococcal Infections

Streptococci are also gram-positive cocci but unlike staphylococci, they are more known for their non-suppurative autoimmune complications than suppurative inflammatory responses.

Streptococcal infections occur throughout the world but their problems are greater in underprivileged populations where antibiotics are not instituted readily.

The following groups and subtypes of streptococci have been identified and implicated in different streptococcal diseases:

1. Group A or Streptococcus: Pyogenes, also called β-haemolytic streptococci, are involved in causing upper respiratory tract infection and cutaneous infections (erysipelas).
   • In addition, β- haemolytic streptococci are involved in autoimmune reactions in the form of rheumatic heart disease (RHD).
2. Group B or Streptococcus: Agalactiae produces infections in the newborn and is involved in non-suppurative post-streptococcal complications such as RHD and acute glomerulonephritis.
3. Group C and G streptococci: Are responsible for respiratory infections.
4. Group D or Streptococcus: Faecalis, also called enterococci are important in causation of urinary tract infection, bacterial endocarditis, septicaemia etc.
5. Untypable α-haemolytic: Streptococci such as Streptococcus viridans constitute the normal
   flora of the mouth and may cause bacterial endocarditis.
6. Pneumococci or Streptococcus: Pneumoniae are etiologic agents for bacterial pneumonia, meningitis and septicaemia.

Clostridial Diseases

Clostridia are gram-positive spore-forming anaerobic microorganisms found in the gastrointestinal tract of herbivorous animals and man. These organisms may undergo vegetative division under anaerobic conditions, and sporulation under aerobic conditions.

These spores are passed in faeces and can survive in unfavourable conditions. On degeneration of these microorganisms, the plasmids are liberated which produce many toxins responsible.

The following clostridial diseases depend upon the species:

1. Gas gangrene by C. perfringens
2. Tetanus by C.tetani
3. Botulism by C.botulinum
4. Clostridial food poisoning by C. perfringens
5. Necrotising enterocolitis by C. perfringens.

1. Gas Gangrene: Gas gangrene is a rapidly progressive and fatal illness in which there is myonecrosis of previously healthy skeletal muscle due to elaboration of myotoxins by some species of clostridia. In majority of cases (80-90%), the source of mycotoxins is C. perfringens
   • Type A: Others are C. novyi and C. septicum. Generally, traumatic wounds and surgical procedures are followed by contamination with clostridia and become the site of myonecrosis.  The incubation period is 2 to 4 days. The most common mycotoxin produced by C. perfringens
   • Type A: Is the alpha toxin which is a lecithinase. The prevention of gas gangrene lies in the debridement of damaged tissue in which the clostridia thrive.  The lesion has a serosanguineous discharge with odour and contains gas bubbles. There is a very scanty inflammatory reaction at the site of gas gangrene.
2. Tetanus:
   • Tetanus or ‘lock jaw’ is a severe acute neurologic syndrome caused by the tetanus toxin, tetanospasmin, which is a neurotoxic exotoxin elaborated by C. tetani.
   • The spores of the microorganism present in the soil enter the body through a penetrating wound.
   • In underdeveloped countries, tetanus in neonates is seen due to the application of soil or dung on the umbilical stump.
   • The degenerated microorganisms liberate the tetanus neurotoxin which causes neuronal stimulation and spasm of muscles. The incubation period of the disease is 1-3 weeks.
   • The earliest manifestation is lock-jaw or trismus. The rigidity of muscles of the back causes backward arching or opisthotonos. Death occurs due to spasm of respiratory and laryngeal muscles.
3.  Botulism:
   • Botulism is characterised by symmetric paralysis of cranial nerves, limbs and trunk.
   • The condition occurs following ingestion of food contaminated with neurotoxins of C. botulinum and less often by contamination of a penetrating wound.
   • The spores of C. botulinum are capable of surviving in unfavourable conditions and contaminate vegetables and other foods, especially if improperly stored or canned.
   • The symptoms of botulism begin to appear within 12 to 36 hours of ingestion of food containing the neurotoxins (type A to type G).
   • The toxins resist gastric digestion and are absorbed from the upper portion of small intestine and enter the blood.
   • On reaching the cholinergic nerve endings, the toxin binds to membrane receptors and inhibits release of acetylcholine resulting in paralysis and respiratory failure.
4.  Clostridial Food Poisoning;
   • Clostridial food poisoning is caused by enterotoxin elaborated by C. perfringens. Out of five serotypes of C. perfringens, type A and C produce alpha-enterotoxin that causes food poisoning.
   • These serotypes of organism are omnipresent in the environment and thus clostridial poisoning occurs throughout the world.
   • Food poisoning from C. perfringens is mostly from ingestion of meat and its products which have been allowed to dry resulting in dehydration and anaerobic conditions suitable for growth of C. perfringens.
   • The contaminated meat contains vegetative form of the organism and no preformed enterotoxin (unlike botulism where preformed neurotoxin of C. botulinum is ingested).
   • On ingestion of the contaminated meat, α-enterotoxin is produced in the intestine.
   • Symptoms of the food poisoning appear within 12 hours of ingestion of contaminated meat and recovery occurs within 2 days.
5. Necrotising Enterocolitis:
   • Necrotising enterocolitis or ‘pig bel’ is caused by beta enterotoxin produced by C. perfringens Type C.
   • The condition occurs especially in undernourished children who suddenly indulge in overeating such as was first reported participation in pig feasts by poor children in New Guinea and hence the name ‘pig bel’.
   • Adults do not develop the condition due to good antibody response. Ingestion of contaminated pork by malnourished children who normally take proteindeficient vegetarian diet causes elaboration of β-enterotoxin.
   • The symptoms appear within 48 hours after ingestion of contaminated meat.

These include:

• Severe abdominal pain
• Distension
• Vomiting and
• Passage of bloody stools.A

Milder form of the disease runs a course similar to other forms of gastroenteritis while fulminant ‘pig bel’ may result in the death of the child.

• Grossly: The disease affects small intestine segmentally. The affected segment of bowel shows green, necrotic pseudomembrane covering the necrotic mucosa and there is associated peritonitis. Advanced cases may show perforation of the bowel wall.
• Microscopically:  There is transmural infiltration by acute inflammatory cell infiltrate with changes of mucosal infarction, oedema and haemorrhage. The pseudomembrane consists of necrotic epithelium with entangled bacilli.

Lyme Disease

Lyme disease or Lyme borreliosis is caused by a spirochete, Borrelia burgdorferi, that is transmitted to humans by deer ticks of the Ixodes genus (Lyme is the name of the city in Connecticut state of US where this disease was first recognised in the 1970s). It is endemic in regions having infected ticks such as some states of US (having high deer populations), throughout Europe and Japan.

The disease involves multiple organs and its clinical manifestations are divided into the following stages:

1. Early localised infection: Stage 1: The organisms multiply at the site of tick bite in the skin. After an incubation period of about 3-30 days, clinical features appear that include fever, headache, fatigue and a characteristic skin rash called erythema migrans. This stage lasts for 4-12 weeks.
2. Early disseminated infection: Stage 2:  The organisms spread by blood route throughout body and produce more disseminated features. These are: stiffness of the neck due to meningitis, migratory musculoskeletal pains, arthralgias, profound malaise and fatigue. Lymphadenopathy and cardiac arrhythmias may occur.
3. Late persistent infection: Stage 3:  Months after infection, patients develop chronic arthritis that may be accompanied with damage to large joints and thus quite disabling. A proportion of patients may continue to suffer from post-Lyme syndrome (chronic Lyme disease) after antibiotic treatment because of neurologic manifestations and features of chronic fatigue.

Bacterial Diseases:

• The plague or black death is caused by Yersinia (Pasteurella) pestis, a small gram-negative coccobacillus.
• Clinicopathologically, bubonic plague is the most common; other forms are septicaemic, typhoidal and pneumonic plague. The last one is invariably fatal.
• Anthrax is caused by Bacillus anthracis and spreads from animals to human beings.
• Depending upon the portal of entry, there are 3 types:

1. 1. Cutaneous form by direct contact with skin and is most common,
   2. Pulmonary form or wool sorter’s disease by inhalation and is most fatal, and
   3. Gastrointestinal form by ingestion and is rare.

• Whooping cough is a highly communicable acute bacterial disease of childhood caused by Bordetella pertussis and is characterised by respiratory mucosal erosions and lymphocytosis.
• Donvanosis or granuloma inguinale is a sexually-transmitted disease affecting the genitalia and inguinal and perianal regions caused by Calymmatobacterium donovani.
• Lymphogranuloma venereum (LGV) is a sexually-transmitted disease caused by Chlamydia trachomatis and is characterised by mucocutaneous lesions and regional lymphadenopathy.
• Cat-scratch disease is caused by Bartonella henselae, an organism linked to rickettsiae.
• Staphylococci cause wide variety of suppurative infections such as skin, burn wounds, upper and lower respiratory tract, joints, bones and meninges.
• Streptococci are known for their non-suppurative autoimmune complications such as in rheumatic heart disease and acute glomerulonephritis.
• Clostridia are spore-forming Gram-positive anaerobic bacteria that cause gas gangrene, tetanus, botulism and food poisoning.
• Lyme disease is caused by spirochete Borrelia burgdorferi transmitted by the vector deer tick.
• Clinically, it passes through three stages:
  • An early infection stage (having characteristic skin rash)
  • A disseminated infection stage (migratory artharlgia) and
  • Persistent infection stage (having chronic arthritis)