Pathology of Salmonellosis

Pathology of Salmonellosis



When we say salmonellosis, we must be remembered the veterinary pathologist daniel salmon who discovered salmonella in 1800 s also we must remmember it kills over than 160000 people every year, yes we are talking about deadly monster but on the next pages we will discuss the causes & symptoms pathogenesis, gross & histopathological lesion that cause by salmonella & also differencial Diagnosis & and we will know what is the gross lesions & histopathological lesion of it & we try to summarized that at the end of the research.

Before that we should know that salmonella is gram negative bacteria & is the biggest causes of food poisoning in the world not just for animal but also for humans.


It is a bacterial infection caused by salmonella, which lives in intestinal tracts of animals & birds, salmonella usually transmitted to human by eating contaminated food by animal or birds fecal matter so,  The source of the infection is usually feces from infected animal. It may be difficult to tell which one is shedding bacteria due to asymptomatic and sub clinically affected animal can shed as a lot of organisms in their manure as the animals that are sick with salmonellosis. Other sources of infection may be rodents, birds (including waterfowl), flies, feral cats, dogs, raccoons and, rarely, people.

It is also very seasonal with most cases happen in the autumn, particularly around October. However cases can be seen at any time of the year and in any part of the country. Although it’s the commonest Salmonella causing disease in cattle, because, unlike other salmonellae, it’s specifically adapted to cattle, cases in humans are very unlikely and thus very rare.

Many Salmonella spp may cause enteric disease, the more common ones (to some extent different  according to geographic location) in each species are as follows: cattle S Typhimurium, S Dublin, and S Newport; sheep and goats S Typhimurium, S Dublin, S Abortusovis, S Anatum, and S Montevideo; pigs S Typhimurium and S Choleraesuis; horses—S Typhimurium, S Anatum, S Newport, S Enteritidis, and Salmonella serovar and poultry S Enteritidis, S Typhimurium, S Gallinarum, and S Pullorum.


The spread of infection varies among host species and countries and is much greater than the incidence of clinical disease, which in food animals is commonly precipitated by stressful situations as sudden taking away  of feed, transportation, drought, crowding, parturition, surgery, and administration of certain medicinal substance , including oral antibiotics. Higher susceptibility in the very young may be the result of high gastric pH, absence of a stable intestinal flora, and limited immunity.

The mainly route of infection in enteritis is fecal-oral, although infection through the upper respiratory tract and the conjunctiva have also been reported. After ingestion, the organism colonizes the digestive tract and invades and multiplies in enterocytes and tonsillar lymphoid tissue. Penetration of bacteria into the lamina propria contributes to gut destruction and diarrhea. “The complex process involves attachment through fimbrial appendages and the injection by the.attached Salmonella organisms into epithelial cells of proteins which induce changes in the actin cytoskeleton that induce membrane ruffling at the cell surface.[1] Figure1.1.This entraps the Salmonella and results in fluid secretion and their ingestion by the cell. The cellular infection leading to in activation of a host alarm process through signalling molecules as a result of the detection of bacterial surface proteins, which in turn induces a strong inflammatory response that generally is able to restrict the bacteria to the intestine  Some serotypes also become localized in the reproductive tract. Serotypes that are able to cause typhoid can modulate the initial host response and suppress the inflammatory response. Cell destruction follows, and the bacteria are ingested by phagocytic cells as macrophages and neutrophils. Although neutrophils are generally able to destroying Salmonella, the bacteria can survive and can make multiplication in side macrophages, which represent the main host cell type during infection.

As the infection continuation the situation was late , a true septicemia may follow, with subsequent localization in many areas such as;  brain and meninges, pregnant uterus, joints and distal aspects of the limbs, and tips of the ears and tails, leading to, respectively, in meningoencephalitis, abortion, osteitis, and dry gangrene of the feet, tail, or ears. The organism also frequently localizes in the gallbladder and mesenteric lymph nodes, and survivors intermittently shed the organism in the feces.

It is rarely to calves to become carriers but virtually all adults do for variable periods up to 10 wk in sheep and cattle and up to 14 mo in horses. Adult cattle infected with S Dublin may excrete the salmonella for years. Infection may also persist in lymph nodes or tonsils, without presence of salmonellae in feces. Latent carriers may begin shedding the organism or even develop clinical disease under stress. A passive carrier acquires infection from the environment but is not invaded, so that if removed from the environment, it ceases to be a carrier.

Gross lesion:-

a)In mice :-

I-Acute inflammation:-

Spleen may be enlarged 2 to 3 times than normal size. Lesions in the small intestine consist of congestion in mucosa of intestine and edema with thrombosis of the mesenteric vasculature.

II-sub-acute infections:-

multiple white to yellow foci occur in the liver, spleen is enlarged, and mesenteric lymph nodes may be enlarged and edematous Figure2.1

b)In sheep:-

1.-Periacute septicaemic form

There may be absence of gross lesions except septicaemic change (extensive submucosal and subserosal petechial hemorrhages, inflammation of lymph nodes

2-.Acute form

  • Intestine :catarrhal to hemorrhagic enteritis. Figure2.5
  • Mesenteric Lymph . Nodes :enlarged, edematous & hemorrhagic2.2
  • Gall bladder :enlarged & thickened Figure2.3
  • Liver: enlarged, pale, foci of Necrosis –>itis size is pin’s head or smaller
  • Spleen: enlarged & pulpy due to congestion then occur acute splenitis
  • There are miliary tiny foci of Necrosis or nodules
  • Serous cavities
  • Contain blood tingal fluid
  • Sub epicaridal hemorrhages
  • Chronic form
  • Intestine :superfacial Necrosis of intestinal mucosa which is proceed to the development of an extensive diphtheretic psoudo membrane appearing as yellowish gray necrotic material

Histopathological lesion:-


  • In acute stage the intestinal villi are swollen
  • The epithelial cell undergo degenerative change and Necrosis & then desquamated
  • The capillaries in the intestinal mucosa is dilated &congested while sub mucosa is edematous & infiltrated by neutrophils but, in characteristic stage intestinal gland atrophied & some are dilated due to closure of ducts by debris
  • Lamina propria is infiltrated by macrophages & lymphocyte


  • Presence of necrotic foci (typhoid granuloma ).Figure 2.4
  • There is coagulative necrosis in hepatic cells
  • Degeneration of endothelial layer & Kuffer’s cell in the affected area
  • At the margin of nicrotic area Kuffers cell well , proliferated &begin in form of cytic granuloma which extend & displace the surrounding hepatic parenchyma.
  • As this granuloma enlarge they ounre more show central necrosis

Spleen:-  Diffuse reaction of  reticulo-endothelial tissue.


lymph nodes & bone marrow show typhoid granuloma but, it is not pathognomonic for salmonellosis as it can be seen in case of tuberculosis infection.

In poultry

Gross pathology:

In Present study. The gross lesions of 17 Salmonella infected layer birds were variable during necropsy 53% liver s is friable. bronzy. discoloration with white focal Necrosis (figr. 1)atotal of 47. 1%livers were congested. & Enlarged  about 53%egg follicls were congested haemorrhagic and discolored with stalk formation while 41.2%egg follicls were mildy congested & haemorrhagic (fig. 2) Atotal of 70.6%Intestine were haemorrhagic to catarrhal enteritis while 29.4%only haemorrhagic and congested. About 64.7% lungs severaly congested and pneumonic while 35.3% lungs showed mild congestion. About 47.1%Spleens were enlarged and discolored. Similar finding with intensity and severity of lesions in different organs were described by many.

Histopathology :-

Only 17 Salmonella positive dead bird tissues of different organs were selected for histopathology. In histopathological investigation. All tissues of different organs of 17 layer birds didnot evoke similar kind of lesions. A total of 76.5%of Liver were congested and formed multifocal nodules with coagulation Necrosis while remaining 23.5%liver showed hepatitis (fig. 4) besides  76.5%lungs were severaly congested and haemorrhagic and 23.5 %lungs showed inflammatory cells in alveoli and bronchi (fig.3) infiltration of heterophils and lymphocytes in the mucosa of intestines were found in 47.1% cases. Several lymphocytic depletion and focal Necrosis in the Spleen was found in 53%birds (fig 5) whereas about 82.4%egg follicles was markedly congested and showed huge leukocytic infiltration

Differential Diagnosis :-

For  Diagnosis of salmonellosis, bacterial Isolation and identification is carried on salmonella which Present in heart blood. Spleen, Liver, lymph nodes Intestine

The most satisfactory method for immediate examination of Salmonella is thick smear from lining of Gall bladder

In cattle :the peracute form of salmonellosis must be differencial form septiceamia of E_coli

The acute enteric form confused e coccidiosis

Chr. Cases resembles the john’s diseases

  1. B: salmonellosis considered as granulomatous diseases?

Because Salmonella cause histocytic granuloma in Liver

Cause typhoid granuloma in kidney, lymph nodes bone marrow

Granuloma May be cellar reaction and called (mono nuclear Serous cells granuloma) with or without caseation and encapsulation

Granuloma – – >no neutrophitis but there is epithiold & gaint cells

Pyogranuloma–>neutrophils & gaint cells, epithiold cells

Abcess–>There is only neutrophils.

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