Download MBBS General Medicine PPT 4 Gn Infections Part II Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) General Medicine 2022 PPT 4 Gn Infections Part II Lecture Notes


Infectious diseases

4/5th Semester Classes on Infectious Diseases, 8-9AM, Tuesdays (LT-1)

Topics

1

Approach to Infectious Diseases and their prevention

2

Antibiotic stewardship practices

3

Community-Acquired Infections

4

Health Care?Associated Infections

5

Gram-Positive Bacteria (part-1)

6

Gram-Positive Bacteria (part-2)

7

Gram-Negative Bacteria (part-1)

8

Gram-Negative Bacteria (part-2)

9

Spirochetal Diseases

10

Diseases Caused by Atypical/Miscellaneous Bacterial Infections

11

Revision-cum-exam on bacteria (Must to know type)

12

Infections Due to DNA Viruses

1

13

Infections Due to RNA Viruses (part 1)

14

Infections Due to RNA Viruses (part 2)

15

HIV/AIDS ? part 1

16

HIV/AIDS ? part 2

17

Fungal Infections

18

Parasitic Infections (part 1)

19

Parasitic Infections (part 2)

20

Revision-cum-exam on Virus, Fungal, and Parasite (Must to know type)

ENTEROBACTERIACEAE

(E. coli, Klebsiella, Proteus, Enterobacter)

In healthy humans, E. coli is the predominant species of gram-negative

bacilli (GNB) in the colonic flora; Klebsiella and Proteus are less prevalent

Multiple bacterial virulence factors are required for the pathogenesis


Certain strains of E. coli are capable of causing diarrheal disease
ExPEC strains are the most common enteric GNB to cause community-acquired and

health care?associated bacterial infections (Al age groups, al types of hosts, and nearly

al organs and anatomic sites)

Humans are the major reservoir [except for STEC/EHEC]

Transmission occurs predominantly via contaminated food and water

for ETEC, STEC/EHEC/STEAEC, EIEC, and EAEC and by person-to-

person spread for EPEC (and occasionally STEC/EHEC/STEAEC)

Except in the cases of EHEC and EAEC, disease occurs primarily in

developing countries

Distinguish noninflammatory (mainly by ETEC, EPEC, and DAEC) from

inflammatory diarrhea (suggested by grossly bloody or mucoid stool

or a positive test for fecal leukocytes)

Definitive diagnosis generally is not necessary except for STEC
The mainstay of treatment for all diarrheal syndromes is replacement

of water and electrolytes, especially for STEC/EHEC/STEAEC infection

where antibiotics may increase the incidence of HUS

If diarrhea persists for >10 days despite treatment, Giardia or

Cryptosporidium should be sought
Person-to-person spread is the predominant mode of acquisition of

Klebsiel a

cKP Causes pneumonia, UTI, abdominal infection, intravascular device

infection, surgical site infection, soft tissue infection, and subsequent

bacteremia

hvKP (of Asian origin) infection distinguished from traditional infections

due to cKP by

(1) presentation as community-acquired pyogenic liver abscess
(2) occurrence in patients lacking a history of hepatobiliary disease,

and

(3) a propensity for metastatic spread to distant sites

Urine samples with unexplained alkalinity should be cultured for Proteus,

and identification of a Proteus species in urine should prompt

consideration of an evaluation for urolithiasis

Enterobacter/citrobacter/serratia/morganel a/edwardsiel a causes a

spectrum of extraintestinal infections similar to other GNB

SALMONELLA
Two species: Salmonella enterica and Salmonella bongori
Serotyping is based on the somatic O antigen (lipopolysaccharide cellwall components),

the surface Vi antigen (restricted to S. typhi and S. paratyphi C), and the flagellar H

antigen

The growth of serotypes Salmonel a typhi and Salmonel a paratyphi is restricted to human

hosts, remaining serotypes (nontyphoidal Salmonella, or NTS) can colonize the

gastrointestinal tracts of a broad range of animals, reptiles, birds, and insects

Ingestion in contaminated food or water with the ingested dose as determinant of

incubation period and disease severity

Conditions that decrease either stomach acidity or intestinal integrity increase

susceptibility to infection

Once reach the smal intestine, they penetrate the mucus layer of the gut, traverse the

intestinal layer through phagocytic microfold (M) cells that reside within Peyer's patches,

phagocytosed by macrophages but in a protective manner, and then via the lymphatics

colonize reticuloendothelial tissues

In contrast to enteric fever, NTS gastroenteritis is characterized by massive

polymorphonuclear leukocyte infiltration into both the large- and smal -bowel mucosa


Enteric (typhoid) fever is a systemic disease characterized by fever and

abdominal pain and caused by dissemination of S. typhi or S. paratyphi

Most commonly, food-borne or waterborne transmission results from fecal

contamination; Sexual transmission between male partners has been

described; Health care workers occasionally acquire too

IP; 10?14 days but ranges from 5 to 21 days
Risk factors include

1. contaminated water or ice,
2. flooding,
3. food and drinks purchased from street vendors,
4. raw fruits and vegetables grown in fields fertilized with sewage,
5. ill household contacts,
6. lack of hand washing and toilet access, and
7. evidence of prior Helicobacter pylori infection

It is estimated that there is one case of paratyphoid fever for every four

cases of typhoid fever

SYMPTOMS

SIGNS

Fever (>75%)

coated tongue (51?56%),

headache (80%)

relative bradycardia at the peak of high

anorexia (55%)

fever (<50%)

chills (35?45%)

rose spots (30%),

Abdominal pain (30-40%)

splenomegaly (5?6%),

cough (30%)

abdominal tenderness (4?5%)

sweating (20?25%)

hepatosplenomegaly (3?6%),

myalgias (20%),

epistaxis,

nausea (18?24%),

vomiting (18%),

diarrhea (22?28%)

Constipation (13?16%)

malaise (10%)

arthralgia (2?4%).

The development of severe disease (which occurs

in ~10?15% of patients) depends on host factors,

strain virulence and inoculum, and choice of

antibiotic therapy

? Gastrointestinal bleeding (10?20%)

? Intestinal perforation (1?3%)

? Neurologic manifestations (2-40%)


Up to 10% of untreated patients excrete S. typhi in the feces for up to 3 months, and 1

?4% develop chronic asymptomatic carriage, shedding S. typhi in either urine or stool

for >1 year

The definitive diagnosis of enteric fever requires the isolation of S. typhi or S. paratyphi

from blood, bone marrow, intestinal secretions,(THESE 3 IN COMBINATION POSITIVE

>90%) other sterile sites, rose spots, and stool

Serologic tests, including the classic Widal test for "febrile agglutinins," and rapid tests

to detect antibodies to outermembrane proteins have lower positive predictive

values than blood culture

Two typhoid vaccines:

(1)Ty21a, (given on days

1, 3, 5, and 7, with a

booster every 5 years);

(2)Vi CPS, (given in a

single dose, with a

booster every 2 years)

cumulative efficacy was

48% for Ty21a at 2.5?3.5

years and 55% for Vi CPS

at 3 years

SHIGELLA
Shigella cannot be distinguished from Escherichia coli by DNA hybridization and

remains a separate species only on hstorical and clinical grounds

Unlike E. coli, is nonmotile and does not produce gas from sugars
Human intestinal tract represents the major reservoir
Bacteria are transmitted most efficiently by the fecal-oral route via hand

carriage, rarely by flies and sexually

Highest prevalences in the most impoverished areas
Shigellosis typically evolves through four phases:

1. Incubation (1?4 days),
2. Watery diarrhea,
3. Dysentery - dysentery--a clinical syndrome of fever, intestinal cramps, and frequent

passage of small, bloody, mucopurulent stools

4. Postinfectious phase ? Reactive arthritis, toxic megacolon, and HUS (in developing

countries)

Ciprofloxacin is recommended as first-line treatment; others like ceftriaxone,

azithromycin, pivmecillinam, and some fifth-generation quinolones


VIBRIO

Cholera now refers to disease caused by V. cholerae serogroup O1 or O139--

i.e., the serogroups with epidemic potential

Responsible for seven global pandemics and much suffering over the past two

centuries

In nature, vibrios most commonly reside in tidal rivers and bays under conditions

of moderate salinity; They proliferate in the summer months

Cholera is predominantly a pediatric disease in endemic areas, but it affects

adults and children equal y when newly introduced into a population

Cholera toxin, toxin-coregulated pilus, and several other virulence factors are

coordinately regulated by ToxR With IP 24- to 48-h

Some individuals are asymptomatic or have only mild diarrhea; others present

with the sudden onset of explosive and life-threatening diarrhea (cholera

gravis); "rice-water" stool WITH absent fever; Complications derive exclusively

from the effects of volume and electrolyte depletion

Clinical suspicion of cholera can be confirmed by the identification in stool
Treatment; first and foremost requires fluid resuscitation with macrolides (DOC)

PSEUDOMONADS (an inability to ferment lactose)
Pseudomonas, Burkholderia, and Stenotrophomonas
The pathogenicity is based on opportunism with the exceptions (melioidosis by

Burkholderia pseudomallei and glanders by B. mallei)

P. aeruginosa remains the most common contributing factor to respiratory

failure in Cystic Fibrosis

B. cepacia gained notoriety as the cause of a rapidly fatal syndrome of

respiratory distress and septicemia (the "cepacia syndrome") in CF patients

Cytotoxic chemotherapy, mechanical ventilation, and broad-spectrum

antibiotic therapy probably paved the way for colonization and infection

P. aeruginosa is found in most moist environments; infection Often occurs

concomitantly with host defense compromise

Of the common gram-negative bacteria, no other species produces such a

large number of putative virulence factors

Among gram-negative bacteria, it probably produces the largest number of

substances that are toxic to cells and thus may injure tissues


P. aeruginosa causes infections at almost all sites in the body but shows a rather

strong predilection for the lungs

Bacteremia; only point differentiating this entity from gram-negative sepsis of other

causes may be ecthyma gangrenosum, which occur almost exclusively in markedly

neutropenic patients and patients with AIDS

Combination therapy became the standard of care, recently newer

antipseudomonal drugs (colistin, tigecycline, cefepime) can be used as

monotherapy

ACINETOBACTER

Acinetobacter baumannii is particularly formidable because of its propensity to

acquire antibiotic resistance determinants

Contrary to previous thought of nonmotile characteristic it demonstrate motility

under certain growth conditions

Widely distributed in nature, like water, soil, on vegetables, a component of the

skin flora, and sometimes a contaminant in blood samples

Colonizes patients exposed to heavily contaminated hospital environments or

to the hands of health care workers

It must be considered in the dif erential diagnosis of hospital-acquired

pneumonia, central line?associated bloodstream infection, posttraumatic

wound infection in military personnel, and postneurosurgical meningitis

It should be suspected when plump coccobacil i are seen in Gram's-stained

samples

Only sulbabctam, cotrimoxazole, carbapenams, amikacin, tigecycline, colistin

are possible treatment


HELICOBACTER

It colonizes the stomach in ~50% of the world's human population, essentially

for life unless eradicated by antibiotic treatment

Humans are the only important reservoir
Lifelong colonization may offer some protection against complications of

gastroesophageal reflux disease (GERD), including esophageal

adenocarcinoma

Treatment against the organism prevent/treat PUD and low-grade gastric MALT

lymphoma, however, no benefit in the treatment of gastric adenocarcinoma

Nongastric (intestinal) Helicobacter species can cause clinical features

resembling those of Campylobacter infections

Prevalence varies with age: H. pylori is usually acquired in childhood, The age

association is due mostly to a birth-cohort effect

Combination of factors lead to disease state: bacterial strain dif erences, host

susceptibility to disease, and environmental factors


Whether or not the ulcers are currently active, H. pylori should be eradicated in

patients with documented ulcer disease to prevent Relapse

Overall most treatment of asymptomatic H. pylori carriage is given without a firm

evidence base

Test-and-treat has emerged as a common clinical practice
CAMPYLOBACTER

Campylobacter, Arcobacter, and Helicobacter
It is more common than that due to Salmonel a and Shigel a combined
Although acute diarrheal illnesses are most common, these organisms may cause

infections in virtually al parts of the body, especially in compromised hosts, and these

infections may have late nonsuppurative sequelae (Reactive A, GBS)

The human pathogens fall into two major groups:

those that primarily cause diarrheal disease (C. jejuni mainly)
those that cause extraintestinal infection (C. fetus mainly)

Transmitted to humans in raw or undercooked food products or through direct contact

with infected animals

The symptoms of Campylobacter enteritis are not sufficiently unusual to distinguish this

illness from that due to Salmonel a, Shigel a, Yersinia, and clostridium (inflammatory

bacterial diarrhea)

Diagnosis of inflammatory bowel disease should not be made until Campylobacter

infection has been ruled out

Indications for therapy include high fever, bloody diarrhea, severe diarrhea, persistence

for >1 week, and worsening of symptoms

A 5- to 7-day course of erythromycin (250 mg orally four times daily) is DOC

Thank you

This post was last modified on 05 April 2022